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Vol. 2, Nr. 4(8), 2007
PRACTICA
MEDICALÅ
Editat de
Societatea Academicå de
Medicinå a Familiei (SAMF)
website: www.samf.ro
Pentru informa¡ii ¿i abonamente vå
rugåm så ne scrie¡i la adresa de
email: info@samf.ro
Copyright © SAMF, 2007
Notå legalå:
Toate datele, informa¡iile ¿i protocoalele
din revista PRACTICA MEDICALÅ pot fi
citate, reproduse sau adaptate, absolut
gratuit ¿i nediscre¡ionar, cu obliga¡ia fermå
de a specifica sursa, astfel: „preluat/adaptat
din/dupå PRACTICA MEDICALÅ“
Publisher: Empire Publishing
Redactor-ªef
Prof. Dr. Adrian RESTIAN
Redactor-ªef adjunct
Conf. Dr. Dumitru MATEI
Redactori coordonatori
Prof. Dr. Elena ARDELEANU – Timi¿oara
Conf. Dr. Lumini¡a BELDEAN – Sibiu
ªef Lucr. Dr. Constantin CÂRSTEA – Bra¿ov
Prof. Dr. Viorela ENÅCHESCU – Craiova
Prof. Dr. Eugeniu ILICEA – Constan¡a
Prof. Dr. Afilon JOMPAN – Arad
Prof. Dr. Pal Istvan KIKELI – Târgu-Mure¿
Prof. Dr. Aurel LAZÅR – Oradea
Prof. Dr. Silvia MÅTÅSARU – Ia¿i
Prof. Dr. Sabin OPREA – Cluj-Napoca
Prof. Dr. Rodica PETROVANU – Ia¿i
Prof. Dr. Georgeta SINIºCHI – Ia¿i
Consiliul Editorial:
Dr. Viorel ALEXANDRESCU – Bucure¿ti (epidemiologie)
Prof. Dr. Eduard APETREI – Bucure¿ti (cardiologie)
Conf. Dr. Corin BADIU – Bucure¿ti (endocrinologie)
Dr. Dorin BEGHER – Arad (medicinå de familie)
Dr. Valer BISTRICEANU – Buzåu (medicinå de familie)
Prof. Dr. Eugen CIOFU – Bucure¿ti (pediatrie)
Conf. Dr. Adrian COSTACHE – Bucure¿ti (ultrasonografie)
Conf. Dr. Floarea DAMASCHIN – Constan¡a (igienå ¿i ecologie)
Prof. Dr. Mircea DICULESCU – Bucure¿ti (hepatogastroenterologie)
Prof. Dr. Constantin DUMITRU – Bucure¿ti (neurologie)
Conf. Dr. Doina FELEA – Ia¿i (medicinå de familie)
Prof. Dr. Adrian GEORGESCU – Bucure¿ti (pediatrie)
Prof. Dr. Ioan GHERGHINA – Bucure¿ti (pediatrie)
ªef Lucr. Dr. Ioana GRÅJDEANU – Bucure¿ti (medicinå de familie)
Dr. George HABER – Alba-Iulia (medicinå de familie)
Prof. Dr. Constantin IONESCU-TÂRGOVIªTE – Bucure¿ti
(diabet, nutri¡ie, metabolism)
Prof. Dr. Nicolae IORDACHE – Bucure¿ti (chirurgie)
Conf. Dr. Constantin MARICA – Bucure¿ti (pneumoftiziologie)
Prof. Dr. Dimitrie NANU – Bucure¿ti (obstetricå-ginecologie)
Prof. Dr. Adriana Sarah NICA – Bucure¿ti (balneofiziokinetoterapie)
Prof. Dr. Alexandru OPROIU – Bucure¿ti (hepatogastroenterologie)
Conf. Dr. Viorel N. PÂRVULESCU – Craiova (medicinå de familie)
Prof. Dr. Florin TUDOSE – Bucure¿ti (psihiatrie)
Prof. Dr. Radu VLÅDÅREANU – Bucure¿ti (obstetricå-ginecologie)
Prof. Dr. Radu VOIOSU – Bucure¿ti (hepatogastroenterologie)
Editor asociat
Dr. Mihai-Cristian POPESCU
 Revista Practica Medicalå – Romanian Journal of Medical Practice (Rom J Med Pract) –
este revistå academicå, mizând pe criterii, autori, colaboratori ¿i subiecte de elitå ¿i care se apleacå
asupra celor mai noi studii, articole originale, descoperiri ¿i controverse din toate specialitå¡ile
medicale.
Revista ¿i-a recâ¿tigat locul pe care îl meritå în doar doi ani de la relansare, fapt confirmat de
o cre¿tere explozivå a tirajului, impunându-se drept norma cercetårii ¿tiin¡ifice actuale. O revistå
care se bucurå de popularitate în rândul medicilor ¿i al celor interesa¡i de subiectele puse în
discu¡ie încå de la primul numår ¿i care se va ridica, în mod constant, la nivelul a¿teptårilor
acestora.
Practica Medicalå este revista oficialå a Societå¡ii Academice de Medicinå a Familiei
(S.A.M.F.) din România. Este vorba de o revistå cu personalitate, dând dovadå de viziune de
ansamblu ¿i perspectivå realistå, prin care a dobândit credibilitate, consecven¡å ¿i integritate.
Parteneriate interne ¿i interna¡ionale:
– Journal of Family Practice, SUA
– Canadian Family Physician, Canada
– Reuters-Health
– principalele reviste oficiale ale celorlalte societå¡i medicale din România.
Indexare interna¡ionalå: Revista Practica Medicalå este indexatå în celebrele baze de date
Scirius, Scopus, getCITED, WAME ¿i EBSCO, ¿i în curs de indexare în MedSci Communications,
Medical-Journals EMBASE, ProQuest ¿i Medline.
Revista Practica Medicalå este acreditatå CNCSIS.
Colaborarea cu departamentele medicale ale companiilor farmaceutice a înlesnit posibilitatea
de a publica în premierå noutå¡ile de pe pia¡a medicalå – legate de indica¡ii noi ¿i medicamente
nou înregistrate, lansåri sau relansåri de produs – ¿i a permis ca revista så devinå o reflectare
fidelå a vie¡ii medicale, ce poate reda cu acurate¡e cursul evenimentelor.
Pornind de la realitatea cå medicina de aståzi este dependentå sau, cel pu¡in, legatå de com-
ponenta economicå, Sec¡iunea Juridicå/Financiarå a revistei î¿i propune så ofere cititorilor såi
informa¡ii ¿i instrumente utile fie în accesarea diferitelor tipuri de fonduri, fie în abordarea diferitelor
situa¡ii ivite în via¡a de zi cu zi a medicului (modele de contracte comentate).
Practica Medicalå se dovede¿te, cu fiecare numår, un instrument indispensabil speciali¿tilor
care vor så fie la curent, în timp real, cu evolu¡ia realitå¡ii medicale.
Pentru autori: Pute¡i trimite articole spre publicare la adresa redactia@samf.ro. Dupå validarea
acestora de cåtre Consiliul Editorial, articolele vor fi publicate în revistå cu maximå prompti-
tudine.
Pentru cititori: Pentru abonamente vå rugåm så scrie¡i pe adresa info@samf.ro, sau så consul-
ta¡i site-ul S.A.M.F. (www.samf.ro).
Web-Site: Practica Medicalå este prezentå ¿i on-line pe site-ul S.A.M.F. (www.samf.ro),
precum ¿i pe site-ul A.M.R. (www.medica.ro), iar pânå la sfâr¿itul anului va fi disponibilå ¿i
varianta electronicå a revistei, în format pdf, atât la nivelul abstractelor, cât ¿i al articolelor
integrale!
 PRACTICA MEDICALÅ

CUPRINS

EDITORIAL
Banii care conduc medicina ....................................................................................... 239
A. Restian

REFERATE GENERALE

1. Actualizåri oportune. Conferin¡a Na¡ionalå de Medicina Familiei

Bucure¿ti, 25-27 Octombrie 2007 ............................................................................. 243
T. Nicolescu

2. Alcoholic hepatitis – current concepts and management ......................................... 246

M. Manuc, M. Diculescu

3. Dislipidemiile ¿i rela¡ia lor cu patologia generalå ..................................................... 254

V.N. Pârvulescu, Rodica Tråistaru, Viorela Enåchescu, L. Mihai, Ligia Florea,
S. Beznå, Vica Ciuvå¡, Cristina Bårbulescu, Cristina Braica-Lupu

4. Canalul atrio-ventricular comun ................................................................................ 262

Silvia Måtåsaru

CAZURI CLINICE

5. Tablou hematologic de împrumut într-un neoplasm mamar cu metastaze

medulare. Importan¡a biopsiei medulare – caz clinic ................................................ 268
Ana-Maria Vladareanu, Irina Voican, Veronica Vasilache, Cristina Ciufu,
H. Bumbea, Madalina Begu, Anca Nicolescu, Minodora Onisai, Sanziana Radesi,
Camelia Dobrea, Carmen Ardeleanu, Viola Popov, D. Jinga

ACTIVITATEA PREVENTIVÅ

6. Which lifestyle interventions effectively lower LDL cholesterol? .............................. 274

Elizabeth Powers, J. Saultz, A. Hamilton

7. Does a low-fat diet help prevent breast cancer? ........................................................ 280

Elizabeth Steiner, D. Klubert, Meg Hayes, A. Hamilton

8. What we really need to do to reduce cardiovascular events

in hypertensive patients ............................................................................................. 283
HT ONG, FRCP (Glas, Edin), FACC, FESC

PREVENºIA ÎN MF
9. BNP ca factor predictiv al morbiditå¡ii ¿i mortalitå¡ii cordului pulmonar acut ......... 291
A. Lazår, L. Lazår, M. Rus

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 235

CUPRINS

10. Riscul cardiovascular la pacien¡ii cu diabet zaharat ¿i hipertensiune

arterialå ...................................................................................................................... 297
A. Jompan, C. Cârstea

11. Postul ¿i beneficiile lui pentru sånåtate ..................................................................... 302

Floarea Damaschin

REVISTA PRESEI MEDICALE

Americans spend most on Lipitor, drug survey finds ................................................ 245

Maggie Fox

Liber la E-uri. Ministerul Sånåtå¡ii introduce aditivi periculo¿i în alimente ............. 260
Claudia Marcu, Andreea Petrescu

Medicii nu mai pot så-¿i cumpere cabinetele medicale ........................................... 261

Alina Enache

Medicii vor cabinetele, cum s-au privatizat fabricile: pe promisiuni

de investi¡ii ................................................................................................................ 267
Gardianul

Food additives may cause hyperactivity: study ........................................................ 272

Maggie Fox

Statin withdrawal after stroke worsens outcome ...................................................... 273

Reuters/Health

Human stem cells heal the hearts of rats .................................................................. 282

Maggie Fox

Elve¡ia: cancerul învins cu ajutorul luminii ¿i metalelor .......................................... 290

Alic Mirza

Too much TV ups kids’ risk of attention problems .................................................... 296

Anne Harding

Santaj?!? ..................................................................................................................... 304

Denisa Mårun¡oiu

236 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007

 PRACTICA MEDICALÅ

CONTENTS

EDITORIAL
The money that controls the medical system ............................................................ 239
A. Restian

GENERAL REPORTS

1. Useful updates. The National Conference of Family Medicine

Bucharest, October 25-27, 2007 ............................................................................... 243
T. Nicolescu

2. Alcoholic hepatitis – current concepts and management ......................................... 246

M. Manuc, M. Diculescu

3. Dyslipidemias and their relationship with general pathology ................................... 254

V.N. Parvulescu, Rodica Traistaru, Viorela Enachescu, L. Mihai, Ligia Florea,
S. Bezna, Vica Ciuvat, Cristina Barbulescu, Cristina Braica-Lupu

4. The common atrioventricular channel ....................................................................... 262

Silvia Matasaru

CLINICAL CASES

5. Bone marrow metastatic breast carcinoma presenting as a full blood

leukemia picture. The importance of bone marrow biopsy – case report ................. 268
Ana-Maria Vladareanu, Irina Voican, Veronica Vasilache, Cristina Ciufu,
H. Bumbea, Madalina Begu, Anca Nicolescu, Minodora Onisai, Sanziana Radesi,
Camelia Dobrea, Carmen Ardeleanu, Viola Popov, D. Jinga

PREVENTIVE ACTIVITY

6. Which lifestyle interventions effectively lower LDL cholesterol? .............................. 274

Elizabeth Powers, J. Saultz, A. Hamilton

7. Does a low-fat diet help prevent breast cancer? ........................................................ 280

Elizabeth Steiner, D. Klubert, Meg Hayes, A. Hamilton

8. What we really need to do to reduce cardiovascular events

in hypertensive patients ............................................................................................. 283
HT ONG, FRCP (Glas, Edin), FACC, FESC

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 237

CONTENTS

PREVENTION IN MF
9. BNP as predictive factor of morbidity and mortality in acute pulmonary
heart disease .............................................................................................................. 291
A. Lazar, L. Lazar, M. Rus

10. Cardiovascular risk of patients with diabetes mellitus and hypertension ................. 297
A. Jompan, C. Carstea

11. The health benefits of fasting ..................................................................................... 302

Floarea Damaschin

MEDICAL PUBLICATIONS REVIEWS

Americans spend most on Lipitor, drug survey finds ................................................ 245

Maggie Fox

No restriction to additives. The Ministry of Health approves

the introduction of potentially dangerous food additives ........................................ 260
Claudia Marcu, Andreea Petrescu

Doctors can no longer purchase their practices ....................................................... 261

Alina Enache

Medics want their practices. The manners in wich factories were

privatized on investment promises ........................................................................... 267
Gardianul

Food additives may cause hyperactivity: study ........................................................ 272

Maggie Fox

Statin withdrawal after stroke worsens outcome ...................................................... 273

Reuters/Health

Human stem cells heal the hearts of rats .................................................................. 282

Maggie Fox

Switzerland: cancer was depleated with the help of light and metals ...................... 290
Alic Mirza

Too much TV ups kids’ risk of attention problems .................................................... 296

Anne Harding

A blackmail?!? ............................................................................................................ 304

Denisa Maruntoiu

238 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007

 EDITORIAL

Banii care
conduc medicina
The money that controls
Prof. As. Dr. Adrian RESTIAN the medical system

Medicina modernå este o ¿tiin¡å, iar medicii cautå så aplice în practica medicalå cele
mai noi cuceriri ale ¿tiin¡ei. Dar dacå unii dintre dumneavoastrå mai cred cå
cercetarea ¿tiin¡ificå pleacå de la observa¡ie, de la curiozitatea ¿i de la pasiunea
proverbialå a cercetåtorului ¿tiin¡ific, se în¿alå. A trecut de mult vremea în care
Isaac Newton ståtea la umbra unui pom ¿i privind cum cad merele din pom a descris
legea gravitå¡ii universale, sau vremea în care Claude Bernard, experimentând pe
animale de laborator, a descoperit mediul intern în care se desfå¿oarå fascinantele
procese ale vie¡ii.

A
ståzi cercetåtorii nu mai pleacå de la
observa¡ie, de la ipotezå ¿i de la
experiment, ci de la nevoile pie¡ii, sau
mai precis de la nevoile companiilor
de medicamente. De aceea aståzi,
Isaac Newton, care a pus bazele mecanicii, nu ar
mai putea så stea lini¿tit la umbra unui pom ¿i så
mediteze asupra merelor care cad ¿i nici Claude
Bernard, care a apus bazele medicinii moderne,
nu ar mai putea så facå experien¡e de dragul
cunoa¿terii ¿tiin¡ifice.
Aståzi, din påcate, aceastå posibilitate a cu-
noa¿terii ¿tiin¡ifice dezinteresate a dispårut. Aståzi,
pentru a cerceta ceva trebuie så ai bani. Nici o
descoperire nu este valabilå dacå nu poate deveni
un business. Acest lucru este valabil ¿i în cerce-
tarea medicalå. Dar atunci cine mai face cercetare
medicalå ¿i cine plåte¿te cercetarea medicalå?
Cercetarea medicalå este plåtitå în mare parte
de stat. Toate ¡årile dezvoltate au institute de cercetåri
foarte bine utilate în care lucreazå mii de cercetåtori,
care au fåcut descoperiri epocale. Acestea desfå-
¿oarå mai ales o cercetare ¿tiin¡ificå fundamentalå,
care ajunge mai târziu în practica medicalå.
Dar cercetare medicalå mai fac ¿i firmele de
medicamente. Se spune cå firmele de medica-
mente investesc 30% din profit în cercetarea
¿tiin¡ificå. ªi este absolut incontestabil cå multe
firme de medicamente au contribuit la progresul
medicinii moderne.
Dar dacå statul investe¿te ace¿ti bani fårå
preten¡ia de a-i recupera imediat, firmele de me-
dicamente sunt societå¡i comerciale care trebuie
så-¿i recupereze cât mai rapid banii investi¡i. ªi
cum pot ele så î¿i recupereze banii investi¡i decât
de la stat, care are obliga¡ia de a asigura într-un
fel sånåtatea cetå¡enilor lui ¿i de la pacien¡i care
trebuie så-¿i plåteascå cel pu¡in o parte dintre
medicamentele de care au nevoie. Dar pentru a
cumpåra medicamentele necesare, bolnavii au
nevoie de o re¡etå sau cel pu¡in de o recoman-
dare. ªi a¿a începe povestea firmelor de medica-
mente de a låmuri bolnavii så cumpere medica-
mentele care se elibereazå fårå re¡etå ¿i de a-i låmuri
pe medici så prescrie medicamentele respective.
ªi pentru aceasta, firmele care nu au nici ele
o via¡å u¿oarå, deoarece concuren¡a este din ce
în ce mai mare, recurg la cele mai ingenioase
metode. Sponsorizeazå conferin¡e ¿i congrese,
apeleazå la somitå¡i sau la liderii de opinie pentru
a ¡ine conferin¡e, oferå pliante, reviste ¿i cår¡i,
cokteiluri ¿i mese festive, excursii în interes ¿tiin¡ific,

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 239

EDITORIAL
dar ¿i în interes turistic, nu numai pentru medici,
ci ¿i pentru familiile acestora, în care pot merge cu
so¡ia, cu copiii sau cu soacra. Fac tot ce pot pentru
a låmuri, pentru a manevra, pentru a manipula ¿i
pentru a corupe pe medici sau pe administratorii
de spitale. Ele ¿tiu cå nici un om nu este inco-
ruptibil, numai cå fiecare om are pre¡ul såu.
Dar pe lângå activitatea de promovare a
produselor care trebuie vândute, firmele desfå-
¿oarå ¿i o intenså cercetare ¿tiin¡ificå pentru gåsirea
unor noi produse. ªi aceastå activitatea nu este
deloc u¿oarå, din câteva mii de substan¡e cerce-
tate numai una reu¿ind så intre pe pia¡å. Pe lângå
cåutarea unor noi substan¡e, ele mai desfå¿oarå
cercetåri postmarketing, efectueazå direct sau
indirect trialuri pentru a demonstra cu dovezi cât
mai valide cå produsele lor sunt cele mai bune.
Pe de altå parte, ele cautå så gåseascå noi calitå¡i
ale produselor aflate deja pe pia¡å ¿i så lårgeascå
sfera lor de ac¡iune. Evident cå toatå aceastå
activitate a contribuit la progresul extrem de rapid
al medicinii moderne
Dar în felul acesta medicina a devenit un business,
iar bolnavul un pretext. În centrul sistemului se
aflå banul ¿i nu bolnavul care a devenit un pretext
în numele cåruia se organizeazå sisteme de
sånåtate tot mai sofisticate ¿i se consumå tot mai
mul¡i bani. Iar atunci când bolnavul apeleazå la
sistemul sanitar se simte hår¡uit ¿i umilit, dupå
cum aratå Silviu Stanciu conform unui interviu
(Editorial, Stetoscop, 61, 2007).
Dar ce dovadå mai bunå dori¡i pentru faptul
cå bolnavul este un pretext, decât adevårul cå
farmaci¿tii câ¿tigå infinit mai bine decât un medic,
iar medicii care lucreazå la firmele de medica-
mente câ¿tigå de 10 ori mai bine decât un medic
care se ocupå de bolnavi, ca ¿i când societatea ar
fi interesatå mai mult de vânzarea de medica-
mente decât de îngrijirea bolnavului.
Aceastå situa¡ie nu este specificå României, ci
întregii lumi. Dupå cum aratå Charles Stein, banii
sunt catalizatorul pentru o medicinå mai bunå
(Money is the catalzst for good medicine, The
Boston Globe, 3 oct. 2004). Fårå bani nu se poate
face nimic. Dar medicina are alte scopuri nu acela
de a face bani. În toate ¡årile statul cheltuie bani
pentru sånåtatea cetå¡enilor såi. Dupå cum aratå
Maggie Mahar, autoarea cår¡ii Money-Driven
Medicine, în 1970 SUA au alocat 7,1% din uria¿ul
lor produs intern brut pentru sånåtate. În 2000
au alocat 16%, iar în 2020 se estimeazå så aloce
21%. Dar câ¡i bani aloca¡i pentru sånåtate ajung
direct sau indirect la bolnav, aceasta este o altå
problemå, pentru cå se gåsesc peste tot båie¡i
de¿tep¡i care s-au specializat în volatilizarea lor.
Maggie Mahar aratå cå peste 30% din bani sunt
cheltui¡i pe investiga¡ii inutile, pe proceduri discu-
240 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
tabile ¿i pe medicamente foarte scumpe, care nu
sunt deloc mai bune decât medicamentele mai
ieftine, dar care î¿i fac o reclamå foarte agresivå,
atât printre medici, cât ¿i printre bolnavi. Iar dupå
cum aratå Don Borwich, aproape 50% din banii
investi¡i pentru sånåtate sunt irosi¡i în alte scopuri.
La noi în ¡arå, dupå cum a aråtat Cristian Vlådescu,
între 2003 ¿i 2005 s-au cheltuit de patru ori mai
mul¡i bani fårå a se ob¡ine rezultate deosebite
(More money for less satisfaction in Romanian’s
Health Insurance System, London, 2005).
Dupå cum aratå Marcia Angell, editorialist la
New England Journal of Medicine, amestecul
dintre bani ¿i medicinå este o combina¡ie foarte
periculoaså. Banii pot compromite medicina. O
pot deturna de la nobila ei misiune, exploatând
nevoile reale ale pacien¡ilor, inducând în rândul
påacien¡ilor false nevoi ¿i chiar false speran¡e.
În acest sens s-ar putea da exemplul obsesiei
colesterolului ¿i a mitului statinelor. Toatå lumea
este de acord cå cre¿terea colesterolului se aflå la
baza multor boli fatale, cum ar fi infarctul de
miocard ¿i accidentele vasculare cerebrale. Pentru
prevenirea ¿i combaterea lor pe lângå regimul
hipolipidic ¿i practicarea exerci¡iilor fizice se admi-
nistreazå o serie de statine. Primul trial efectuat
în 1994 denumit 4S (Scandinavian Simvastatin
Survival Studz Group: Randomised trial of choles-
terol lowering in 4444 patients with coronarz
heart disease, Lancet 344, 1994, 1383-1389) a
aråtat cå simvastatina poate reduce cu 5% morta-
litatea cardiovascularå.
Al¡i cercetåtori au aråtat cå tratând 1000 de
pacien¡i cu statine putem preveni 2 decese, 6
infacte miocardice non-fatale ¿i 2 accidente
vasculare cerebrale non-fatale.
Ulterior s-a constatat cå statinele au efecte
favorabile nu numai la bolnavii cu hipercoleste-
rolemie, ci ¿i la bolnavii cu o colesterolemie
normalå ¿i s-a emis ipoteza cå acest efect se
datoreazå activitå¡ii antiinflamatoare a statinelor.
Astfel s-a atras aten¡ia asupra rolului pe care îl
are inflama¡ia în procesul de aterosclerozå, pre-
cum ¿i în alte boli, cum ar fi boala Alzheimer.
Astfel statinele au ajuns så fie cele mai prescrise
medicamente din lume. 11 milioane de americani
folosesc zilnic o statinå. Iar Atorvastatina, sau
Lipitor, este cel mai prescris medicament din lume.
Tratatamentul cu statine este foarte bun, dar
foarte scump. El costå aproximativ 1,4 dolari pe
zi. Firmele câ¿tigå foarte bine. Dar de¿i realizau
o cifrå de afaceri foarte bunå, firmele producå-
toare au încercat så lårgeascå aria de utilizare a
statinelor. În acest sens s-a încercat utilizarea
statinelor la indivizii sånåto¿i pentru preven¡ia pri-
marå a bolilor cardiovasculare. Înså trialul WOSCOP
(West Scotland Coronarz Prevention Study)

efectuat pe 10.000 de indivizi sånåto¿i nu a dat
rezultatele a¿teptate.
Inten¡ia de a extinde administrarea medica-
mentelor ¿i la oamenii sånåto¿i au avut-o ¿i alte
firme de medicamente, cum ar fi cele care produc
antihipertensive. Dupå cum aratå Stephanie Saul
(The New York Times, 20 mai 2006), unele com-
panii producåtoare de antihipertensive au donat
Societå¡ii Americane de Hipertensiune suma de
700.000 de dolari pentru ca aceasta så modifice
în a¿a fel defini¡ia prehipertensiunii arteriale încât
cel pu¡in o parte dintre pacien¡ii cu prehiper-
tensiune (120/80-139/89) så fie încadra¡i în HTA
stadiul I ¿i deci så li se recomande un tratament
medicamentos. Dupå schimbarea defini¡iei 65 de
milioane de americani au devenit hipertensivi, iar
al¡i 59 de milioane de americani se aflå la grani¡a
HTA. Încasårile firmelor au crescut de la 15 bi-
lioane dolari la 17 bilioane dolari. Purtåtoarea
de cuvânt a Societå¡ii Americane de Hiperten-
siune, Susan Rood a recunoscut cå exper¡ii soci-
etå¡ii au primit granturi de peste 700.000 de
dolari de la firmele respective.
Constatând cå administrarea atorvastatinului
la oamenii sånåto¿i nu då rezultatele a¿teptate,
firmele producåtoare de statine au cåutat så
creascå dozele. Au fåcut studiile respective ¿i în
2005 au comunicat medicilor, dar ¿i pacien¡ilor
cå în doze mai mari atorvastatinul då rezultate
mai bune (Cholesterol drug best in the large doses,
The Vancuver Sun, 9 martie 2005). Dar compa-
niile nu au specificat cå de¿i dozele mari de ator-
vastatin previn mai bine evenimentele cardiace,
ele nu reduc mortalitatea generalå. Diferen¡a de
mortalitate fiind determinatå probabil tocmai de
efectele adverse ale dozelor mai mari. De aceea,
pe bunå dreptate, John Abramson ¿i-a intitulat
cartea sa Overdosed America. Pe de altå parte,
dupå cum aratå Margaret Munro (Media, medicine
and big time money, The Thunderbird, 28 aprilie,
2005), 11 dintre autorii studiilor respective au avut
legåturi financiare cu firmele producåtoare.
De¿i statinele au efecte secundare destul de
rare, cum ar fi dispepsia, crampele musculare,
pruritul, vertijul, mialgiile ¿i rabdomioliza, se
vorbe¿te ¿i mai pu¡in despre ele. Totu¿i, apro-
ximativ 2% dintre pacien¡i sunt obliga¡i så între-
rupå tratamentul din cauza reac¡iilor adverse.
Una dintre reac¡iile adverse ale statinelor cel
mai pu¡in discutatå este reprezentatå de redu-
cerea sintezei coenzimei Q10. Julian Whitaker
aratå cå inhibând HMO-CoA reductaza, statinele
inhibå ¿i sinteza de coenzimå Q10, care intervine
în lan¡ul respirator, de producere a energiei
celulare ¿i care este unul dintre cei mai puternici
antioxidan¡i ai celulei, contracarând astfel efectele
devastatoare ale stresului oxidativ. De aceea
EDITORIAL
scåderea coenzimei Q10 poate contribui la
apari¡ia cardiomiopatiei ¿i a insuficien¡ei cardiace.
Dar se vorbe¿te foarte pu¡in despre asta. În acest
sens, David Blumental de la Institute for Health
Policy, Massachusetts, aratå cå firmele cautå de
obicei så minimalizeze efectele negative ale me-
dicamentelor pe care le produc.
Cazul statinelor, care sunt cele mai comercia-
lizate medicamente, este înså un caz fericit, în
care de¿i s-a constatat tendin¡a de a interveni în
cercetarea ¿tiin¡ificå ¿i de a lårgi cât mai mult
posibil indica¡ia terapeuticå, cercetarea ¿tiin¡ificå
sus¡inutå de firmele producåtoare a contribuit
totu¿i la progresul medicinii moderne.
Nu acela¿i lucru se poate spune înså despre
alte medicamente, cum ar fi inhibitoarele de
COX2, în care existau încå de la început anumite
indicii privind efectele adverse cardiovasculare.
Dupå ce li s-au fåcut o reclamå foarte agresivå,
s-a constatat cå afectarea cardiacå a fost mai mare
decât protec¡ia digestivå. Dupå cum aratå Margaret
Munro, Vioxx, a¿a numita superaspirinå, ar fi
contribui la moartea a 60.000 de americani ¿i a
6.000 de canadieni. De aceea Richard Horton,
editorul revistei Lancet, a considerat Vioxx ca o
catastrofå medicalå.
Iatå deci cå trialurile, ghidurile ¿i dovezile pe
care noi ne chinuim så ni le însu¿im cât mai re-
pede, sunt de fapt ni¿te lucruri foarte relative.
Nu pentru cå trialurile ¿i dovezile (la care eu ¡in
atât de mult ¿i militez pentru o medicinå bazatå
pe dovezi) ar fi de vinå, ci pentru cå banii au
infectat cercetarea ¿tiin¡ificå medicalå, a¿a dupå
cum aratå Amy Barett ¿i Kerry Capell (When
medicine and money don’t mix, Business Week,
28 iunie, 2004).
Banii de la firmele de medicamente au påtruns
în mediul academic. În acest sens, Marcia Angell
se întreabå dacå banii au compromis medicina ¿i
dacå mediul academic este de vânzare. Dupå
cum aratå cercetåtorii de la Yale University, dacå
în 1980 aproximativ 32% dintre studiile universi-
tare erau finan¡ate de firmele de medicamente,
în 2000 peste 62% dintre studiile universitare sunt
finan¡ate de firmele de medicamente. ªi cum
toate se plåtesc, s-a ajuns în situa¡ia în care ne
aflåm aståzi, în care nu mai ¿tim care este gradul
de încredere pe care trebuie så îl avem într-o
cercetare ¿tiin¡ificå ¿i uneori ne este foarte greu
så vorbim despre o medicinå bazatå pe dovezi. Ce
dovezi? Dovezile plåtite de firmele de medicamente.
Aceasta l-a determinat pe George Soros så
aloce 15 milioane de dolari pentru a combate
corup¡ia ¿i influen¡a banilor în medicinå (www.
Soros.org/initiative/map/news). Dar suma s-ar
putea så fie mult prea micå în compara¡ie cu
sumele vehiculate de firmele de medicamente.
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 241
EDITORIAL
ªi atunci ce este de fåcut? Ei bine, mare lucru
nu se poate face. Tendin¡a omului de a recurge
la toate mijloacele pentru a câ¿tiga cât mai mul¡i
bani nu poate fi combåtutå. Probabil înså cå
situa¡ia nici nu este chiar atât de gravå cum s-ar
pårea la prima vedere. În fond nu existå un adevår
absolut ¿i nici un medicament perfect. Încå nu
s-a descoperit piatra filosofalå a tinere¡ii fårå
båtrâne¡e ¿i a vie¡ii fårå boli. Toate medicamentele
au pe lângå efectele pozitive ¿i efecte negative.
Evident cå unele sunt mai bune, iar altele sunt
mai rele. Deosebirea dintre medicamentele stu-
diate este înså de multe ori foarte micå. Aceastå
diferen¡å nu depå¿e¿te uneori diferen¡a dintre
medicament ¿i placebo. Evident cå firmele exa-
gereazå pu¡in, iar uneori exagereazå chiar mai
mult. Evident cå reclama lor agresivå ne poate
duce în eroare ¿i tendin¡a de a ne corupe ar putea
så dea roade. Evident cå agresivitatea firmelor ar
mai putea fi potolitå pu¡in. Dar fårå medicamente
nu se poate tråi. Iar obiectivitatea absolutå nu
existå. De aceea toatå greutatea cade pe capul
medicului practician care trebuie så aibå o ati-
tudine criticå. El trebuie så priveascå cu oarecare
rezervå toate afirma¡iile care se fac. El trebuie så
discearnå ce este bine ¿i ce este råu. Afirma¡iile
cercetåtorilor ar putea fi corecte, dar ar putea fi
¿i exagerate. Din påcate aceea¿i rezervå va trebui
så o manifeståm ¿i asupra trialurilor, a meta-
analizelor, a recenziilor sistematizate ¿i a dovezilor
pe care ni le aduc firmele. ªi aceasta este o
problemå foarte dificilå deoarece ele erau un
foarte bun instrument de lucru.
242 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
De aceea dupå ce în 1992 D.H. Sackett a
definit medicina bazatå pe dovezi ca activitatea
de aplicare con¿tientå ¿i judicioaså a celor mai bune
dovezi în practica medicalå, våzând probabil cå nici
dovezile nu sunt chiar atât de clare ¿i de simplu de
aplicat în practica medicalå, în 2002 el a redefinit
medicina bazatå pe dovezi considerând-o ca o
activitate de integrare a celor mai bune dovezi cu
experien¡a medicului ¿i cu valorile bolnavului. În
felul acesta se amestecå de fapt dovezile cele mai
bune oferite de trialurile randomizate ¿i de
metaanalize, cu dovezile cele mai slabe reprezentate
de opiniile medicilor ¿i a exper¡ilor. Dar nu avem
ce face, oricum nu putem renun¡a la experien¡a
medicului care trebuie så personalizeze tratamentul
recomandat de ghiduri ¿i de trialuri.
Astfel, judecate prin prisma experien¡ei
medicului, medicamentele cele mai bune vor
supravie¡ui, iar cele mai proaste vor dispårea,
indiferent de dovezile pe care le aduc firmele de
medicamente, deoarece pânå la urmå via¡a le
a¿azå pe toate la locul lor, chiar dacå vor exista,
din påcate, ¿i unele pierderi colaterale. Oricum,
un medicament nu-¿i gåse¿te locul lui în porto-
foliul de medicamente ale medicului practician
decât dupå câ¡iva ani de utilizare. Pentru a putea
face fa¡å acestei situa¡ii trebuie så dåm dovadå de
multå, de foarte multå experien¡å. De aceea cred
cå se în¿alå aceia care cred cå pot så transforme
medicul într-un prestator de servicii sau cå folosind
acela¿i ghid un student poate pune acela¿i
diagnostic ca un medic cu multå experien¡å. ‰

Bucure¿ti, 25-27 Octombrie 2007
Dr. Tiberiu NICOLESCU
The National Conference of Family Medicine,
Bucharest, October 25-27, 2007
Unitatea de Management a Proiectului Fondului Global, Ministerul Sånåtå¡ii
C
elor are au asistat ¿i la precedenta
edi¡ie (vezi Practica Medicalå nr. 3-
4/2006), participarea la Conferin¡a
Na¡ionalå de Medicina Familiei –
2007 le-a oferit, nemijlocit, cel pu¡in
douå constatåri. Prima, cå evenimentul vine în
întâmpinarea unor nevoi recunoscute; a doua,
cå instituirea anualå a unui început de tradi¡ie atrage
consecin¡e dincolo de up-date-ul profesional.
Så må explic. Mai întâi, orice profesionist onest
implicat în medicinå resimte nevoia de a-¿i actu-
aliza cuno¿tin¡ele prin revizitarea bazelor teoretice
sau a rezultatelor cercetårii aplicate. Individual, e o
nevoie perceputå. Participarea înså, în numår atât
de mare, la o conferin¡å, a fost o recunoa¿tere
public asumatå a nevoii profesionale de bazå ¿i a
unui mod în care aceasta poate fi satisfåcutå. A fost
cazul recentei conferin¡e. A doua observa¡ie:
reîntâlnirea universitarilor ¿i a colegilor practicieni a
avut efect de rapel: al sentimentului apartenen¡ei
la breaslå ¿i, contingent, a celui de relativå siguran¡å.
În economia afectivå, ambele sunt esen¡iale. Odatå
stimulate, confra¡ii au devenit mai deschi¿i comu-
nicårii profesionale, adevårata mizå a reuniunii.
Conferin¡a a beneficiat de organizarea eficace a
Societå¡ii Academice de Medicinå a Familiei, cu
sprijinul a numeroase companii farmaceutice, care
s-au constituit în expozan¡i genero¿i cu participan¡ii,
furnizând ¿i teme pentru simpozioane. Mai pu¡in
omogene tematic decât în 2006, dar interactiv
moderate, sesiunile (câte 2 în fiecare jumåtate de
zi) au reunit prezentåri acoperind o plajå largå a
cazuisticii din medicina primarå, prin sec¡iunile:
patologie respiratorie, imunoprofilaxie, diabet
PRACTICA MEDICALÅ
REFERATE GENERALE 1
Actualizåri oportune.
Conferin¡a Na¡ionalå
de Medicina Familiei
Useful updates.
Dr. TIBERIU NICOLESCU
zaharat ¿i boli endocrine, pediatrie, patologie on-
cologicå, cardiologie preventivå ¿i boli cardio-
vasculare, hepato-gastro-enterologie, neuropsi-
hiatrie, reumatologie, medicinå alternativå. Dintre
lucrårile unor nume sonore ale medicinei româ-
ne¿ti ¿i ale practicienilor, am re¡inut pe cele mai
apreciate de asisten¡å. ‰
ZIUA 1
Prof. Dr. F. Tudose a deschis seria prezentårilor
cu „Depresia din patologia cardiacå în practica
medicinei de familie“. Bolile cardiovasculare î¿i
vor påstra primul loc între cauzele de mortalitate,
dar pânå în 2020 depresia va ajunge, ubicuu pe
mapamond, a doua în topul morbiditå¡ii. Comor-
biditatea e prezentå la cca 45% dintre pacien¡i,
iar sindromul depresiv al coronarienilor este cauzå
de necomplian¡å la tratament ¿i factor agravant
al evolu¡iei BCI. Noile antidepresive din categoria
ISRS nu mai au efecte secundare cardiotoxice,
asocierea antiischemic – antidepresiv devenind
lipsitå de risc cardiovascular.
Abordând subiectul la modå al inteligen¡ei
emo¡ionale, Prof. Dr. D. Constantin a fost în asen-
timentul asisten¡ei afirmând cå „ceea ce ne distruge
e via¡a afectivå“, dar a încheiat printr-un discutabil
raccourci sus¡inând cå “de boala cauzatå de emo¡ii
distructive ne vindecåm acceptând iertarea”.
Inciden¡a Attention Deficit Hyper Activity
Disorder (ADHD) ¿i Tulburårii de Spectru Autist
a crescut în ultimii 10 ani, a comunicat Prof. Dr.
Iuliana Dobrescu. Doar 15% dintre adul¡ii care
au suferit în copilårie de ADHD mai fac controale
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 243
ACTUALIZÅRI OPORTUNE. CONFERINºA NAºIONALÅ DE MEDICINA FAMILIEI
de specialitate, consecin¡ele tulburårii impietând,
chiar la distan¡å în timp, asupra comportamentului
lor social.
Simpozionul Lilly a supus aten¡iei disfunc¡ia
erectilå, din recomandårile Dr. V. Iconaru re¡i-
nând cå reglatorul acesteia nu trebuie administrat
concomitent cu nitra¡i sau alfa-blocan¡i, în doze
mai mari de 1 Cp/zi, iar efectul lui trebuie precedat
de stimulul sexual natural.
Continuându-¿i cercetarea aplicatå ¿i spiritul
ludic, Prof. Dr. R. Vlådåreanu a prezentat noutå¡i
de profilaxie a cancerului de col uterin. 50-80%
dintre femeile active sunt la risc de contaminare
cu Human Papiloma Virus, riscul maxim este sub
vârsta de 25 ani, iar contactul sexual complet nu
e necesar, fiind suficient cel genital cutanat. În
99,7% dintre biopsiile de col uterin cu displazii
premergåtoare cancerului a fost gåsit HPV, aso-
cierea HPV-CCU fiind de 50 de ori mai puternicå
decât cea fumat-cancer pulmonar. Vaccinurile
recent apårute con¡in primele 2 cele mai frecvente
tipuri HPV (16, 18); pot fi administrate la femei
între 15 ¿i 55 de ani, au efect protector pentru un
interval de 4 ani, AC råmânând în circula¡ie timp
de 5 ani ¿i jumåtate; optim este ca prima dozå så
fie fåcutå în adolescen¡å, înaintea debutului vie¡ii
sexuale. Mai ales acolo unde programele de
screening pentru depistarea CCU nu au eficien¡a
scontatå, vaccinarea HPV este cea mai bunå
strategie preventivå.
Profesionist având experien¡å mai mare decât
vârsta tinerilor medici, d-na Dr. Carmen Ciofu a
oferit un regal de semiologie pediatricå în imagini,
animat de convingerea pedagogicå „un doctor tânår
care n-a våzut niciodatå, nu recunoa¿te citind cår¡i“.
În stilul såu binecunoscut, Prof. Dr. D.D. Ionescu
a fåcut o legåturå ¿tiin¡ificå ¿i pragmaticå între
cercetarea aplicatå ¿i terapiile cardio-vasculare
accesibile în ambulator (simpozionul Teva). Citåm
3 idei: (i) România e pe primul loc în UE la procentul
de AVC care duc la invaliditå¡i, (ii) în monoterapie,
orice antihipertensiv este asemånåtor de eficient,
(iii) costul unui medicament nu mai are importan¡å
dacå este eficace ¿i bine tolerat de pacient. ‰
ZIUA 2
Adesea, copilul poate tu¿i o lungå perioadå.
Cum, la adult, primele 3 cauze de tuse sunt
astmul, refluxul gastro-esofagian ¿i „scurgerile post-
nazale“, un copil care tu¿e¿te 3-4 såptåmâni este,
frecvent, etichetat cu astm. Conf. Dr. I. Cernåtescu
a subliniat cå astmul – varianta tuse, trebuie
suspectat doar când tusea recurentå se asociazå
cu hiper-reactivitate bron¿icå, atopie ¿i råspuns bun
la medica¡ia bronho-dilatatoare. ªi diferen¡iat de
rino-sinuzita cronicå, refluxul gastro-esofagian,
fumatul pasiv, în copilårie (pårin¡i fumåtori – copii
tu¿itori) sau activ, în adolescen¡å.
244 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
Cu privire la aceea¿i temå, îmbinând datele
actuale din literaturå cu experien¡a personalå,
colectivul de la Ia¿i coordonat de d-na Conf. Dr.
Doina Felea a subliniat rolul medicinei primare
¿i al ambulatorului de specialitate în diagnostica-
rea corectå ¿i în timp util a etiologiei tusei cronice
sau recidivante.
Un colectiv de speciali¿ti de la INDNBM, condus
de Prof. Dr. C. Ionescu-Târgovi¿te, a propus un scor
de risc al DZ bazat pe factori de predictibilitate
precum ereditatea, vârsta, sexul, talia, BMI (IMC),
TA, dislipidemia. Medicii de familie au fost invita¡i
så se implice în validarea protocolului, ¿tiind cå
determinarea glicemiei à jeun identificå DZ în doar
60% dintre cazuri ¿i cå proba hiperglicemiei
provocate nu poate fi efectuatå sistematic.
În continuare, colectivul d-nei Prof. Dr. Rodica
Petrovanu, UMF Ia¿i, a prezentat riscul cardiome-
tabolic ¿i terapia adaptatå riscului cardiometabolic
în contextul depistårii clinice ¿i monitorizårii în
medicina primarå ¿i ambulatorul de specialitate
ale hipertensiunii arteriale. Preven¡ia ¿i abordarea
holisticå a sindromului metabolic este o prioritate
în medicina primarå; el reune¿te diabetul zaharat
¿i hipertensiunea arterialå esen¡ialå pe „solul
comun“ al insulinorezisten¡ei. Abordårile terape-
utice urmåresc ghidurile din 2007.
În pauza mare a celei de-a doua zi a avut loc
o dublå lansare: „Esen¡ialul în Medicina Familiei“,
a Conf. Dr. D. Matei (carte riguros sistematizatå,
incluså în mapa conferin¡ei, oferitå de editura
Amaltea tuturor participan¡ilor) ¿i „Medicamentele
medicului de familie“, a Prof. Dr. B. Cuparencu
¿i Conf. Dr. D. Mure¿an.
Pe parcursul discu¡iilor care au urmat, Prof.
Dr. A. Restian a abordat problema îmbåtrânirii
în practica medicalå, comentând douå concepte
la modå în ultimii ani: (1) Radicalii liberi (cu rol
mai mic decât cel prezumat) ¿i Antioxidan¡ii (de
asigurat printr-o dietå consistent vegetarianå,
reducåtoare a ra¡iei calorice) ¿i (2) Medicina Bazatå
pe Dovezi (EBM) – care, de la aplicarea judicioaså
a celor mai bune dovezi, ¿i-a flexibilizat semni-
ficativ defini¡ia în fa¡a realitå¡ii, recomandând
acum aplicarea dovezilor integrând experien¡a
medicului ¿i specificul cazului tratat.
În simpozionul Servier au fost apreciate, cu
deosebire, douå prezentåri. „Controlul HTA –
ghiduri de practicå noi cu obiective cunoscute“,
a ¿ef de lucr. Dr. Roxana Darabon¡, a relevat cå
doar 25% dintre hipertensivii trata¡i ating ¡inta
terapeuticå, 61% au TA deasupra acesteia, iar
prevalen¡a HTA e constantå în popula¡ie în timp
ce utilizarea medicamentelor în cre¿tere. A doua,
„Angina pectoralå – abordåri multiple înseamnå
tratament optim“ a apar¡inut Dr. V. Vintilå.
Dna Prof. Dr. Silvia Måtåsaru a prezentat mal-
forma¡iile cordului la copil (PCA), cauze ¿i terapii
adecvate.
 ACTUALIZÅRI OPORTUNE. CONFERINºA NAºIONALÅ DE MEDICINA FAMILIEI

Alte douå subiecte au avut, la sfâr¿itul celei de-a
doua zi, vådit impact. Minicursul ilustrat de eco-
grafie, al Conf. Dr. A. Costache – care a exem-
plificat utilitatea ¿i beneficiile ultrasonografiei la
nivelul consulturilor de medicinå primarå; MF au
fost încuraja¡i så urmeze cursul de formare atestatå.
ªi simpozionul GSK, „Managementul actual al
RGE“, al Prof. Dr. M. Diculescu ¿i Dr. M. Ciocârlan.
Inhibitorii pompei de protoni se pot administra ¿i
în tratamentul bolilor cronice – nefiindu-le, la 10-
20 ani, dovedit riscul de mortalitate; dar dozele ¿i
schemele de administrare trebuie adaptate tipu-
rilor de leziuni ¿i prezen¡ei/absen¡ei Hp. ‰
ZIUA 3
Dupå impactul asupra auditoriului, ultima zi
a avut 3 puncte de interes major. „Bolile cronice
la copil“, prezentarea Prof. Dr. E. Ciofu – pre¿e-
dinte al conferin¡ei, a amintit cå în România nu
existå statistici clare asupra prevalen¡ei bolilor
cronice la copii, aspect ce ar merita discutat la o
întâlnire de anvergurå na¡ionalå. Dintre pro-
bleme, au fost aduse în discu¡ie obezitatea ¿i HTA
primitivå la copii.
De cel mai mare succes la public s-au bucurat
titlurile Conf. Dr. Lumini¡a Beldean, „Aspecte de
diagnostic ¿i tratament al disfunc¡iilor endocrine
la copil“ ¿i „Pubertatea“ – savuros comentatå prin
butada „un båiat se maturizeazå cu 2 ani mai
devreme decât cred pårin¡ii lui ¿i cu 3 ani mai
târziu decât crede el“.
„Pacientul oncologic în practica medicului de
familie“ – lucrare unui colectivului condus de Prof.
Dr. Viorela Enåchescu a sumarizat recomandåri
pentru depistarea precoce a cancerului la indivizi
asimptomatici cu risc mediu.
Unele prezentåri vor fi publicate, in extenso,
în revistele de specialitate „Practica Medicalå“ ¿i
„Maedica“. Pentru profesioni¿tii deja sensibiliza¡i,
conferin¡a a devenit un reper anual de ne-ratat.
Pentru cei care încå nu au descoperit-o, ecourile
ei, speråm, le vor stârni curiozitatea. ‰

Revista presei medicale

Americans spend most on Lipitor,
drug survey finds
Reporting by MAGGIE FOX,
editing by JULIE STEENHUYSEN and BILL TROTT

WASHINGTON, Sept 12 (Reuters):
U.S. consumers spent more money on
the cholesterol-lowering drug Lipitor –
more than $9 billion – than any other
prescription drug in 2004, according
to federal estimates released on
Wednesday.
Cholesterol drugs in general raked
in the most money for their makers,
according to the survey by the Agency
for Healthcare Research and Quality.
While adults of all ages spent more
on Pfizer’s (PFE.N: Quote, Profile,
Research) Lipitor than any other
single drug, the survey found Merck
and Co’s (MRK.N: Quote, Profile)
Zocor was second with $4.7 billion in
sales.
Stomach acid drugs also accounted
for a large chunk of prescription spen-
ding. AstraZeneca’s (AZN.L: Quote,
Profile, Research) Nexium accounted
for $4.2 billion in 2004 spending while
Prevacid, sold by a joint venture of
Abbott Laboratories Inc (ABT.N:
(The Reuters Messaging: Maggie.Fox.Reuters.com@reuters.net; tel: Washington Newsroom 202-898-8300)
Quote, Profile, Research) and Takeda
Pharmaceutical Co Ltd (4502.T:
Quote, Profile, Research), brought in
more than $2.4 billion.
Antidepressant Zoloft, also made
by Pfizer, took in $1.9 billion in
spending by adults aged 18 to 64.
For children aged 17 and under,
the most money was spent on Merck’s
asthma drug Singulair – $680 million.
Johnson & Johnson’s attention deficit
drug Concerta ranked second, with
spending of $490 million.
Rival ADHD drugs Strattera,
made by Eli Lilly and Co (LLY.N:
Quote, Profile, Research) and Adderall,
made by Shire Plc (SHP.L: Quote,
Profile, Research), both also brought
in more than $400 million in annual
spending each.
The allergy drug Zyrtec, made by
Belgian pharmaceutical group UCB
(UCBBt.BR: Quote, Profile, Research),
made $420 million in sales to the
under-18 group.
Key words: DRUGS SPENDING/USA
For Americans aged 65 and older,
Lipitor and Zocor ranked first and
second in total 2004 spending,
followed by Plavix, an antiplatelet
drug made by Sanofi-Aventis (SASY.
PA: Quote, Profile, Research) (SNY.
N: Quote, Profile, Research) at $1.7
billion.
Seniors spent $1.5 billion on Pfizer’s
Norvasc, a calcium channel blocker
drug that treats high blood pressure
and chest pain.
The survey did not include spen-
ding on generic and over-the-counter
drugs, which are far cheaper than
prescription drugs that have few or no
generic rivals. Many of the drugs in
the study are now sold generically.
The survey also excluded drugs that
are administered in a doctor’s office or
hospital, such as cancer drugs. The full
survey is available at http://www.
meps.ahrq.gov/mepsweb/data_files/
publications/st180/stat180.pdf.

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 245

 2 PRACTICA MEDICALÅ
REFERATE GENERALE

Alcoholic hepatitis – current

concepts and management
MIRCEA MANUC, MD, PhD; MIRCEA DICULESCU, Prof., MD, PhD
“Fundeni” Clinical Institute, National Center of Gastroenterology and
MD, Mircea MANUC Hepatology, Bucharest, Romania

ABSTRACT
Alcoholic hepatitis is a form of acute injury to liver tissue that is also a precursor of cirrhosis, and carries
significant morbidity and mortality. Severe alcoholic hepatitis in particular causes a high short-term mortality,
and also places an enormous burden on healthcare resources.
The treatment of alcoholic hepatitis remains one of the most debated topics in medicine and a field of continued
research. In this review, we discuss the clinical point of view (evolution of scoring systems), the current
solutions on management, and the perspectives of new drugs.
Nutritional support, medical therapy with glucocorticoids, pentoxifylline, infliximab, s-adenosyl-methionine,
colchicine and other drugs are reviewed, as well as the role othotopic liver transplantation (OLT). Glucocorticoids
currently remain the mainstay of treatment for severe alcoholic hepatitis.

INTRODUCTION term for “alcohol use” with “alcohol abuse”, and

A
lcoholic liver disease is one of the top
ten leading causes of death in
developed countries, responsible for
3% of all deaths (1). Age adjusted
death rate from alcohol induced liver
disease accounts for 40% of deaths from cirrhosis
or 28% of all deaths from liver disease (2).
The syndrome of alcoholic hepatitis develops
in only a minority of chronic alcohol abusers (3),
with a clinical spectrum ranging from an asymp-
tomatic histological diagnosis to a life-threatening
clinical illness that may include jaundice, ascites,
gastrointestinal bleeding or encephalopathy.
While alcoholic hepatitis is common, its patho-
genesis, predictors for survival, and treatment
remain debated. The prevalence of the disease,
its high fatality rate, and the elusiveness of cure
keeps this disease in the forefront of topic reviews
and scientific investigations. ‰
EPIDEMIOLOGY AND CLINICAL DATA
Alcohol intake – how much is “too much”?
This topic is of major importance in current
medical practice, as many people confuse the
other people believe that they do not actually
drink if they use low alcohol concentration
beverages. It has to be said from the beginning
that, regarding the hepatic toxicity, it is not the
type of drink that matters, but only the amount
of pure alcohol that is used.
According to epidemiological data, a man who
drinks more than 4 units/day or 14 units/week,
respectively a woman who drinks 3 units/day or
7 units/week are exposed to the risk of developing
chronic liver disease (1 unit equivalent to 14 grams
of absolute alcohol) (4).
Although, we must not forget that, in the
presence of additional factors (age over 65 (5),
co-morbidities – HCV (6), hemochromatosis,
diabetes mellitus (7), drug use (8) even intake
below this doses may cause liver injury (9). Also,
during pregnancy, abstinence must be recom-
mended in order not to affect the mother and
the child (10).
Population-based studies show that in USA,
as in Western Europe, 68% of the population
drinks alcohol at least once a month. About 10%
of the population drinks at least 2 units/day. From
these alcohol abusers, in time 80-100% will

246 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007

 ALCOHOLIC HEPATITIS – CURRENT CONCEPTS AND MANAGEMENT
develop liver steatosis, 13-35% alcoholic hepatitis
and 10-20% liver cirrhosis (11).
Alcoholic hepatitis – clinical and laboratory
data
This entity covers a large clinical spectrum,
from subclinical, asymptomatic forms (consisting
of biochemical and histological changes) to the
acute fulminant hepatic failure.
This large clinical variability is the main cause
for the underdiagnose of this entity. On the other
hand, the occurrence of steatohepatitis is an
important prognostic factor in the evolution of
chronic liver disease (12).
Severe forms present fever, anorexia, painful
liver enlargement (90%), splenomegaly (50%),
jaundice, ascites (40-50%), encephalopathy. In
a severe evolution, renal failure occurs and the
general condition is worsening. The patients who
need hospitalization for this reason have a short-
term mortality (one month) of 40-50% (13).
Lab results show leukocytosis with neutrophilia
(correlated to the severity of liver injury) and high
levels of aminotrasferases (usually below 400 IU/
l) (14). The increased seric levels of bilirubin and
prothrombin time are correlated to the degree
of liver involvement, being included in the scores
for the stratification of the severity of the disease
(15).
Scoring systems
Patients stratification for therapy allocation and
prognostic evaluation is important in current
medical practice. There are several scoring
systems that may be used in alcohol-induced liver
disease (Child-Pugh, Maddrey, MELD, or recently
published Lille model).
1. The Child-Pugh score is the most fre-
quently used score in cirrhotic patients, irrespec-
tive of etiology, with an uncontestable prognostic
value (16). There is although evidence that in
alcoholic hepatitis other scoring systems have a
better prognostic value.
2. The Maddrey score takes into account the
prothrombin time and bilirubin, two parameters
that proved to be independent mortality factors
in patients with ethanolic hepatitis (17). A
Maddrey score > 35 shows a severe alcoholic
hepatitis with bad prognosis and the addition of
encephalopathy predicts a mortality rate > 50%
(18). The value of this score is diminished by some
interfering elements such as the large variability
of prothrombin time among different centers(19).
For this reason, some authors recommend other
scoring systems.
3. The MELD score (Mayo Endstage Liver
Disease) was developed for patients with terminal
liver cirrhosis and include parameters that also
appear in the Madrrey score. In addition, it also
includes parameters that have a prognostic role,
such as creatinin levels, which predicts an eventual
development of the hepato-renal syndrome.
There is evidence that the MELD score may also
be used in patients with alcoholic cirrhosis, having
a predictive value similar to the Maddrey score
(20). Although, there are also some restraints in
using this score in the current clinical practice,
mainly concerning the lack of a well defined cut-
off value and the fact that the MELD on day 7
after admission would be more useful than the
score at admission (21).
4. The GAHS score (Glasgow Alcoholic
Hepatitis Score) was especially created for
alcoholic hepatitis, taking into account the
variables that are independently associated to
mortality by this disease (22). Patients with a
GAHS greater than or equal to 9 have an
extremely poor prognosis if they are not treated
with corticosteroids, or if such treatment is
contraindicated (23). The superiority of this score
compared to those formerly presented is still
uncertain, further studies being needed to reach
this conclusion.
5. The Lille model is the last proposed scoring
system for evaluating the prognosis of alcoholic
hepatitis (24), and of course is not yet validated
A specific prognostic model was generated by
logistic regression in order to identify candidates
early on for alternative therapies. The model
combining six reproducible variables (age, renal
insufficiency, albumin, prothrombin time, bil-
irubin, and evolution of bilirubin at day 7) was
highly predictive of death at 6 months. Patients
above an ideal cutoff of 0.45 showed a marked
decrease in 6-month survival as compared with
others (25% versus 85%). This cutoff was able to
identify approximately 75% of the observed
deaths, showing a better prognostic value than
MELD and GASH.
Liver biopsy
Liver biopsy is the only one able to distinguish
an alcoholic hepatitis from liver cirrhosis. More-
over, alcoholic hepatitis lesions may overlap in a
patient with preexistent ethanolic cirrhosis. Since
it was reported first (25), the morphology of
alcoholic liver disease has been well described
(26).
Moreover, several histological characteristics as
the presence of perivenular fibrosis, steatosis and
giant mitochondria in a known alcoholic may
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 247
ALCOHOLIC HEPATITIS – CURRENT CONCEPTS AND MANAGEMENT
herald the transition from alcoholic hepatitis to
cirrhosis (27).
While histologic changes from steatosis and
steatohepatitis to cirrhosis are known, correlating
degree of steatosis with liver function and survival
is currently under investigation. Few studies finds
a correlation between low grade steatosis and
advanced liver failure as well as lowered sensitivity
to steroid treatment (28). However, patients with
low grade steatosis had higher Maddrey dis-
criminant function scores, which can also predict
poor survivals. That’s why liver biopsy for staging
and predicting survival has been replaced by the
discussed scoring systems.
It is generally accepted to perform a liver
biopsy if the diagnosis of alcoholic hepatitis is
either in question or a concomitant pathology,
such as hepatitis C, is suspected (29).
Another important indication for the liver
biopsy is the distinction between alcoholic hepatitis
alone and the concomitance of liver cirrhosis in
patients with severe disease (30). In clinical
practice, transjugular liver biopsy is recommended
in these cases (given the presence of coagulopathy
and/or ascites) if leukocytosis, fever and hepatic
bruit are absent (31).
In conclusion, the role of liver biopsy in defining
prognosis and treatment of alcoholic hepatitis in
the clinical setting remains unclear, in the absence
of the above recommendations. ‰
THERAPY OF ALCOHOLIC HEPATITIS
1. Abstinence
It is the key point in the management of every
clinical form of alcohol-induced liver disease,
being even able to reverse the lesions of hepatic
steatosis or alcoholic hepatitis. The persistence
of alcohol intake is an independent risk factor
with a bad prognosis in patients with alcoholic
hepatitis, liver cirrhosis and after liver trans-
plantation (32.). Liver steatosis may be completely
reversible in case of abstinence in a few weeks.
Alcoholic hepatitis may be partially reversible after
stopping the alcohol intake (33).
Reaching this goal is not easy in alcohol-
addicted patients and therefore a therapeutic plan
is needed, which has to involve a psychological
component and a pharmaceutical one. The
psychological intervention involves strategies for
educating and informing the patients about the
problems related to chronic consumption and
alcohol addiction and also for recommending
behavioral changes (34).
In addition to psychotherapy, alcohol addic-
ted patients could benefit from a pharmacologic
248 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
therapy (35). Acamprosate proved itself useful
in reducing the number of intake days and
increasing the abstinence ratio (36), with also a
good tolerability (except for cirrhotic Child C
patients). Naltrexone had similar effects, but a
lower tolerability. Disulphiram (inhibitor of the
acetaldehyde dehydrogenase) is being used for
many years in alcohol addicted patients, although
the results are uncertain and the adverse events
are significant (37).
Not to forget the “other side of the coin” in
abstinent patients – the alcohol withdrawal
syndrome. Symptoms usually start within a few
hours (tremors, sweating, elevated pulse and
blood pressure, nausea, insomnia, anxiety. The
delirium may follow after 1-3 days (altered
sensorium, disorientation, hallucinations, poor
shot-term memory, altered sleep-wake cycle).
Mild withdrawal can be managed in an outcare
setting, while severe cases require hospitalization
and intensive treatment (thiamines, benzodi-
azepines, anticonvulsivants, beta-adrenergic
blockers, or antipsychotics) (38).
2. Nutrition
Malnutrition is found in a significant number
of patients, having various etiology and important
consequences in amplifying the toxicity of the
ethanol (39). Prognostic studies showed benefits
for nutritional therapy similar to corticotherapy
and their association might result in a synergic
therapeutic effect (40). One-year mortality was
lower in patients with nutritional therapy (41).
Thus, supportive nutritional therapy still re-
presents a therapeutic alternative in the manage-
ment of these patients although some authors
consider it’s efficacy “unproven” (42). It is nec-
essary to supplement proteins (1g/kg/day), cal-
ories (2000-3000 kcal/day) and vitamins (mainly
thiamine). Vitamin K is routinely administered in
patients with prolonged prothrombin time,
although this is not completely benefic because
liver failure causes complex abnormalities of the
coagulation.
Conventional amino acids may be used in
enteral or parenteral administration, branched-
chain amino acids being reserved for patients with
encephalopathy. Medium-chain triglycerides may
also be used.
If oral nutrition is not possible (severe disease,
encephalopathy, dynamic ileus), total parenteral
nutrition must be started. In the other situations
one may choose oral or parenteral catheter
nutrition.
Hyperhydration must be avoided in paren-
teral nutrition, because it could increase the
 ALCOHOLIC HEPATITIS – CURRENT CONCEPTS AND MANAGEMENT
ascites, cause a dilutional hyponatremia or favor
a variceal bleeding by increasing the pressure in
the portal vein.
3. Medical therapy
Corticoids
They have been used for treating alcoholic
hepatitis starting from the ‘60s and represent the
main discussed drugs in this disease. Although,
their use is still controversial to date, even if every
author agrees that they are the most efficient
available therapy at this moment (43).
The mechanism of action is centered on
blocking the pathogenic inflammatory and
cytotoxic routes, by decreasing the level of pro-
inflammatory cytokines such as TNF-alpha and
reducing the expression of ICAM-1 (44).
The therapeutic indication is the severe
alcoholic hepatitis (Maddrey score > 35) (43).
Although in variable proportions, therapeutic
trials showed a benefic result of steroid therapy,
demonstrating decrease of mortality, clinical and
biological improvement and even histological
improvement.
Thus, response ratio ranged between 67% and
87%, with an NNT (number of treated patients to
obtain a therapeutic response) between 2 and 6.
In the absence of infection or upper digestive
bleeding, the presence of encephalopathy is an
additional reason to administer corticoids (31).
Overall mortality after one month of corticoid
therapy decreased from 35% to 15%.
The duration of administration is one month.
A number of studies showed that the best marker
to evaluate the benefits of corticoid therapy is
the early decreasing of total bilirubin level (after
7 days of therapy) (45). If total bilirubin level after
7 days of therapy is lower than its level at
admittance, then there is a therapeutic response;
if not, corticoids can be stopped. 6 month
survival was 84% if there had been an early
decreasing of bilirubin level and only 23% if
bilirubin levels had not changed in 7 days.
Though, regarding 2 years survival, no significant
difference was found in patients with
corticotherapy compared to the other patients.
On the other hand, we must not omit the
adverse events of corticotherapy, especially the
infectious ones, which may cause mortality by
themselves (46). Therefore, corticoids should not
be administered with mild and moderate disease,
while overall survival in this category exceeds 90%
anyway.
In conclusion, in selected cases, corticotherapy
is benefic in patients with severe alcoholic
hepatitis, resulting in a significant decrease in
mortality.
Pentoxifylline
This is a phosphodiesterase inhibitor, whose
mechanism of action is related to the inhibition
of TNF-alpha (47). The recommended dose is 3
x 400 mg/day for 4 weeks. Relatively recently
added to the therapeutic arsenal, pentoxifylline
proved useful in severe alcoholic hepatitis (48),
increasing overall survival by 20% (49). It must
be stated that the improvement in survival was
related to the decrease in number of deaths due
to hepatorenal syndrome, the benefit of the
pentoxifylline being strictly related to the decrease
of this complication (50).
Anti TNF-alpha therapy
This therapy is based on the premise that
cytotoxic effect of TNF alpha is a key element in
the etiopathogeny of alcohol-induced liver injury.
The administration of these drugs was proposed
for the therapy of severe alcoholic hepatitis
(Madrey score > 35), in association with corti-
costeroids, but to date, this category of drugs
cannot be recommended in current medical
practice, further efficacy and safety trials being
needed for the usage of etanercept and infliximab.
a) Infliximab
It was used in a 5mg/kg or 10 mg/kg i.v. dose;
a single or multiple administration (weeks 0, 2,
4) has been proposed. If the 5 mg/kg dose in
single administration proved itself useful (51), the
therapy with 10mg/kg in 3 doses was inferior to
corticotherapy, resulting in a higher mortality by
infectious complications (52). Moreover, except
the increased risk of infection, infliximab was
associated with cases of acute liver failure in
patients with Crohn’s disease and rheumatoid
arthritis. And this risk may preclude its use in
patients with underlying severe liver injury who
are less capable of withstanding an additional
insult to the liver.
b) Etanercept
This drug is a soluble TNF p75 receptor, which
neutralizes the soluble TNF. The usage of this drug
in patients with severe and moderate alcoholic
hepatitis (score >15) showed a possible improve-
ment in 30-days survival (92%), but also a high
ratio of adverse events (infections, renal failure,
digestive hemorrhage) which led therapy discon-
tinuation in 23% of patients (53).
c) Thalidomide
The proposed mechanism of action is the
reduction in the synthesis of TNF-alpha and the
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 249
ALCOHOLIC HEPATITIS – CURRENT CONCEPTS AND MANAGEMENT
inhibition of the Kupffer cells response to bacterial
endotoxins. Experimental studies showed a
decrease of necro-inflammatory processes,
respectively of hepatic steatosis after the
administration of alcohol in association with
thalidomide during 8 weeks (54). Moreover, this
drug has been shown to reduce the hepatic
venous pressure gradient in stable alcoholic
cirrhotics (55). On the other hand, major side
effects result in not using this drug in medical
practice for alcoholic hepatitis. To date, researches
are ongoing for synthesizing thalidomide
analogues with no teratogenic effect.
d) Pioglitazone
It is a PPAR-g (peroxisome proliferator-
activated receptor-gamma) agonist, which inhibits
the production of TNF-alpha by Kupffer cells in
response to endotoxinemia. Animal studies
showed that pioglitazone prevents alcohol-
induced hepatic lesions (56). There are no studies
on humans to date, but in the future this drug
could be useful for patients with severe alcoholic
hepatitis.
Antioxidant therapy
This therapeutic alternative is based on the
concept that oxidative stress is in a high degree
responsible for the development of alcohol-
induced liver injury. Moreover, chronic alcohol
abusers have a low intake of antioxidants
(selenium, vitamin A, vitamin C, coenzyme Q).
a) Antioxidant coktails
Relatively recent studies compared corticos-
teroids to a cocktail containing beta-caroten,
vitamin A and C, selenium, methionine, allo-
purinol, desferoxamine and N-acetylcysteine (57).
Corticotherapy was superior to this therapy after
one month, but after one year, the mortality rates
were similar. Other studies that associated
antioxidant therapy to corticotherapy showed no
additive benefit, suggesting the lack of efficacy of
this kind of therapy (58).
b) Vitamin E
Studies performed in patients with mild and
moderate ethanolic hepatitis, who received vit. E
1000 IU/day for 3 months, showed a decrease
in the seric level of hialuronic acid (serologic
marker of liver fibrogenesis), but had no effect
concerning the improvement of hepatic function
or mortality after the firs year of therapy (59).
Thus, this therapy remains a subject of contro-
versy.
c) Silymarin
This is an antioxidant compound widely used
in patients with liver cirrhosis, irrespective of the
etiology. The mechanisms of action are numerous,
250 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
including regulation of membrane permeability,
inhibition of 5-lipooxygenase, decrease of oxygen-
centered free radicals, suppression of the nuclear
factor NF-kappaB (60).
The recommended dosage is 150 mg x 3/day
orally. While experimental studies showed that
silymarin delays the development of alcohol-
induced liver fibrosis, therapeutic trials showed
discordant results, some of those showing a
decrease by 20% of 4-years mortality, while the
others showed no significant difference to placebo
(61).
Counting currently available data, we could
state that silymarin might have a favorable
therapeutic effect in some groups of patients with
alcoholic cirrhosis, but this effect might not be
superior to that resulting from abstinence.
Though, considering that these drugs have a good
tolerability and a low cost, silymarin may be
recommended in current practice.
Propylthiouracil
The mechanism of action is related to the
inhibition of the hypermetabolic status and
reduction of oxygen consumption (62). The
therapeutic indication is moderate and severe
alcoholic hepatitis. While initial studies revealed
a benefit in terms of decreasing the complications
and mortality rates, a meta-analysis of data in
the literature did not show any benefit regarding
histological improvement, complications, liver
injury related mortality or overall mortality (63).
Under these circumstances, this drug cannot be
to date recommended in current medical
practice.
Anabolic steroids (oxandrolone)
There is a measurable and clinically apparent
decline in gonadal function in patients with
alcoholic liver disease, but available data could
not demonstrate a significant effect of anabolic-
androgenic steroids on the symptoms improve-
ment and mortality of patients with alcoholic liver
disease (64). Currently, anabolic steroids are no
longer recommended for the treatment of
alcoholic hepatitis.
S-adenosyl-methionine
In the setting of alcoholic hepatitis, there is a
measurable decrease in hepatic methionine, and
glutathione levels The proposed mechanism of
action for this drug concerns the reduction of liver
alcoholic injury by diminishing the oxidative stress
and raising the level of mitochondrial glutathione
(65).
 ALCOHOLIC HEPATITIS – CURRENT CONCEPTS AND MANAGEMENT

Administered in dose of 1200 mg/day for 1-
2 years in cirrhotic patients, led to a decrease of
mortality rate and number of liver transplants
compared to placebo, but the differences were
not statistically significant in different studies (66).
Furthermore, currently there are no available
trials studying the effect of the drug in acute
alcoholic hepatitis. Therefore, this drug cannot
be recommended in current clinical practice.
Colchicine
The mechanism of action is anti-inflammatory
and antifibrotic. Its use in alcoholic hepatitis (1
mg/day, orally) did not prove efficacy (67), and
long-term use in cirrhotic patients resulted in dis-
cordant data regarding the benefits (com-
plications, liver transplant, death) and negative
results concerning the adverse events (68).
Therefore, this drug cannot be recommended
to date in current medical practice.
Dilinoleoylphosphatidylcholine
The mechanism of action is antifibrotic by
reducing the activity of stellate cells (Ito cells) and
stimulating the activity of the colagenases, but also
anti-inflammatory by reducing the activity of
cytochrome P450-2EI and inhibiting TNF-alpha
(69). There are few clinical trials, which makes it
difficult to evaluate the efficacy of this drug.
Current data show that a 2 year administration
led to a decrease of the bilirubin and amino-
transferases levels, but did not influence the
progression of liver fibrosis (70).
Therapy of the hepatorenal syndrome
The occurrence of this complication rep-
resents a bad prognosis factor, while it is associated
with a mortality rate of 90%. In liver cirrhosis,
combination therapy with i.v. albumin and a
splanchnic vasoconstrictor (terlipressin) has been
successfully implemented (71). There are no
studies in alcoholic hepatitis to date, but the-
oretically this kind of approach could be useful
in reducing the mortality rate in patients with
hepatorenal syndrome, in association with
pentoxifylline.
Transplant for alcoholic hepatitis
Liver transplant is the only permanent the-
rapeutic option in patients with terminal liver
disease, including patients with alcohol-induced
liver cirrhosis. But also severe forms of alcoholic
hepatitis may evolve with fulminant liver failure,
which could represent another indication for liver
transplant, in the absence of a therapeutic
response to medical treatment (72).
At this moment, there is no absolute recom-
mendation for transplant in these patients, be-
cause there is no pre-transplant abstinence
period, comorbidities are frequently found and
there is no appropriate psychiatric evaluation (73).
There are only isolated case reports concerning
patients who survived the transplant. There is
probably at least one subgroup of patients with
severe alcoholic hepatitis who could benefit from
transplant, but further studies are needed to asses
this indication (if it does exist). ‰
CONCLUSION
Alcoholic hepatitis is still a “difficult to diagnose” entity
because of its large variability in clinical presentation. Severe
onsets represents a “difficult to treat” group, in which the
actually recommended therapies are still modest, and short/
long-term mortality is significant.
Despite the recent advances in understanding the path-
ways of ethanol liver injuries, attempts to link therapeutic
options to the pathogenesis prove no major benefit for the
moment. ‰

REFERENCES
1. Rehm J, Room R, Monteiro M,
et al. – Alcohol as a risk factor for
global burden of disease. Eur Addict
Res 2003; 9:157-164
2. Kim WR, Brown RS Jr, Terrault NA,
et al. – Burden of liver disease in the
United States: summary of a
workshop. Hepatology 2002; 36:227-
242
3. Pirmohamed M, Gilmore IT –
Alcohol abuse and the burden on the
NHS – time for action. J R Coll
Physicians London 2000; 34:161-162
4. Dawson DA, Grant BF, Li TK –
Quantifying the risks associated with
exceeding recommended drinking
limits. Alcohol Clin Exp Res 2005;
29(5):902-908
5. Seitz HK, Stikel F – Alcoholic liver
disease in the elderly. Clin Geriatr
Med 2007; 23(4):905-921
6. Szabo G – Pathogenic interanctions
between alcohol and hepatitis C, Curr

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 251

ALCOHOLIC HEPATITIS – CURRENT CONCEPTS AND MANAGEMENT
Gastroenterol Rep 2003; 5(1):86-92
7. Picardi A, D’avola D, Gentilluci
UV, et al. – Diabetes in chronic liver
disease: from old concepts to new
evidence. Diabetes Metab Res Rev 2006,
22(4):274-283
8. Gonzalez MJ – Role of cytochromes
P450 in chemical toxicity and
oxidative stress. Studies with
CYP2E1, Mutat Res 2005, 569(1-
2):101-110
9. Tsukamoto H – Conceptual
importance of identifying alcoholic
liver disease as a lifestyle disease.
2007; 42(8):603-609
10. US Surgeon General release advisory
on alcohol use in pregnancy.
Washington DC US Departament of
Health and Human Services. In
press, press release 21 feb. 2005
11. Mann RE, Smart RG, Govoni R –
The epidemiology of alcoholic liver
disease. Alcohol Res Health 2003;
27:209-220
12. Reuben EA – Alcohol and the liver.
Curr OpinGastoenterol 2007, 23(3),
283-291
13. Tome S, Lucey MR – Review article:
current management of alcoholic liver
disease. Aliment Pharmacol Ther
2004;19:707-714
14. Orrego H, Blake JE, Blendis LM, et
al. – Prognosis of alcoholic cirrhosis
in the presence and absence of
alcoholic hepatitis. Gastroenterology
1987; 92:208-214
15. Chedid A, Mendenhall CL,
Gartside P, et al. – Prognostic
factors in alcoholic liver disease. VA
Cooperative Study Group. Am J
Gastroenterol 1991; 86:210-216
16. Sarin SK, Chari S, Sundaram KR,
et al. – Young v adult cirrhotics: a
prospective, comparative analysis of
the clinical profile, natural course
and survival. Gut 1988; 29:101-107
17. Maddrey WC, Boitnott JK, Bedine
MS, et al. – Corticosteroid therapy
of alcoholic hepatitis.
Gastroenterology 1978; 75:193-199
18. Ramond MJ, Poynard T, Rueff Bet
al. – A randomized trial of
prednisolone in patients with severe
alcoholic hepatitis. N Engl J Med
1992; 326:507-512
19. Kulkarni K, Tran T, Medrano M, et
al. – The role of the discriminant
factor in the assessment and
treatment of alcoholic hepatitis. J
Clin Gastroenterol 2004; 38:453-459
20. Dunn W, Jamil LH, Brown LS,
et al. – MELD accurately predicts
mortality in patients with alcoholic
hepatitis. Hepatology 2005; 41:353-
358
21. Forrest EH – Prognostic evaluation
of alcoholic hepatitis. J Hepatol 2005;
43:738-739
22. Forrest TH, et al. – Analysis of
factors predictive of mortality in
alcoholic hepatitis and derivation
252 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
and validation of the Glasgow
alcoholic hepatitis score. Gut 2005;
54(8):1174-1179
23. Forrest TH, et al. – The Glasgow
alcoholic hepatitis score identifies
patients who may benefit from
corticosteroids, Gut 2007;
56(12):1743-1746
24. Louvet A et al. – The Lille model: a
new tool for therapeutic strategy in
patients with severe alcoholic
hepatitis treated with steroids.
Hepatology 2007; 45(6):1348-1354
25. Mallory F, et al. – Cirrhosis of the
liver. Five different types of lesions
from which it may arise. Bull Johns
Hopkins Hospital 1911; 22:69-74
26. Lefkowitch JH – Morphology of
alcoholic liver disease. Clin Liver Dis
2005; 9:37-53
27. Teli MR, Day CP, Burt AD, et al. –
Determinants of progression to
cirrhosis or fibrosis in pure alcoholic
fatty liver. Lancet 1995; 346:987-990
28. Duvoux C, Radier C, Roudot-
Thoraval F, et al. – Low-grade
steatosis and major changes in portal
flow as new prognostic factors in
steroid-treated alcoholic hepatitis.
Hepatology 2004; 40:1370-1378
29. Sougioultzis S, Dalakas E, Hayes
PC, et al. – Alcoholic hepatitis: from
pathogenesis to treatment. Curr Med
Res Opin 2005; 21:1337-1346
30. Levitsky J, Mailliard ME, et al. –
Diagnosis and therapy of alcoholic
liver disease. Semin Liver Dis 2004;
24:233-247
31. Rongey C, Kaplowitz N – current
concepts and controversies in the
treatment of alcoholic hepatitis.
World J Gastroenterol 2006;
12(43):6909-6921
32. Alexander JF, Lichner MW,
Galambos JT – Natural history of
alcoholic hepatitis. The long-term
prognosis. Am J Gastroenterol 1971;
56:515-525
33. Galambos JT – Natural history of
alcoholic hepatitis. III. Histological
changes. Gastroenterology 1972;
63:1026-1035
34. Project MATCH Research Group –
Matching alcoholism treatments to
client heterogeneity. Alcohol Clin Exp
Res 1998; 22(6):1300-1311
35. Anton RF, et al. – Combined
pharmacotherapies and behavioural
interventions for alcohol dependence.
A randomized control trial. JAMA
2006; 295(17):2003-2017
36. Lieber CS – Liver diseases by
alcohol and hepatitis C: early
detection and new insights in
pathogenesis lead to improved
treatment. Am J Addict 2001;10
Suppl:29-50
37. Dilts SL, Dilts SL Jr – Assessing
liver function before initiating
disulfiram therapy. Am J Psychiatry
1996; 153(11):1504-1505
38. Mayo-Smith MP, et al. –
Management of alcohol witdrawal
delirium An evidence-based practice
guideline. Arch Intern Med 2004;
164(13):1405-1412
39. Halsted CH – Nutrition and
alcoholic liver disease. Semin Liver
Dis 2004; 24:289-304
40. Cabre´ E, Rodriguez Iglesias P,
Caballeria J, et al. – Short and long-
term outcome of severe alcohol-
induced hepatitis treated with
steroids or enteral nutrition: a
multicenter randomized trial.
Hepatology 2000; 32:36-42
41. Mendenhall CL, Tosch T, Weesner
RE, et al. – VA cooperative study on
alcoholic hepatitis. II. Prognostic
significance of protein-calorie
malnutrition. Am J Clin Nutr 1986;
43:213-218
42. Stickel F, Hoehn B, Schuppan D, et
al. – Nutritional therapy in alcoholic
liver disease. Aliment Pharmacol Ther
2003; 18:357-373
43. Mathurin P, Mendenhall CL,
Carithers RL Jr, et al. –
Corticosteroids improve short-term
survival in patients with severe
alcoholic hepatitis (AH): individual
data analysis of the last three
randomized placebo controlled
double blind trials of corticosteroids
in severe alcoholic hepatitis. J Hepatol
2002; 36:480-487
44. Spahr L, Rubbia-Brandt L, Pugin J,
et al. – Rapid changes in alcoholic
hepatitis histology under steroids:
correlation with soluble intercellular
adhesion molecule-1 in hepatic
venous blood. J Hepatol 2001; 35:582-
589
45. Mathurin P, Abdelnour M,
Ramond MJ, et al. – Early change in
bilirubin levels is an important
prognostic factor in severe alcoholic
hepatitis treated with prednisolone.
Hepatology 2003; 38:1363-1369
46. Cabr. E, et al. – Short- and long-term
outcome of severe alcohol-induced
hepatitis treated with steroids or
enteral nutrition: a multicenter
randomized trial. Hepatology 2000;
32:36-42
47. Shirin H, Bruck R, Aeed H, et al. –
Pentoxifylline prevents concanavalin
A-induced hepatitis by reducing
tumor necrosis factor alpha levels
and inhibiting adhesion of T
lymphocytes to extracellular matrix.
J Hepatol 1998; 29:60-66.
48. McAvoy NC, Forrest EH,
Hayes PC – The Glasgow Alcoholic
Hepatitis Score and the effect of
pentoxifylline in alcoholic hepatitis.
Gut 2005; 54 (Suppl.2):44A
49. Akriviadis E, Botla R, Briggs W, et
al. – Pentoxifylline improves short-
term survival in severe acute
alcoholic hepatitis: a double-blind,

placebo-controlled trial.
Gastroenterology 2000; 119:1637-1640
50. Baccaro ME, Guevara M –
Hepatorenal syndrome. Gastroenterol
Hepatol 2007; 30(9):548-555
51. Mookerjee RP, Tilg H, Williams R,
et al. – Infliximab and alcoholic
hepatitis. Hepatology 2004; 40:499-
500
52. Naveau S, Chollet-Martin S,
Dharancy S, et al. – A double-blind
randomized controlled trial of
infliximab associated with
prednisolone in acute alcoholic
hepatitis. Hepatology 2004; 39:1390-
1397
53. Menon KV, Stadheim L, Kamath
PS, et al. – A pilot study of the
safety and tolerability of etanercept
in patients with alcoholic hepatitis.
Am J Gastroenterol 2004; 99:255-260
54. Austin AS, Mahida YR, Clarke D,
et al. – Freeman, J.G. Thalidomide
prevents alcoholic liver injury in rats
through suppression of Kupffer cell
sensitization and TNF-alpha
production. Gastroenterology 2002;
123(1):291-300
55. Austin AS, Mahida YR, Clarke D,
et al. – Freeman, J.G A pilot study to
investigate the use of oxpentifylline
(pentoxifylline) and thalidomide in
portal hypertension secondary to
alcoholic cirrhosis. Aliment Pharmacol
Ther 2004; 1(19):79-88
56. Tomita K, et al. – Pioglitazone
prevents alcohol-induced fatty liver
in rats through up-regulation of c-
Met. Gastroenterology 2004 Mar;
126(3):873-885
57. *** – Steroids or cocktails for
alcoholic hepatitis. J Hepatol 2006;
44(4):633-636
SOCIETźII ACADEMICE
ALCOHOLIC HEPATITIS – CURRENT CONCEPTS AND MANAGEMENT
58. Stewart S, Prince M, Bassedine M,
et al. – A randomized trial of
antioxidant therapy alone or with
corticosteroids in acute alcoholic
hepatitis. J Hepatol 2007; 47(2):277-
283
59. Mezzey E, Potter JJ, Rennie-
Tankersley L, et al. – A randomized
placebo controlled trial of vitamin E
for alcoholic hepatitis. J Hepatol
2004, 40:40-46
60. Song J, et al. – Silymarin protects
against acute ethanol-induced
hepatotoxicity in mice. Alcohol Clin
Exp Res 2006; 30(3):407-413
61. Rambaldi A, Jacobs BP, Iaquinto
G, et al. – Milk thistle for alcoholic
and/or hepatitis B or C liver
diseases—a systematic cochrane
hepato-biliary group review with
meta-analyses of randomized clinical
trials. Am J Gastroenterol 2005;
100(11):2583-2591
62. Iturriaga H, Ugarte G, Israel Y –
Hepatic vein oxygenation, liver blood
flow, and the rate of ethanol
metabolism in recently abstinent
alcoholic patients. Eur J Clin Invest
1980; 10:211-218
63. Rambaldi A, Gluud C – Meta-
analysis of propylthiouracil for
alcoholic liver disease – a Cochrane
Hepato-Biliary Group Review. Liver
2001; 21:398-404
64. Rambaldi A, Iaquinto G, Gluud C –
Anabolic-androgenic steroids for
alcoholic liver disease. Cochrane
Database Syst Rev 2003; CD003045
65. Lieber CS – Role of S-adenosyl-L-
methionine in the treatment of liver
diseases. J Hepatol 1999; 30:1155-
1159
Vizita¡i site-ul
DE MEDICINÅ
www.samf.ro
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
66. Mato JM, Camara J, Fernandez de
Paz J, et al. – S-adenosylmethionine
in alcoholic liver cirrhosis: a
randomized, placebo-controlled,
double-blind, multicenter clinical
trial. J Hepatol 1999; 30:1081-1089
67. Rambaldi A, Gluud C – Colchicine
for alcoholic and non-alcoholic liver
fibrosis and cirrhosis. Cochrane
Database Syst Rev 2001; 3:CD002148
68. Morgan TR, Weiss DG,
Nemchausky B, et al. – Colchicine
treatment of alcoholic cirrhosis: a
randomized, placebo-controlled
clinical trial of patient survival.
Gastroenterology 2005; 128:882-890
69. Cao Q, Mak KM, Lieber CS –
Dilinoleoylphosphatidylcholine
decreases acetaldehyde-induced
TNF-alpha generation in Kupffer
cells of ethanol-fed rats. Biochem
Biophys Res Commun 2002; 299:459-
464
70. Lieber CS, Weiss DG, Groszmann
R, et al. – Veterans Affairs
cooperative study of
polyenylphosphatidylcholine in
alcoholic liver disease. Alcoholism:
Clin Exp Res 2003; 27:1765-1772
71. Arroyo V, Terra C, Gines P – New
treatments of hepatorenal syndrome.
Semin Liver Dis 2006; 26(3):254-264
72. Mathurin P – Is alcoholic hepatitis
an indication for transplantation?
Current management and outcomes.
Liver Transpl 2005 Nov; 11(11 Suppl
2):S21-24
73. Zetterman RK – Liver
transplantation for alcoholic liver
disease, 2005; 9(1):171-181
A FAMILIEI
253
 3 PRACTICA MEDICALÅ
REFERATE GENERALE

Dislipidemiile ¿i rela¡ia lor cu

patologia generalå
Dyslipidemias and their relationship
with general pathology
Conf. Dr. VIOREL-NICU PÂRVULESCU1,
ªef Lucr. Dr. RODICA TRÅISTARU1, Prof. Dr. VIORELA ENÅCHESCU1,
Dr. MIHAI LAURENºIU2, ªef Lucr. Dr. LIGIA FLOREA1,
Conf. Dr. Viorel-Nicu
ªef Lucr. Dr. SORIN BEZNÅ1, Dr. VICA CIUVź2,
PÂRVULESCU
Asist. Univ. Dr. CRISTINA BÅRBULESCU1, Dr. CRISTINA BRAICA-LUPU2
1
UMF, Craiova
2
Spitalul „Filantropia“, Craiova

REZUMAT
Dislipidemiile reprezintå perturbarea metabolismului lipoproteinelor, al frac¡iunilor lipidice sanguine, în
sensul unei produc¡ii crescute sau al unui deficit. Dislipidemiile nu determinå manifeståri clinice directe dar
reprezintå factor de risc pentru afec¡iuni cardiovasculare aterosclerotice. În studiul retrospectiv derulat am
stabilit rela¡iile între prezen¡a dislipidemiilor ¿i alte aspecte de patologie generalå. Rezultatele ob¡inute se
încadreazå în datele de literaturå medicalå, care subliniazå cå dislipidemiile reprezintå factorul de risc major
la pacien¡ii obezi ¿i/sau cardiovasculari.

Cuvinte cheie: dislipidemii, boala cardiovascularå, patologie generalå, factor de risc

ABSTRACT
Dyslipidemia is a disorder of lipoprotein metabolism, including lipoprotein overproduction or deficiency.
Dyslipidemia itself causes no symptoms but can lead to symptomatic vascular disease, including coronary
artery disease and peripheral arterial disease. In our retrospective study we established the relations between
dyslipidemia and other general pathology entities. Our results confirm the medical literature data about
incidence of dyslipidemia like a risk factor in cardiovascular and obese patients.

Key words: dyslipidemia, cardiovascular disease, general pathology, risk factor

NOºIUNI INTRODUCTIVE consecin¡ele complexe patogenice ¿i clinice,

T
ermenul de dislipidemii define¿te
diver¿i factori genetici sau de mediu
care altereazå produc¡ia, catabolismul
sau clearance-ul lipoproteinelor
plasmatice din circula¡ie.
Pe plan mondial, dislipidemiile se constituie
într-o realå problemå de sånåtate publicå, aspect
justificat de prevalen¡a ¿i inciden¡a crescutå,
costurile implicate.
În România, dislipidemiile sunt prezente la
46% din popula¡ie, sub diverse forme: hipercoles-
terolemia totalå a 24%, LDL peste 130 mg/dl sau
peste 100 mg/dl la diabetici la 24%, TGL peste
150 mg/dl la 23% din populatie, procentele fiind
mai ridicate în Moldova ¿i Oltenia.
Clasificårii tradi¡ionale a dislipidemiilor stabilitå
de Fredrickson i s-a adåugat una mai practicå,

254 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007


recomandatå de Asocia¡ia Europeanå de Atero-
sclerozå; în prezent se folose¿te ¿i clasificarea
etiopatogenicå (conform cåreia dislipidemiile, mai
exact hiperlipidemiile sunt primare – genetice ¿i
secundare – dobândite).
Elementele semiologice existente la un pacient
dislipidemic reprezintå expresia patogenicå a
diferitelor afec¡iuni care au ca factor de risc
perturbarea metabolismului lipidic.
În conformitate cu aprecierile Societå¡ii Euro-
pene de Cardiologie, Societå¡ii Europene de
Aterosclerozå ¿i Societå¡ii Europene de Hiperten-
siune, cre¿terea colesterolului plasmatic (LDL
colesterol) ¿i a nivelului plasmatic scåzut al HDL
colesterol reprezintå factori de risc pentru bolile
cardiovasculare aterosclerotice.
În anul 2001, NCEP-ATPIII (National
Cholesterol Education Program - Adult Treatment
Panel III) reactualizeazå un ghid ce aduce noi
modificåri în detec¡ia, evaluarea ¿i tratamentul
dislipidemiilor la adult, precum ¿i în interpretarea
celorlal¡i factori de risc. Acest ghid continuå så
considere nivelul LDL colesterolului ¡inta primarå
a tratamentului, dar în acela¿i timp a fost mo-
dificatå abordarea terapeuticå, în sensul includerii
în ¡inta scåderii LDL sub 100 mg/dl ¿i a acelor
pacien¡i care sunt la risc înalt pentru cardiopatia
ischemicå, dar care nu au încå eviden¡å clinicå
de cardiopatie ischemicå.
Din hiperlipoproteinemi, hipercolesterolemia
reprezintå factorul de risc principal care a fost
asociat statistic cu riscul cel mai mare pentru
boala coronarianå ¿i mortalitatea prin aceasta.
LDL colesterolul, ca frac¡iunea lipidicå care
transportå aproximativ 70% din colesterolul
plasmatic, prezintå o rela¡ie direct propor¡ionalå
cu riscul cardiovascular indiferent de na¡ionalitate
sau rasa etnicå. Nivelul scåzut al HDL-coles-
terolului reprezintå un alt factor de risc cardio-
vascular. Implicarea trigliceridelor în aterogenezå
continuå så fie un subiect discutat, studiile clinice
¿i epidemiologice nereu¿ind så adopte o decizie
finalå asupra importan¡ei acestora în patologia
cardiovascularå.
Pornind de la aceste no¡iuni fundamentale,
am studiat inciden¡a dislipidemiilor în contextul
unor afec¡iuni din patologia generalå, legate sau
nu prin verigi patogenice cunoscute cu tulburårile
metabolismului lipidic.
PACIENºI ªI METODÅ
Studiul a fost unul de tip retrospectiv ¿i a
cuprins pacien¡ii consecutiv interna¡i pe parcursul
a doi ani (între 1 ianuarie 2005 ¿i 31 decembrie
2006) în Spitalul Clinic Municipal Craiova la
Clinica Medicalå III. Lotul a cuprins un numår
DISLIPIDEMIILE ªI RELAºIA LOR CU PATOLOGIA GENERALÅ
de 1050 de pacien¡i (555 de femei, 495 de
bårba¡i).
Fiecårui subiect din lot i s-a realizat un bilan¡
lipidic din datele clinice (anamnezå, antecedente,
istoric personal de boli cardiovasculare, date ale
examenului clinic – înål¡ime, greutate, indice de
maså corporalå, circumferin¡a abdominalå, gro-
simea pliurilor cutanate, alte modificåri clinice
caracteristice) ¿i paraclinice (lipide totale, colesterol
total, HDL colesterol, trigliceride, LDL colesterol
calculat). Determinarea lipidelor sanguine s-a
fåcut folosind un analizor semiautomat Hospitex
Screen master plus, utilizând teste enzimatice
colorimetrice. Interpretarea statisticå a rezultatelor
a fost fåcutå folosind programul SPSS Windows
98, apreciindu-se riscul relativ estimat (OR) ¿i
intervalul de încredere 95% (CI 95%). Am ¡inut
seama de urmåtoarea interpretare statisticå:
• OR > 1, variabila de expunere reprezintå
un factor de risc,
• OR = 1, variabila de expunere este factor
indiferent,
• OR< 1, variabila de expunere reprezintå
un factor de protec¡ie,
• dacå intervalul de încredere include cifra
1, nu se pot face considera¡ii de protec¡ie
sau risc,
• dacå limita superioarå a intervalului de
încredere este mai micå decât 1, atunci se
vorbe¿te despre factor de protec¡ie,
• dacå limita inferioarå a intervalului este
mai mare decât 1, atunci se vorbe¿te des-
pre factor de risc.
În derularea studiului au fost respectate
normele de eticå medicalå ale spitalului.
REZULTATE ªI DISCUºII
Raportând prezen¡a sau absen¡a dislipidemiei
la datele biografice ale pacien¡ilor studia¡i, am
ob¡inut urmåtoarele rezultate:
• frecven¡å scåzutå a dislipidemiilor la
pacien¡ii cu vârsta pânå la 40 de ani atât
din mediul rural, cât ¿i din mediul urban;
o frecven¡å ridicatå a dislipidemiilor a
existat la pacien¡ii cu vârsta cuprinså între
50 ¿i 60 de ani, atât la cei din mediu rural,
dar mai ales la pacien¡ii din mediul urban
(70% au dislipidemie) (Figura 1);
• predominan¡å minimå a numårului fe-
meilor în rândul bolnavilor cu dislipidemii
(Figura 2);
• grupul pacien¡ilor dislipidemici din mediul
urban, în special la bårba¡i a fost relativ
mai mare (Figura 3).
Ulterior, am apreciat frecven¡a dislipidemiei
pentru aspectele de patologie generalå descrise
la lotul studiat.
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 255
DISLIPIDEMIILE ªI RELAºIA LOR CU PATOLOGIA GENERALÅ
Figura 1. Frecven¡a dislipidemiilor în func¡ie
de vârstå ¿i mediu social
Figura 2. Distribu¡ia dislipidemiilor în func¡ie de sex
Figura 3. Frecven¡a dislipidemiilor în fun¡ie de mediu ¿i
sex
256 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
Am constatat o asociere frecventå a obezitå¡ii
cu dislipidemia (Figura 4). Persoanele cu dislipi-
demie au prezentat un risc al obezitå¡i mai mare
de 2,87 ori decât cei fårå dislipidemie. Rezultatele
prelucrårii statistice au fost: OR = 2,87, CI 95% =
2,08 – 3,97. Cum limita inferioarå a intervalului
de încredere este mai mare decât 1, dislipidemia
reprezintå un factor de risc pentru apari¡ia obe-
zitå¡ii.
Figura 4. Situa¡ia stårii de nutri¡ie în cadrul
lotului studiat
A existat o asociere importantå între afec¡iunile
cardiovasculare ¿i dislipidemii. Mai multe de 4/5
dintre subiec¡ii cu dislipidemie au avut ¿i afec¡iuni
cardiovasculare (88% la femei ¿i 86% la bårba¡i)
(Figura 5).
La bolnavii cardiovasculari, numårul pa-
cien¡ilor cu dislipidemie a fost mai crescut în
ambele medii, dar mai ales în mediul urban
(Figura 6).
Rezultatele statistice au fost: OR = 5,15, CI
95% = 3,79 – 6,98. Interpretarea este urmå-
toarea: pentru persoanele cu dislipidemie, riscul
så aibå o boalå cardiovascularå este cu 5,15 mai
mare decât la persoanele fårå dislipidemie. Cum
limita inferioarå a intervalului de încredere este
mai mare decât 1, dislipidemia reprezintå un
factor de risc important pentru apari¡ia bolii car-
diovasculare.
În lotul de pacien¡i studiat nu s-a gåsit o co-
rela¡ie între dislipidemii ¿i bolile hepatice. Numårul
bolnavilor cu afec¡iuni hepatice este u¿or crescut
în cazul celor care prezintå ¿i dislipidemii (61%)
fa¡å de cei non-dislipidemici (56%) (Figura 7). Su-
biec¡ii cu dislipidemie nu prezintå risc semnificativ
så aibå boalå hepaticå fa¡å de persoanele fårå
 DISLIPIDEMIILE ªI RELAºIA LOR CU PATOLOGIA GENERALÅ

Figura 7. Asocierea cu afec¡iuni hepatice

Figura 5. Corela¡ia dislipidemiei cu bolile 1, nu se pot face considera¡ii de protec¡ie sau

cardiovasculare ¿i sexul pacien¡ilor risc referitoare la variabila dislipidemiei pentru
boala colecistului.

Figura 8. Corela¡ia dislipidemiilor cu

colecistopatiile

În lotul studiat se observå o rela¡ie de tip

invers, prevalen¡a afec¡iunilor endocrine este mai
scåzutå la pacien¡ii care au ¿i dislipidemie fa¡å de
cei fårå dislipidemie (OR = 0,70) (Figura 9). Cum
Figura 6. Corela¡ia dislipidemiilor cu bolile
cardiovasculare ¿i mediul social limita superioarå a intervalului de încredere este
mai micå decât 1 (CI 95% = 0,54 – 0,91) se
poate concluziona cå variabila dislipidemiei nu
este factor de risc pentru boala endocrinå.
dislipidemie (OR = 1,24). Cum intervalul de
încredere include cifra 1 (CI 95% = 0,97 – 1,95),
nu se pot face considera¡ii de protec¡ie sau risc
referitoare la variabila dislipidemie pentru boala
hepaticå.
Nu existå o corela¡ie între dislipidemii ¿i
colecistopatii, poate doar o u¿oarå scådere a
numårului de afec¡iuni ale colecistului la pacien¡ii
cu dislipidemii (Figura 8).
Rezultatele ob¡inute au fost: OR = 0,76, CI
95% = 0,53 – 1,10. Interpretarea este urmå-
toarea: pentru persoanele cu dislipidemie, nu
existå risc semnificativ så aibå o suferin¡å a cole-
cistului mai mare decât la persoanele fårå disli-
pidemie. Cum intervalul de încredere include cifra Figura 9. Asocierea dislipidemiilor cu bolile endocrine

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 257

DISLIPIDEMIILE ªI RELAºIA LOR CU PATOLOGIA GENERALÅ
Pentru persoanele cu dislipidemie, nu existå
risc semnificativ så aibå o suferin¡å reumatismalå
(articularå) mai mare decât la persoanele fårå
dislipidemie (OR = 1,16); singura asociere a celor
douå boli ar putea fi explicatå doar prin cre¿terea
în greutate ¿i suprasolicitarea articula¡iilor (Figura
10). Cum intervalul de încredere (CI 95% = 0,90 –
1,49) include cifra 1, nu se pot face considera¡ii
de protec¡ie sau risc referitoare la variabila disli-
pidemiei pentru boala articularå.
Figura 10. Asocierea dislipidemiilor cu afec¡iunile articulare
Rela¡ia dislipidemiilor cu bolile digestive este
una inverså, frecven¡a afec¡iunilor digestive scade
de la 29% la pacien¡ii fårå dislipidemie la 13% la
pacien¡ii care prezintå dislipidemie (Figura 11).
Pentru persoanele cu dislipidemie existå risc mai
redus så aibå o boalå digestivå, decât la persoanele
fårå dislipidemie (OR = 0,38, CI 95% = 0,27 –
0,52). Cum limita superioarå a intervalului de
încredere este mai micå decât 1, se poate con-
cluziona cå variabila dislipidemiei nu este factor
de risc pentru boala digestivå.
Figura 11. Asocierea cu boli digestive
258 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
La lotul studiat se observå o rela¡ie inverså
între prezen¡a dislipidemiei ¿i afec¡iunile renale;
frecven¡a afec¡iunilor renale scåzând de la 34%
la pacien¡ii fårå dislipidemii, pânå la 25% la
pacien¡ii care prezintå dislipidemie (Figura 12).
Pentru persoanele cu dislipidemie existå risc mai
redus så aibå o boalå urogenitalå, decât la per-
soanele fårå dislipidemie (OR = 0,64, CI 95% =
0,49 – 0,83). Cum limita superioarå a intervalului
de încredere este mai micå decât 1, se poate
concluziona ca variabila dislipidemiei nu este
factor de risc pentru boala urogenitalå.
Figura 12. Asocierea cu afec¡iuni urogenitale
Dislipidemiile prezintå o rela¡ie inverså cu
afec¡iunile pulmonare, frecven¡a acestora din
urmå scåzând de la 28 % la pacien¡ii fårå
dislipidemii pânå la 20 % la cei ce nu prezintå
dislipidemie (Figura 13). Subiec¡ii cu dislipidemie
au un risc mai redus så aibå o boalå pulmonarå
decât cei fårå dislipidemie (OR = 0,65, CI 95% =
0,48 – 0,86). Cum limita superioarå a interva-
lului de încredere este mai micå decât 1 se poate
concluziona cå variabila dislipidemiei nu este
factor de risc pentru boala pulmonarå.
Figura 13. Legåtura cu afec¡iuni pulmonare
 DISLIPIDEMIILE ªI RELAºIA LOR CU PATOLOGIA GENERALÅ

Cea mai frecventå formå de dislipidemie a fost lot de pacien¡i.

reprezentatå de hipercolesterolemia izolatå cu
cre¿teri moderate sau severe ale colesterolului.
Valorile trigliceridelor au fost crescute într-o
propor¡ie mai reduså, iar HDL-colesterol a fost
în general normal. Severitatea hipercoleste-
rolemiei ar fi putut fi datå de predispozi¡ia gene-
ticå, dar ¿i de coexistenta altor factori de risc pre-
cum vârsta, sedentarismul sau fumatul. Frecven¡a
hipercolesterolemiilor severe, în special a formelor
primare (genetice) a fost reduså, dar în acela¿i
timp ace¿ti pacien¡i au prezentat riscul cardiovas-
cular cel mai înalt.
În ciuda scåderii drastice a riscului de boli
cardiovasculare în ultimii 15 ani, ca urmare a
måsurilor de sånåtate publicå luate de diverse
state ale lumii, boala cardiovascularå råmâne pe
primul loc, cauzând aproape 37% din totalul
cauzelor de mortalitate din lume. O cauzå in-
trinsecå a bolii cardiovasculare sunt dislipidemiile,
uneori exprimate discret clinic. Ac¡ionând din
timp asupra acestor factori de risc, prevalen¡a
bolilor cardiovasculare poate scådea, de¿i aceasta
este în cre¿tere ca urmare a cre¿terii speran¡ei de
via¡å ¿i paradoxal a îmbunåtå¡irii calitå¡ii asisten¡ei
medicale.
În studiul nostru, pacien¡ii cu dislipidemie au
avut un risc de 5,15 ori mai mare pentru bolile
cardiovasculare decât cei fårå dislipidemie.
CONCLUZII
1. Dislipidemiile prezintå o inciden¡å ridicatå
la pacien¡ii spitaliza¡i, cu vârsta peste 50
ani, mai ales la cei din mediul urban, pre-
dominând la bårba¡i. Diversele tipuri de
dislipidemii ajung în total la 68,72%, pro-
cent semnificativ ¿i îngrijoråtor din întregul
2. Prevalen¡a dislipidemiilor se gåse¿te la
valori ridicate, inclusiv la pacien¡ii diag-
nostica¡i cu suferin¡å cardiovascularå
ateroscleroticå, ace¿tia necon¿tientizând
riscul pe care îl reprezintå hipercoles-
terolemiile.
3. Dislipidemiile reprezintå factorul de risc
major pentru patologia cardiovascularå
(riscul relativ = 5,15).
4. Interrela¡ia dintre dislipidemie ¿i obezitate
(risc relativ = 2,87), aratå cå dislipidemia
reprezintå un factor de risc pentru obezitate
(¿i invers!), iar sumarea lor reprezintå un
factor de risc important pentru bolile car-
diovasculare.
5. Conform datelor ob¡inute în studiul de-
rulat, nu existå o rela¡ie semnificativå între
alte aspecte de patologie (boli hepatice,
digestive, pulmonare, renale, reumatis-
male) ¿i dislipidemii, adicå dislipidemiile nu
pot fi considerate un factor de risc pentru
aceste boli.
6. Dislipidemiile, ca o alterare calitativå ¿i/sau
cantitativå a metabolismului lipoprote-
inelor, se manifestå prin cre¿terea sau des-
cre¿terea concentra¡iei sangvine a coles-
terolului total, LDL colesterolului ¿i a triglice-
ridelor ¿i/sau descre¿terea concentra¡iei
LDL colesterolului. Sunt cele mai întâlnite
patologii în practica medicalå, iar prin riscul
cardiovascular ce îl implicå, prin costurile
ridicate de tratament, se impune o aten¡ie
sporitå ¿i permanentå în vederea depistårii,
diagnosticårii precise ¿i aplicårii precoce a
måsurilor terapeutice.

BIBLIOGRAFIE
1. Blake GH, Triplett LC –
Management of
hypercholesterolemia. Am Fam
Physician 1995; 51:1157-1166
2. Charrois TL, Johnson JA, Blitz S, et
al. – Relationship between number,
timing, and type of pharmacist
interventions and patient outcomes,
Am J Health Syst Pharm
September 1, 2005; 62(17):1798-
1801
3. Cheta D – HIperlipoproteinemiile, în
Medicina Internå, vol 2.: Bolile
cardiovasculare ¿i metabolice, L.
Gherasim, Editura Medicalå,
Bucure¿ti, 1996; 1323-1338
4. Genest J, Frohlich J, Fodor G,
et al. – Recommendations for the
management of dyslipidemia and the
prevention of cardiovascular disease:
summary of the 2003 update, Can
Med Assoc J, October 28, 2003;
169(9):921-924
5. Geurian KL – The cholesterol
controversy. Ann Pharmacother 1996;
30:495-500
6. Grundy SM, Pasternak R,
Greenland P, et al. – Assessment of
cardiovascular risk by use of
multiple-risk-factor assessment
equations. A statement for healthcare
professionals from the American
Heart Association and the American
College of Cardiology. Circulation
1999; 100:1481-1492

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 259

DISLIPIDEMIILE ªI RELAºIA LOR CU PATOLOGIA GENERALÅ
7. Grundy S – Hypertriglyceridemia,
atherogenic dyslipidemia and
metabolic syndrome. Am J Cardiol
1998; 81:18B-25B
8. Haskell W, Alderman E, Farin J, et
al. – Effects of intensive multiple risk
factor reduction on coronary
atherosclerosis and clinical cardiac
events in men and women with
coronary artery disease. The Stanford
Coronary Risk Intervention Program
(SCRIP). Circulation 1994; 89:975-990
9. Hâncu N – Obezitatea ¿i
dislipidemiile în practica medicalå.
Ghid de buzunar pentru medicul
Revista presei medicale
Liber la E-uri. Ministerul Sånåtå¡ii
introduce aditivi periculo¿i în alimente
No restriction to additives. The Ministry of Health approves the introduction of potentially dangerous
Ordinul nr. 438/295/2002, pri-
vind aditivii alimentari va fi modificat
printr-un proiect de act normativ
elaborat de ministrul sånåtå¡ii Eugen
Nicolaescu. La prima vedere pare cå,
în sfâr¿it, autoritå¡ile din România
s-au trezit ¿i vor så ne scape de E-urile
periculoase. În realitate, proiectul
scoate câteva E-uri, de ochii lumii, ¿i
adaugå altele, mai nocive. În plus,
actul normativ majoreazå considerabil
cantitå¡ile maxime admise ale aditivi-
lor din produsele alimentare. Potrivit
acestuia, prezen¡a unui aditiv alimen-
tar nu va mai fi autorizatå pentru
preparatele pe bazå de cereale prelu-
crate ¿i alimentele pentru sugari ¿i
copii de vârstå micå. Totodatå, E 400-
404, E 406, E 407, E 410-415, E 417,
E 418 ¿i E 440 vor fi interzise la
fabricarea minijeleurilor, definite ca
jeleuri de consisten¡å durå, ingerate
dintr-o singurå înghi¡iturå dupå in-
troducerea în gurå. Din lista cu con-
servan¡i ¿i antioxidan¡i autoriza¡i
condi¡ionat, adicå în doze cu maxime
stabilite de lege, din cauza faptului
cå sunt dåunåtori, dispar E 216 ¿i E
260 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
practician. Bucure¿ti, Infomedica,
1998
10. Harrison – Principii de Medicinå
Internå, Edi¡ia 14, Editura Teora,
2001; 2353-2360
11. Kronenberg F, Kronenberg M,
Kiechl S, et al. – Role of
lipoprotein(a) and apolipoprotein(a)
phenotype in atherogenesis.
Prospective results from the Bruneck
Study. Circulation 1999; 100:1154-
1160
12. Sacks F, Pfeffer M, Moye L, et al. –
The effect of pravastatin on coronary
events after myocardial infarction in
food additives
CLAUDIA MARCU, ANDREEA PETRESCU
217. De precizat cå E 217 era deja
interzis în mai multe ¡åri. Conser-
van¡ii ¿i antioxidan¡ii autoriza¡i
condi¡ionat se eliminå definitiv din
compozi¡ia creve¡ilor prepara¡i, a
cozilor de raci preparate ¿i preambalate
¿i a molu¿telor preparate ¿i marinate,
precum ¿i din suplimentele alimentare
dietetice lichide. În schimb, acestea vor
fi permise la prepararea crustaceelor ¿i
molu¿telor tratate termic ¿i în supli-
mentele alimentare comercializate sub
formå lichidå.
Liber la nitrit de potasiu
E 249, nitrit de potasiu, este un
fixator de culoare ¿i agent de con-
servare pentru carne. Acesta poate
produce ame¡eli, dureri de cap ¿i este
poten¡ial cancerigen, nefiind permiså
utilizarea în alimentele pentru sugari
¿i copii. În ordinul actual era admis,
în cantitate de 150 mg/kg, în pro-
dusele din carne netratate termic,
afumate ¿i uscate. În modificårile
legislative, cantitatea este permiså în
toate produsele din carne. E 250, nitrit
de sodiu – poate provoca hiperreac-
patients with average cholesterol
levels. N Engl J Med 1996; 335:1001-
1009
13. Wilson P, D’Agostino R, Levy D, et
al. – Prediction of coronary heart
disease using risk factor categories.
Circulation 1998; 97:1837-1847
14. Third Report of the National
Cholesterol Education Program
(NCEP) Expert Panel on Detection,
Evaluation, and Treatment of High
Blood Cholesterol in Adults (Adult
Treatment Panel III). Final report.
Circulation 2002; 106:3143-3421
tivitate ¿i alte reac¡ii adverse, fiind
poten¡ial cancerigen, fiind restric-
¡ionat în multe ¡åri. În prezent, este
admiså o cantitate de 150 mg/kg la
alte produse din carne afumatå ¿i
produse din carne în conservå. Po-
trivit proiectului de ordin, în produse
din carne tradi¡ionale conservate, cum
ar fi Paprikas ¿i Selsky salam, canti-
tatea maximå permiså de nitrit de
sodiu va fi de 180 mg/kg.
În proiectul de act normativ se aflå
¿i o confuzie dubioaså. E 251 este
trecut ca nitrat de potasiu, iar E 252
este nitrat de sodiu. În realitate, E 251
este nitrat de sodiu ¿i E 252 este nitrat
de potasiu. Confuzia este destul de
gravå, având în vedere cå E 252 poate
provoca hiperactivitate ¿i alte reac¡ii
adverse, este poten¡ial cancerigen, iar
folosirea sa este restric¡ionatå în multe
¡åri. Din proiect reiese cå E 252 poate
fi utilizat în cantitå¡i de 300 mg/kg
în produse din carne tradi¡ionale,
conservate prin inserare în solu¡ie de
saramurå, în cele conservate prin
uscare. Totodatå, E 252, în cantitate
de 150 mg/kg, se va introduce, ca

noutate, ¿i în brânzå cu pastå tare,
semitare ¿i semimoale, înlocuitori de
brânzå pe bazå de produse lactate.
Heringul marinat ¿i sprotul vor putea
con¡ine E 252 în cantitate de 500 mg/
kg, pânå acum nefiind permiså decât
o cantitate rezidualå de nitrat de
potasiu de 50 mg/kg. Un antioxidant
Revista presei medicale
Medicii nu mai pot så-¿i cumpere
Doctors can no longer purchase their practices
Legea care permite primåriilor så vândå spa¡iile a fost declaratå neconstitu¡ionalå
Medicii nu vor mai putea så-¿i
cumpere cabinetele în care î¿i desfå-
¿oarå activitatea. Curtea Constitu¡io-
nalå a declarat legea în baza cåreia
cabinetele medicale pot fi cumpårate
ca fiind neconstitu¡ionalå.
Oamenii în halate albe sunt ne-
mul¡umi¡i pentru cå spun cå au
investit în cabinetele respective cu
gândul cå, în viitor, le vor apar¡ine.
Curtea Constitu¡ionalå a declarat
Legea 236/2006, care modificå ¿i
completeazå Ordonan¡a de Urgen¡å a
Guvernului nr. 110/2005, în baza
cåreia primåriile puteau så vândå
medicilor spa¡iile aflate în proprietatea
consiliilor locale, ca fiind neconsti-
tu¡ionalå. Asta înseamnå cå legea nu
mai poate fi aplicatå.
Pre¡ul de vânzare este „neserios“
Decizia Cur¡ii Constitu¡ionale nr.
871, din 9 octombrie 2007, a fost luatå
în urma depunerii excep¡iei de ne-
constitu¡ionalitate ridicatå de Consi-
liul Local al comunei Bon¡ida, jude¡ul
Cluj. În motivarea excep¡iei se sus¡ine
cå actele sunt neconstitu¡ionale, în-
trucât „bunurile la care acestea se
referå fac parte din domeniul public
al unitå¡ii administrativ – teritoriale,
iar nu din domeniul privat”. Conform
deciziei Cur¡ii Constitu¡ionale, pre¡ul
la care urmau så fie vândute cabinetele
DISLIPIDEMIILE ªI RELAºIA LOR CU PATOLOGIA GENERALÅ
periculos, E 319 (Tert-butilhidro-
chinona) va putea fi introdus în
unturå, ulei de pe¿te, gråsime de vitå,
pasåre ¿i oaie. E 319 este un produs
pe bazå de ¡i¡ei ¿i se recomandå evi-
tarea sa. Aceasta poate cauza gre¡uri,
vårsåturi, delir – o dozå de 5 grame
fiind consideratå letalå. Cantitatea de
cabinetele medicale
este catalogat drept „neserios“, în-
trucât nu ¡ine cont de valoarea pe
pia¡å a bunului. Astfel, conform
Ordonan¡ei 110/2005, pre¡ul maxi-
mal de vânzare al cabinetelor medicale
este stabilit pe categorii de localitå¡i,
iar în privin¡a terenului aferent este
stabilit un pre¡ fix de 1 euro pentru
un metru påtrat. Întrucât Constan¡a
este localitate de rangul I, pre¡ul
maximal de vânzare ar fi fost de 50 de
euro pe metrul påtrat, asta în con-
di¡iile în care pre¡ul maximal de
vânzare pe pia¡a imobiliarå este de
1.500-1.600 de euro.
Curtea Constitu¡ionalå mai moti-
veazå decizia de declarare a neconsti-
tu¡ionalitå¡ii prin faptul cå, vânzând
aceste spa¡ii, statul nu mai poate lua
„måsuri de asigurare a igienei ¿i
sånåtå¡ii publice“ ¿i nu mai poate crea
„condi¡iile care så asigure prestarea de
servicii medicale“, obliga¡ii prevåzute
în Constitu¡ia României, întrucât
existå riscul ca dupå ce vor fi vândute,
cabinetele så-¿i schimbe destina¡ia.
Medicii de familie sunt foarte
nemul¡umi¡i de aceastå decizie ¿i spun
cå au investit în spa¡iile în care î¿i
desfå¿oarå activitatea cu gândul cå le
vor cumpåra în timp. Dr. Elena
Dråghici, medic de familie în Con-
stan¡a, ne-a declarat: „Vara trecutå
cred cå am investit 16.000-18.000 de
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
E 385 cre¿te la crustacee congelate sau
înghe¡ate de la 75 mg/kg la 250 mg/
kg. E 385 produce perturbåri sale
echilibrului electrolitic, afec¡iuni gas-
trointestinale ¿i crampe intestinale,
fiind interzis în unele ¡åri.
Sursa: GARDIANUL, 15.11.2007
ALINA ENACHE
lei în cabinetul unde îmi desfå¿or
activitatea. Noi am fost deconecta¡i
de la centrala cartierului ¿i ne-au låsat
în frig o iarnå. Am folosit re¿ouri
electrice, s-a format mucegai, a¿a cå
am decis så cumpår centralå. Am
investit foarte mul¡i bani. Cabinetul
în care lucrez a fost, demult, magazie,
a¿a cå a trebuit så creez condi¡iile
necesare, fiindcå nu aveam nici måcar
o chiuvetå. De ¿apte ani am investit
în acest cabinet. Acum ce fac, îmi då
primåria banii înapoi?“, ne-a declarat
medicul.
De cealaltå parte, autoritå¡ile sa-
nitare spun cå decizia Cur¡ii Consti-
tu¡ionale este îndreptå¡itå. Dr. Tan¡a
Cule¡u, directorul adjunct al Auto-
ritå¡ii de Sånåtate Publicå a jude¡ului
Constan¡a, spune cå nu ar fi fost
normal ca medicii så cumpere cabi-
netele la un pre¡ atât de mic, în com-
para¡ie cu pre¡ul de pe pia¡å. „Or fi
investit în cabinete! Unii ¿i-au luat
termopane, au pus linoleum, dar au
beneficiat de deduceri de impozit.
Altceva nu au fåcut! ªi eu a¿ fi decla-
rat legea necostitu¡ionalå!“, a declarat
dr. Cule¡u.
Cât timp legea a fost aplicabilå, la
Constan¡a nu a fost vândut nici un
cabinet medical, dupå cum a precizat
directorul adjunct al ASPJ.
Sursa: CUGET LIBER, 07.11.2007
261
 4 PRACTICA MEDICALÅ
REFERATE GENERALE

Prof. Dr. Silvia MÅTÅSARU
Canalul atrio-ventricular
comun
The common atrioventricular channel
Prof. Dr. SILVIA MÅTÅSARU
Disciplina Medicina de Familie – copii, UMF „Gr.T. Popa“, Ia¿i

DEFINIºIE
Malforma¡ie complexå datoratå unei tulburåri
în dezvoltarea burele¡ilor endocardici, care in-
tervin în formarea por¡iunii inferioare a SIA,
por¡iunii superioare a SIV ¿i a valvei mitrale ¿i
tricuspide.
Malforma¡ia asociazå:
• DSA OP
• DSV înalt
• Cleft de valvå mitralå ± tricuspidå
Severitatea anomaliilor variazå considerabil,
de la un DSA OP + cleft de valvå mitralå pânå la
forma completå în care existå un singur canal
atrio-ventricular.
Ca frecven¡å, reprezintå cam 2-5% din totalul
malforma¡iilor congenitale cardiace.
Se poate asocia cu:
– boala Down
– sdr. Ellis van Creveld (displazie ectodermicå
+ polidactilie) ‰
EMBRIOLOGIE
Închiderea regiunii atrio-ventriculare începe în
såptåmâna a 4-a embrionarå prin apari¡ia a 4
burele¡i (burjoni) endocardici, situa¡i în lumenul
canalului atrio-ventricular, care separå atriul
primitiv de ventriculul primitiv. Anomaliile de
dezvoltare ale burele¡ilor endocardici vor produce
defecte structurale de grade variate ale SIA, SIV
¿i valvelor atrio-ventriculare. ‰
Clasificare
Existå 3 tipuri de canal atrio-ventricular comun
(CAV):
• par¡ial:
– DSA OP + cleft VMA
– atriu unic
– comunicare VS-AD
• intermediar (DSA OP ± DSV ± cleft VMA/
VT)
• complet: din cauza absen¡ei totale a fu-
ziunii burele¡ilor endocardici între ei ¿i cu
structurile septale existå un singur inel atrio-
ventricular cu 4-6 cuspe sau 2 hemivalve
mitro-tricuspidiene.
În func¡ie de anatomia hemivalvei anterioare
(Rastelli) se disting 3 tipuri:
A. Cordajele plecând din cleft (fantå) se inserå
pe creasta SIV sau pe marginea sa dreaptå;
jumåtatea stângå se inserå pe pilierul anterior al
mitralei, jumåtatea dreaptå pe pilierul anterior al
tricuspidei.
B. Cordajele plecând din cleft se inserå pe un
pilier accesoriu în ventriculul drept.
C. Hemivalva anterioarå nedivizatå se inserå
în VS ¿i VD pe pilierii anteriori ai mitralei ¿i
tricuspidei.
Defecte asociate (în afara carefurului atrio-
ventricular):
• Scurtarea camerei de umplere a VS, com-
parativ cu camera de golire, rezultând
verticalizarea inelului mitral;

262 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007

 CANALUL ATRIO-VENTRICULAR COMUN

Figura 1. Schematizarea celor 3 forme

de CAV: par¡ialå, intermediarå ¿i
completå.
(dupå Coppin M ¿i Corone P. Canal
atrio-ventriculaire. Encycl. Med.Chir.
Paris, coeur-vaisseaux, 11041 G10, 3-
1981)

Figura 2. Forma completå de CAV Figura 3. Dispozi¡ia în spa¡iu a CAV

(dupå Blondeau PH, Henry E) (dupå M. Toussaint)

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 263

CANALUL ATRIO-VENTRICULAR COMUN

• Anomalii de pozi¡ionare ¿i orientare a ori-

ficiului aortic;
ASPECTE CLINICE
• Defect septal atrial tip ostium secundum, Descoperirea se face:
stenozå pulmonarå, transpozi¡ie de vase • la un examen de rutinå, sau
• din cauza dispneii de efort, pneumopatiilor
mari, ventricul unic, tetralogie Fallot.
repetate, hipotrofiei staturo-ponderale.
• Anomalii ale cåilor de conducere:
În formele grave, descoperirea poate fi mai
– deplasare postero-inferioarå a nodului
precoce, uneori chiar dupå na¿tere.
Tawara,
Examenul fizic deceleazå:
– lungirea sau scurtarea trunchiului sau ra-
• suflul sistolic ejec¡ional în spatiul II intercostal
murilor fascicolului Hiss.
stâng, legat de hiperdebitul pulmonar;
• Asplenie, polisplenie
• dedublarea sg. II în focarul pulmonarei
CAV neechilibrat: un ventricul este hipoplazic,
• suflul diastolic xifoidian, datorat hiperde-
iar celalalt de¡ine cea mai mare parte din valva
bitului tricuspidian;
atrio-ventricularå. ‰
• în IM – suflu holosistolic dulce apexo-
axilar;
FIZIOPATOLOGIE • hiperactivitate precordialå ventricularå
Douå elemente dominå fiziopatologia CAV: dreaptå.
1. Importan¡a ¿untului stg.-dr.: Când ¿untul este important ¿i IM severå apar:
• atrial (AS-AD) 1. dispneea de efort
• ventricular: VS -VD; VS-AD 2. insuficien¡a cardiacå congestivå, hepato-
În func¡ie de: megalie
– mårimea comunicårilor (CIA, CIV) 3. cardiomegalia
– importan¡a regurgitårii mitrale 4. bombarea regiunii precordiale
– raportul dintre circula¡ia pulmonarå ¿i 5. pneumopatiile recurente
sistemicå, (nivelul rezisten¡elor pulmonare), 6. falimentul cre¿terii
exceptând ¿untul VS-AD, unde gradientul În formele complete de CAV:
dintre cele 2 cavitå¡i este totdeauna sufi- – sg. I accentuat
cient pentru men¡inerea lui. – sg. II dedublat
Contribuie la cre¿terea debitului pulmonar ¿i – suflul sistolic 3-4/6 pe marginea stângå a
la apari¡ia mai rapidå a modificårilor vasculare sternului (CIV)
pulmonare. – suflul sistolic apexian dulce (IM)
2. Importan¡a regurgitårii mitrale (care se face – suflul diastolic xifoidian (hiperdebit tricus-
în mare parte cåtre atriul drept), din cauza: pidian)
• pierderilor de substan¡å Odatå cu apari¡ia bolii vasculare obstructive
• polisegmentårilor pulmonare:
• inser¡iei VMA pe cordaje anormale – se diminueazå pânå la dispari¡ie suflul sis-
IM agraveazå alterårile patului vascular pul- tolic parasternal stâng,
monar prin majorarea presiunilor în AS ¿i a – sg. II este întårit în focarul pulmonarei ¿i
¿untului stg.-dr. atrial. poate apårea
Simplul cleft nu produce totdeauna insufi- – suflul diastolic de insuficien¡å pulmonarå.
cien¡å. Eventuala regurgitare tricuspidianå nu are
råsunet hemodinamic notabil. Formele par¡iale Examene complementare
de CAV, în ciuda debitului pulmonar crescut au • EKG:
mult timp o toleran¡å hemodinamicå bunå, în – CAV par¡ial:
timp ce formele complete, reunind mai multe – bloc minor de ram drept
cauze de HTP evolutivå ¿i o tendin¡å precoce de – bloc A-V gr. I
cre¿tere a rezisten¡elor vasculare pulmonare ¿i – axå electricå deviatå la stânga (- 60°)
insuficien¡å cardiacå sunt grevate de o mortalitate – P de suprasolicitare atrialå dreaptå
precoce, în cazul în care corec¡ia chirurgicalå nu – SDVD
se face în timp util. Poate apårea un ¿unt drept- – CAV formå completå:
stâng la nivel atrial ¿i ventricular, conducând la o – axå electricå deviatå la stânga (- 60-120°)
desaturare arterialå. În timp, boala vascularå – bloc A-V gr.
pulmonarå accentueazå ¿untul drept-stâng, încât – HAD, HVD/HBV
apare cianoza (sdr. Eisenmenger). ‰ – HAS (în IM severå)

264 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007


• Fonocardiograma confirmå suflurile pre-
zentate la ex. clinic.
• Examenul radiologic:
– cardiomegalia mai mult sau mai pu¡in
importantå, pe seama:
– AD (arcul inferior drept)
– HVD ± VS ± AS
– AP largi ± expansive
– vasculariza¡ia pulmonarå crescutå
În boala vascularå obstructivå pulmonarå
(BVOP) cre¿te transparen¡a la periferia câmpurilor
pulmonare.
• Ecocardiografia:
Cele mai bune incidente:
– apicalå 4 camere
– subcostalå
– sec¡iunea transversalå a VS (pentru cleftul
mitral)
În CAV total se eviden¡iazå:
– DSA-OP
– DSV
– o hemivalvå care trece pe deasupra SIV,
baleind ambele cavitå¡i ventriculare sau
– 2 hemivalve ce se deschid în oglindå
– determinarea punctelor de inser¡ie ale
cordajelor valvelor A-V comune ± even-
tuale cordaje la nivelul septului interven-
tricular
– VD mårit
– pozi¡ie joaså anormalå a valvei atrio-
ventriculare ® deformare în gât de ga¿cå
a tractului de ie¿ire al VS (¿i angiografic)
– ambele valve (mitralå ¿i tricuspidå) se inse-
reazå la acela¿i nivel din cauza absen¡ei
septului interventricular (SIV)
– în CAV complet SIV poate lipsi
Dopplerul pulsatil ¿i color demonstreazå:
• ¿untul stâng – drept la nivel:
– atrial
– ventricular
– ventriculo-atrial
• cuantificå gradul insuficien¡ei valvei atrio-
ventriculare
• evaluarea leziunilor asociate: persisten¡a de
canal arterial, coarcta¡ia de aortå, stenozå
pulmonarå etc.
Cateterismul ¿i angiocardiografia pot fi
necesare pentru confirmarea diagnosticului, de¿i
majoritatea pacien¡ilor pot fi opera¡i fårå cate-
terism. Acestea demonstreazå:
– mårimea ¿untului stg.-dr.
– severitatea HTP ¿i a cre¿terii rezisten¡elor
vasculare pulmonare
– severitatea insuficien¡ei valvei comune
A-V
CANALUL ATRIO-VENTRICULAR COMUN
Prin oximetrie este demonstrat ¿untul la nivel
atrial/ventricular. Saturarea arterialå în oxigen este
normalå sau u¿or reduså, exceptând boala
vascularå pulmonarå severå. Copiii cu DSA-OP
au presiune arterialå pulmonarå normalå sau
u¿or crescutå. Din contrå, CAV forma completå
se asociazå cu HTP ¿i ventricularå dreaptå, iar
pacien¡ii mai în vârstå cu cre¿terea rezisten¡elor
vasculare pulmonare.
Ventriculografia selectivå stângå este edifica-
toare în diagnosticul defectelor septale A-V.
Deformarea valvei mitrale sau valvei comune A-
V ¿i distorsiunea tractului de ie¿ire al VS då
acestuia aspectul de gât de gâscå.
Se poate observa inser¡ia anormalå a VMA ¿i
regurgitarea atât în AS, cât ¿i în AD. Se poate
demonstra ¿i ¿untul direct VS®AD.
În comunicarea VS®AD se constatå o
îmbogå¡ire în O2 exclusivå sau esen¡ialå în AD,
care sugereazå un ¿unt stâng-drept, dar sonda
nu poate fi dirijatå din AD în AS. ‰
EVOLUºIE, PROGNOSTIC,
COMPLICAºII
CAV par¡ial este bine tolerat într-un numår
apreciabil de cazuri, fiind mult timp compatibil
cu o via¡å normalå (pânå în decada a 3-a, a 4-a
de via¡å). Pot totu¿i surveni unele complica¡ii:
• sub vârsta de 10 ani:
– insuficien¡a cardiacå
– infec¡iile pulmonare repetate (mai frecvent
în IM importantå)
• dupå vârsta de 20 de ani:
– tulburårile de ritm ¿i de conducere:
– extrasistolele
– TSV
– flutterul, fibrila¡ia atrialå
– bloc A-V complet cu accese Adams-Stokes
– grefa oslerianå, abcesul cerebral
CAV-formå completå: prognosticul depinde
de:
– importan¡a ¿untului stâng-drept
– gradul cre¿terii rezisten¡elor vasculare
pulmonare
– severitatea insuficien¡ei valvulei atrio-
ventriculare
Înaintea chirurgiei corective, ace¿ti copii
mureau în perioada de sugar, iar cei ce supra-
vie¡uiau dezvoltau boala vascularå obstructivå
pulmonarå, în aceastå situa¡ie nemaiexistând nici
o posibilitate terapeuticå.
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 265
CANALUL ATRIO-VENTRICULAR COMUN

TRATAMENT Totu¿i, ¿i în formele complete, la orice grupå

• Medical:
– digitalo-diuretic în insuficien¡å cardiacå
– prevenirea endocarditei infec¡ioase
– vasodilatatoare (captopril)
• Chirurgical: este tratamentul de elec¡ie în
toate formele.
DSA-OP – prin defectul atrial se reparå cleftul
mitral ¿i apoi se închide DSA prin petec sintetic.
Mortalitatea este scåzutå.
În CAV – forma completå, tratamentul chi-
rurgical este mai dificil din cauza insuficien¡ei
cardiace ¿i hipertensiunii pulmonare, dar trebuie
realizat la vârsta de sugar, datoritå riscului bolii
vasculare pulmonare. În cazul în care copilul e
prea mic sau riscul e prea mare din cauza unor
leziuni asociate, se poate efectua, ini¡ial, banding
de arterå pulmonarå.
de vârstå e preferatå corec¡ia per primam. DSA
¿i DSV se închid printr-un singur petec sau prin
douå petece separate, iar valvele, mitralå ¿i
tricuspidå, se reconstruiesc.
Complica¡iile postoperatorii:
– blocul A-V gr. III necesitå pacemaker
permanent
– îngustarea tractului de ie¿ire al VS sau ste-
nozå mitralå necesitând revizuire chirur-
gicalå
– agravarea regurgitårii mitrale necesitå plas-
tie sau protezare mitralå.
Mortalitatea operatorie poate ajunge la 15-
50% în formele complete de CAV. Formele cu
arteriolitå pulmonarå contraindicå tratamentul
chirurgical. ‰

BIBLIOGRAFIE
1. Tweddell JS, Litwin SB, Berger S,
et al. – Twenty-year experience with
repair of complete atrioventricular
septal defects. Ann Thorac
Surg. Aug 1996; 62(2): 419-424.
2. Bando K, Turrentine MW, Sun K,
et al. – Surgical management of
complete atrioventricular septal
defects. A twenty-year experience. J
Thorac Cardiovasc Surg. Nov 1995;
110(5): 1543-1552; discussion 1552-
1554
3. Najm HK, Coles JG, Endo M,
et al. – Complete atrioventricular
septal defects: results of repair, risk
factors, and freedom from
reoperation. Circulation. Nov 4 1997;
96(9 Suppl): II-311-315
4. De Oliveira NC, Sittiwangkul R,
McCrindle BW, et al. – Biventricular
repair in children with
atrioventricular septal defects and a
small right ventricle: anatomic and
surgical considerations. J Thorac
Cardiovasc Surg, Aug 2005; 130(2):
250-257
5. Alexi-Meskishvili V, Ishino K,
Dahnert I, et al. – Correction of
complete atrioventricular septal
defects with the double-patch
technique and cleft closure. Ann
Thorac Surg, Aug 1996; 62(2): 519-
524; discussion 524-5
6. Backer CL, Mavroudis C, Alboliras
ET, Zales VR – Repair of complete
atrioventricular canal defects: results
with the two- patch technique. Ann
Thorac Surg, Sep 1995; 60(3): 530-537
7. Cabrera A, Pastor E, Galdeano JM,
et al. – Cross-sectional
echocardiography in the diagnosis of
atrioventricular septal defect. Int
Cardiol, Jul 1990; 28(1): 19-23
8. LeBlanc JG, Williams WG, Freedom
RM, Trusler GA – Results of total
correction in complete
atrioventricular septal defects with
congenital or surgically induced right
ventricular outflow tract obstruction.
Ann Thorac Surg, Apr 1986; 41(4):
387-391
9. Monro JL, Alexiou C, Salmon AP,
Keeton BR – Reoperations and
survival after primary repair of
congenital heart defectsin children. J
Thorac Cardiovasc Surg, Aug 2003;
126(2): 511-520
10. Tedziagolska M – Two-patch repair
of atrioventricular canal. Ann Thorac
Surg, May 1996; 61(5): 1589-1590
11. Yamaki S, Yasui H, Kado H, et al. –
Pulmonary vascular disease and
operative indications in complete
atrioventricular canal defect in early
infancy. J Thorac Cardiovasc Surg, Sep
1993; 106(3): 398-405
Zellers TM, Zehr R, Weinstein E,
et al. – Two-dimensional and
Doppler echocardiography alone can
adequately define preoperative
anatomy and hemodynamic status
before repair of complete
atrioventricular septal defect in
infants < 1 year old. J Am

266 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007


Revista presei medicale
Medicii vor cabinetele, cum s-au privatizat
fabricile: pe promisiuni de investi¡ii
Medics want their practices. The manners in wich factories were privatized on investment promises
Ministrul sånåta¡ii, Eugen
Nicolaescu, a declarat, vineri, la Cluj-
Napoca cå vrea adoptarea, în procedurå
de urgen¡å, a proiectul de lege privind
vânzarea cabinetelor medicale. Mi-
nistrul sus¡ine cå a stat de vorbå cu
unii parlamentari despre adoptarea
unui proiect de lege în acest sens pânå
la începerea vacan¡ei parlamentare.
„Såptåmâna viitoare voi avea acea
formå finalå, dupå care voi merge la
fiecare grup parlamentar så cer sprijin
pentru adoptarea acestui act normativ
în procedurå de urgen¡å“, a afirmat
ministrul. El a adåugat cå procesul
de vânzare a cabinetelor a fost blocat
prin decizia Cur¡ii Constitu¡ionale,
care a declarat neconstitu¡ionalå Or-
donan¡a Guvernului nr. 110 privind
vânzarea spa¡iilor proprietate privatå
a statului sau a unitå¡ilor adminis-
trativ-teritoriale, cu destina¡ia de
cabinete medicale. Nicolaescu sus¡ine
cå pânå la mijlocul såptåmânii vi-
itoare ministerul va avea un proiect
concret, pe care îl va depune la Senat,
pentru a fi adoptat în procedura de
urgen¡å pânå la Cråciun. Tot pânå la
aceastå datå, ministrul apreciazå cå
va fi finalizat ¿i proiectul de lege
SOCIETźII ACADEMICE
CANALUL ATRIO-VENTRICULAR COMUN
privind reziden¡iatul pe post, aflat în
dezbatere cu Asocia¡ia Medicilor Rezi-
den¡i, ce are unele propuneri pe aceastå
temå.
Medicii spun cå nu vor mai investi
în spa¡iile cu destina¡ia de cabinete
medicale decât dupå ce autoritå¡ile vor
gåsi o nouå solu¡ie de vânzare a
acestora, deoarece din data de 17
octombrie, procesul de vânzare a fost
sistat prin declararea neconstitu¡io-
nalitå¡ii legii care permitea achizi¡ia
lor.
Curtea Constitu¡ionalå a decis
cå guvernul nu poate obliga pri-
måriile så-¿i vândå spa¡iile
Potrivit deciziei cu numårul 870
a Cur¡ii Constitu¡ionale, argumentele
invocate pentru declararea neconstitu-
¡ionalitå¡ii articolelor ce permit vân-
zarea cabinetelor cåtre medicii care î¿i
desfå¿oarå activitatea în spa¡iul lor au
fost cu privire la încålcarea drepturilor
la proprietate prin obligativitatea
primåriilor de a vinde spa¡iile, dar ¿i
pre¡ul metrului påtrat de cabinet, a
explicat pentru NewsIn profesorul
George Borcean de la Colegiul Medi-
cilor. Dr. Rodica Tånåsescu a precizat
Vizita¡i site-ul
DE MEDICINÅ
www.samf.ro
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
cå o vânzare la pre¡ul pie¡ei nu ar fi
justificatå deoarece medicii care
cumpårau cabinetele medicale în care
î¿i desfå¿oarå activitatea aveau
anumite condi¡ionåri.
„Primåriile nu au investit nici un
ban în aceste spa¡ii ca så î¿i justifice
în vreun fel preten¡ia de a stabili
pre¡ul, iar medicii s-au såturat så facå
repara¡ii ¿i så renoveze spa¡ii care nu
le apar¡in“, a spus pre¿edinta AMFB.
„Pentru 15 metri påtra¡i, cât revine
în medie unui medic pe cabinet me-
dical ¿i pe care primåria trebuie så-i
vândå, agita¡ia aceasta cu declararea
legii drept neconstitutionalå este re-
voltåtoare, mai ales ca ¿tim cu to¡ii
cå fabrici întregi au fost vândute ieftin
din diferite motive, iar în cazul nostru
existå atâtea opozi¡ii“, a mai spus
Rodica Tånåsescu. „Am fi bucuro¿i
dacå påstrându-le (n.r. - spa¡iile),
acele primårii î¿i iau råspunderea så
le renoveze, modernizeze, doteze în cel
mai scurt timp, cåci normele europene
de func¡ionare a cabinetelor bat la u¿å,
iar noi nu vom mai investi în pere¡ii
altor proprietari“, a adåugat medicul.
Sursa: GARDIANUL, 04.11.2007
A FAMILIEI
267
 5 PRACTICA MEDICALÅ
CAZURI CLINICE

Tablou hematologic de
împrumut într-un neoplasm
poza
mamar cu metastaze
medulare.
Importan¡a biopsiei medulare –
Conf. Dr. Ana-Maria
VLÅDÅREANU
caz clinic
Bone marrow metastatic breast carcinoma
presenting as a full blood leukemia picture.
The importance of bone marrow biopsy –
case report
Conf. Dr. ANA-MARIA VLÅDÅREANU*, Dr. IRINA VOICAN*,
Dr. VERONICA VASILACHE*, Dr. CRISTINA CIUFU*, Dr. HORIA BUMBEA*,
Dr. MÅDÅLINA BEGU*, Dr. ANCA NICOLESCU*, Dr. MINODORA ONISAI*,
Dr. SÂNZIANA RADESI*, Dr. CAMELIA DOBREA**,
Prof. Dr. CARMEN ARDELEANU**, Dr. VIOLA POPOV***, Dr. DAN JINGA****
*Clinica de Hematologie, Spitalul Universitar de Urgen¡å Bucure¿ti
**Institutul Na¡ional „Victor Babe¿“
***Sec¡ia Medicalå, Spitalul Jude¡ean Arge¿
****Compartimentul de Oncologie, Spitalul Universitar de Urgen¡å Bucure¿ti

REZUMAT
Multe afec¡iuni maligne pot determina modificåri hematologice ce mimeazå perfect patologia hematologicå.
Prezentåm cazul unei paciente în vârstå de 45 ani, la care, de¿i analizele primare sugerau diagnosticul de
eritroleucemie, investiga¡iile aprofundate au eviden¡iat cå determinårile hematologice erau în cadrul unei alte
neoplazii.

Cuvinte cheie: eritroleucemie, neoplazie, hemoleucograma, biopsie

ABSTRACT
Many malignant disorders can induce hematological features that perfectly mimic a hematologic disease. We
present the case of a 45 years old female patient in which although the preliminary investigation suggested the
diagnosis of erythroleukemia, the more detailed subsequent assays revealed that the hematological picture was
the consequence of another neoplastic disease.

Key words: erythroleukemia, neoplasia, blood cell count, biopsy

268 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007

 TABLOU HEMATOLOGIC DE ÎMPRUMUT ÎNTR-UN NEOPLASM MAMAR CU METASTAZE MEDULARE
B
olile neoplazice hematologice ¿i non-
hematologice pot induce o paletå
variatå de modificåri ale tabloului
sangvin periferic. Modificårile tabloului
sanguin pot include citopenii izolate
(frecvent anemie, mai rar leucopenie sau trom-
bocitopenie izolatå), pancitopenii, bicitiopenii,
precum ¿i cre¿teri ale numårului de leucocite ¿i
modificåri ale formulei leucocitare constituindu-se
în a¿a numitul tablou leucoeritroblastic. Mecanis-
mele patogenice implicate în aceste modificåri
sunt complexe ¿i nu în totalitate elucidate. Este
¿tiut în prezent cå modificårile hematologice
descoperite la pacien¡ii cu cancer pot fi consecin¡å
directå a bolii sau secundare unor complica¡ii ale
cancerului.
Tumorile maligne ¿i în special cele hemato-
poietice pot fi cauza primarå a uneia sau mai
multor citopenii. La pacien¡ii cu sindroame
mielodisplazice sau mieloproliferative, o clonå
anormalå de celule stem hematopoietice înlocu-
ie¿te hematopoieza normalå în måduva osoaså.
Aceastå clonå prezintå frecvent anomalii genetice
care determinå atât modificåri privind citologia
medularå, cât ¿i func¡ia acestor celule, scåzând
capacitatea de matura¡ie a precursorilor medulari,
cât ¿i durata de supravie¡uire a celulelor mature.
Dintre neoplaziile solide, carcinoamele de sân
¿i prostatå afecteazå mai frecvent måduva osoaså.
Aceste tumori produc în måduvå o reac¡ie
desmoidå sau fibroaså cu fibrozå medularå care
determinå distrugerea spa¡iului medular ¿i sinu-
soidal, ceea ce poate afecta eliberarea celulelor
mature (diabaza) ¿i poate produce tablou
hematologic leucoeritroblastic. Metastazele din
måduva osoaså pot afecta hematopoieza
normalå prin dislocarea sau distrugerea celulelor
progenitoare, afectarea micromediului medular,
produc¡ie inadecvatå a factorilor hematopoetici
de cre¿tere sau producerea de citokine care
inhiba hematopoieza. Mieloftizia este deci o
formå de insuficientå medularå datoratå înlocuirii
¡esutului hematopoietic cu ¡esut anormal
(metastatic sau fibros), situa¡ie frecvent întâlnitå
în cazul metastazelor carcinomatoase (1). Acest
proces se soldeazå uneori cu hematopoieza
extramedularå, frecvent splenica (9), ducând la
eliberarea prematurå a celulelor hematopoietice
în circula¡ie (tablou leucoeritroblastic). Exami-
narea frotiului de sânge periferic eviden¡iazå
în aceste cazuri poikilocitoza (ovalocite, da-
criocite, schizocite), prezen¡a de eritrobla¿ti
¿i leucocite imature (deviere „la stânga“ a
formulei eritrocitare uneori pânå la mieloblast)
¿i uneori anizocitoza trombocitarå cu trombo-
cite gigante.
ªi cancerele care nu invadeazå måduva pot
afecta hematopoieza normalå prin producerea
¿i eliberarea în circula¡ie a citokinelor care in-
fluen¡eazå negativ producerea de factori de cre¿-
tere hematopoietici.
La aceste mecanisme ale citopeniei, în cazul
pacien¡ilor cu boli neoplazice diagnosticate ¿i
tratate se poate asocia iunosupresia medularå
prin tratamentul chimioterapic ori radioterapic
efectuat. De asemenea, la ace¿ti pacien¡i pot apårea
infec¡ii care så determine supresie medularå (ex.
infec¡ia cu parvovirusul B19 poate produce sin-
dromul de aplazie eritroidå purå cu anemie se-
verå. Medulograma aratå pronormobla¿ti gigan¡i
având incluzii virale intranucleare ¿i frecvent
intracitoplasmatice, ca ¿i hipoplazie eritroidå se-
verå. Celelalte serii sunt normale). Alteori, din
cauza statusului imun alterat infec¡iile bacteriene
degenereazå în ståri septice severe cu neutropenie
importantå prin consum periferic de leucocite
în focarele de infec¡ie, cât ¿i prin inhibarea pre-
cursorilor medulari. Medica¡ia antibacterianå,
antifungicå sau antiviralå poate accentua supresia
medularå.
Un tablou hematologic complex ce ridicå
deseori probleme de diagnostic diferen¡ial se
întâlne¿te cu precådere în cazul unor carcinoame
de regulå metastazate (de sân, prostatå, gastrice,
pulmonare) care induc distruc¡ie eritrocitarå prin
anemie hemoliticå microangiopaticå (7,8,10).
Tabloul hematologic poate fi ¿i mai mult complicat
de asocierea trombocitopeniei, adeseori severå,
datoratå fie produc¡iei medulare scåzute (prin
metastazele medulare), fie consumului periferic
al plachetelor, în cadrul unei coagulåri intra-
vasculare diseminate (situa¡ia cea mai frecvent
întâlnitå în practicå) sau rareori în contextul unei
purpure trombotice trombocitopenice/sindrom
hemolitic uremic. ªi în aceste cazuri examinarea
frotiului de sânge periferic relevå tablou leuco-
eritroblastic. ‰
PREZENTAREA CAZULUI
Pacienta, în vârstå de 45 de ani, a fost internatå
în Clinica de Hematologie SUUB în ianuarie
2006, fiind trimiså cu suspiciunea de eritroleu-
cemie.
Principalele acuze la internare ale pacientei
au fost: metroragii abundente, astenie fizicå,
scådere ponderalå importantå – 10 kg în 6 luni –
simptomatologie pentru care se adreseazå unei
sec¡ii de Medicinå Internå.
Din antecedentele patologice re¡inem: Boala
Behcet de 10 ani, tratatå cu Prednison, Imuran
¿i intermitent cu Ciclofosfamida, osteoporozå de
6 ani, tratatå cu Miacalcic ¿i Fosamax, hiper-
tensiune arterialå de 6 ani. De asemenea, în timpul
internårii în clinica medicalå, pacientei i s-a
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 269
TABLOU HEMATOLOGIC DE ÎMPRUMUT ÎNTR-UN NEOPLASM MAMAR CU METASTAZE MEDULARE
descoperit o forma¡iune nodularå tumoralå la
nivelul sânului drept.
Examenul clinic a eviden¡iat tegumente palide,
cu echimoze diseminate, microadenopatii latero-
cervicale ¿i axilare, ficatul cu marginea inferioarå
la 2 cm sub rebordul costal ¿i splinå la 1 cm sub
rebordul costal. Tabloul clinic orienta cåtre o
afec¡iune de sistem cu råsunet general, o posibilå
neoplazie.
Date paraclinice:
Hematologic, pacienta prezenta anemie
severå, trombopenie importantå ¿i tablou leuco-
eritroblastic. Hemograma eviden¡ia: hemoglobina
7,1 mg/dl, cu reticulocite 18% ¿i eritrobla¿ti 86%,
leucocite numeric normale, dar cu o formulå
leucocitarå deviatå la stânga – cu 2% mielobla¿ti,
4% Promielocite, 4% Metamielocite, Nesegmentate
+ Segmentate 53% ¿i trombocite 28000/mm3.
Frotiul de sânge capilar ilustra anizocitozå eri-
FIGURA 1a. Frotiuri de sânge periferic MGG, 20x –
poikilocitozå cu dimorfism eritrocitar, eritrobla¿ti maturi,
unii binuclea¡i, deviere la stânga a formuei leucocitare,
anizocitozå trombocitarå cu trombocite gigante.
FIGURA 1b. Frotiuri de sânge periferic MGG, 100x –
eritrobla¿ti cu puncta¡ii bazofile, în diferite stadii de
matura¡ie (stânga); anizocitozå eritrocitarå, poikilocitozå
(ovalocite, dacriocite), policromatofilie, eritroblast cu corp
Jolly (dreapta)
270 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
trocitarå, sferocite, schizocite, hematii cu corpi
Jolly, eritroblasti normoblasti. Aspectul hematolo-
gic periferic era dominat de modificårile pe seria
eritrocitarå cu dismorfism eritrocitar impresionant
¿i cu descårcare masivå de eritrobla¿ti în periferie
asociat elementelor tinere leucocitare, fiind prin-
cipalul argument pentru diagnosticul de suspi-
ciune de trimitere de eritroleucemie (Figura 1a ¿i
b).
Biologic, s-a remarcat un sindrom inflamator
cu VSH 95 mm/h ¿i un acid uric crescut 14mg/dl.
Sideremia era de 90 µ/dl. Tabloul coagulårii
prezenta un AP 67%, în condi¡iile tuturor celorla¡i
timpi alungi¡i, cu nivel al fibrinogenului normal ¿i
D-dimerii prezen¡i sugerând un CID cronic.
Electroforeza proteinelor serice relevå hipalbumi-
nemie, fårå hipergamaglobulinemie de tip mono
sau policlonal.
La examenul genital uterul apårea mårit de
volum, neomogen, cu o anexå stângå volumi-
noaså. Echografia genito-abdominalå repetatå a
eviden¡iat mårirea de volum a anexei stângi, ovar
stâng cu aspect polichistic.
Din bilan¡ul clinic, biologic ¿i hematologic s-au
ridicat urmåtoarele supozi¡ii de diagnostic:
1. Eritroleucemie – LAM6, diagnostic de
suspiciune ridicat de tabloul hematologic periferic
(descårcarea importantå de eritrobla¿ti, apari¡ia
câtorva forme tinere pe seria granulocitarå,
prezen¡a anemiei ¿i a trombocitopeniei severe
periferice), în concordan¡å ¿i cu sindromul de
impregnare tumoralå (scådere ponderalå), cu
hepatosplenomegalia, cu hiperuricemia ¿i cu
sindromul hemoragipar cutaneo-mucos.
2. Sindrom mieloproliferativ cronic (posibil
MMM- metaplazie mieloidå cu mielofibrozå)
incriminat în diagnosticul diferen¡ial din cauza
tabloului leucoeritroblastic cu anizopoikilocitoza
importantå, cu hepatosplenomegalie ¿i sindrom
hipercatabolic de impregnare tumoralå.
3. Neoplasm cu punct de plecare genital
(uter sau anexå) sau neoplasm mamar cu
determinåri secundare medulare, tablou leuco-
eritroblastic ¿i coagulopatie de consum.
S-a efectuat punc¡ie medularå care a fost albå,
la o dublå execu¡ie, neputând astfel orienta diag-
nosticul. Imunofenotiparea realizatå prin citome-
trie în flux din sângele periferic a eviden¡iat o
popula¡ie de celule nucleate corespunzåtoare
imunologic eritrobla¿tilor (Glicoforin A+ CD33+
- popula¡ia de culoare verde), dar fårå a putea
stabili natura lor leucemicå (Figura 2).
Testele de hemolizå efectuate au eviden¡iat
prezen¡a unui grad de hemolizå imunå (test Coobs
direct pozitiv ++) ¿i o tara talasemicå (electro-
foreza hemoglobinei sugestivå). Totodatå au
 TABLOU HEMATOLOGIC DE ÎMPRUMUT ÎNTR-UN NEOPLASM MAMAR CU METASTAZE MEDULARE

Figura 2

infirmat un alt tip de hemolizå (test Ham negativ),
dar nu au putut exclude participarea hemolizei
microangiopatice în tabloul hematologic.
Biopsia medularå a fost cea care a transat
diagnosticul prin identificarea metastazelor me-
dulare compacte excluzând totodatå o afec¡iune
hematologicå cu tablou periferic ¿i medular.
Astfel, examenul histopatologic a aråtat prezen¡a
metastazelor masive de carcinom mamar (Figura
3a, 3b) reprezentate de celule cu citoplasmå bo-
gatå ce determinå o reac¡ie stromalå importantå
cu dislocarea marcatå a hematopoiezei normale.
Testele imunohistochimice au eviden¡iat natura
epitelialå a celulelor metastatice (CK7 pozitiv ¿i
MNF 116 pozitiv – Figura 3f) care exprimå în cca
50% receptori pentru estrogeni (Figura 3c), în 60%

Figura 3c. IHC: ER Figura 3d. IHC: PGR

Figura 3a. Metastazå Figura 3b. Metastazå (receptori estrogenici) (receptori progesteronici)
medularå de carcinom medularå de carcinom pozitiv 50% în celulele pozitiv 60% în celulele
mamar – HE, 10x mamar – HE, 10x tumorale (10x) tumorale (10x)

Figura 3e. GCDFP15 (gross cystic Figura 3f. IHC: MNF116 pozitiv în Figura 3g. IHC (20x) CerbB2
disease fluid protein) pozitiv în celulele tumorale (10x) (proteina oncogenei CerbB2): slab
tumorå (10x) pozitivå (20x)

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 271

TABLOU HEMATOLOGIC DE ÎMPRUMUT ÎNTR-UN NEOPLASM MAMAR CU METASTAZE MEDULARE

receptori pentru progesteron (Figura 3d); poziti-

vitatea pentru GCDFP15 (Figura 3e) atestå
originea mamarå a metastazelor medulare.
Totodatå, slaba expresie a CerbB2 este un factor
de prognostic pozitiv ¿i un element important de
orientare a tratamentului.
Investiga¡iile s-au orientat apoi preferen¡ial
cåtre forma¡iunea tumoralå mamarå. Astfel,
markerii tumorali de neoplasm mamar au fost
gåsi¡i cu valori mult crescute: CA 15-3 cu valoarea
de 647 uI/ml (valoarea normalå fiind sub 30 uI/
ml). Ecografia mamarå a identificat la nivelul
cadranului intern al sânului drept o forma¡iune
hipoecogenå cu diametrul cd 1,3 cm, imprecis
delimitatå. Documenta¡ia mamograficå ulterioarå
a trasat diagnosticul eviden¡iind nodulul mamar,
cu metastaze medulare, osoase. ‰
CONCLUZII
De¿i tabloul clinic, aspectul hemoleucogramei ¿i al
frotiului de sânge periferic ar ridica suspiciunea unei afec¡iuni
hematologice, examenul hematologic complex (5,6), cu
respectarea tuturor treptelor de diagnostic specifice, poate
confirma sau exclude un diagnostic hematologic definitiv.
Aceste trepte de investiga¡ie includ punc¡ia medularå
aspirativå ¿i examenul histopatologic medular cu testele
imunohistochimice aferente (1,2).
Multe afec¡iuni, în special neoplazii, pot determina
modificåri hematologice ce mimeazå perfect patologia
hematologicå (1,4), motiv pentru care investigarea unui
pacient trebuie så fie completå ¿i multidisciplinarå,
modificårile hematologice trebuind interpretate în contextul
general al pacientului. ‰

BIBLIOGRAFIE
1. Makoni SN, Laber DA – Clinical
spectrum of myelophthisis in cancer
patients. Am J Hematol 2004 May;
76(1):92-93
2. Srinivas U, Kumar R, Pati H,
et al. – Sub classification and clinico-
hematological correlation of 40 cases
of acute erythroleukemia - can
proerythroblast/myeloblast and
proerythroblast/total erythroid cell
ratios help subclassify? Hematology
2007 Jun 27; 1
3. Kowal-Vern A, Mazzella FM,
Cotelingam JD, et al. – Diagnosis and
characterization of acute erythro-
leukemia subsets by determining the
percentages of myeloblasts and
proerythroblasts in 69 cases. Am J
Hematol 2000 Sep; 65(1):5-13
4. Domingo-Claros A, Larriba I,
Rozman M, et al. – Acute erythroid
neoplastic proliferations. A biological
study based on 62 patients.
Haematologica 2002 Feb; 87(2):148-
153
5. Davey FR, Abraham N Jr, Brunetto
VL, et al. – Morphologic
characteristics of erythroleukemia
(acute myeloid leukemia; FAB-M6):
a CALGB study. Am J Hematol 1995
May; 49(1):29-38
6. Jun KR, Park CJ, Cho YW, et al. –
Recommendation of the use of
myeloblast percentage among non-
erythroid cells instead of percentage
among total nucleated cells for
therapeutic response assessment in
acute erythroid leukemia. Leuk
Lymphoma 2006 Apr; 47(4):683-687
7. Pasquau Liaño F, Pasquau Liaño J,
Amador Prous C, et al. –
Microangiopathic hemolytic anemia
and leukoerythroblastosis as the
presenting form of a gastric
adenocarcinoma. Rev Esp Enferm
Apar Dig. 1989 Oct; 76(4):397-400
8. Oliveira A, Frazão A, Duarte PC, et
al. – Microangiopathic hemolytic
anemia. A form of presentation of
stomach neoplasm. Acta Med Port.
1998 Jun; 11(6):569-572
9. O’Keane JC, Wolf BC, Neiman RS –
The pathogenesis of splenic
extramedullary hematopoiesis in
metastatic carcinoma. Cancer. 1989
Apr 15; 63(8):1539-1543
10. Bondar GV, Dumanskii IuV,
Iakovets IuI, et al. – Immediate
results of surgical treatment of
gastric cancer complicated by
anemia. Klin Khir 1992; (5):1-4

Revista presei medicale

Food additives may cause hyperactivity: study

MAGGIE FOX, Health and Science Editor

WASHINGTON (Reuters) – Cer-
tain artificial food colorings and other
additives can worsen hyperactive
behaviors in children aged 3 to 9, British
researchers reported on Wednesday.
Tests on more than 300 children
showed significant differences in their
behavior when they drank fruit drinks
spiked with a mixture of food colorings
and preservatives, Jim Stevenson and
colleagues at the University of
Southampton said.
“These findings show that adverse
effects are not just seen in children
with extreme hyperactivity (such as

272 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007

 TABLOU HEMATOLOGIC DE ÎMPRUMUT ÎNTR-UN NEOPLASM MAMAR CU METASTAZE MEDULARE
ADHD) but can also be seen in the
general population and across the range
of severities of hyperactivity,” the
researchers wrote in their study, pub-
lished in the Lancet medical journal.
Stevenson’s team, which has been
studying the effects of food additives
in children for years, made up two
mixtures to test in one group of 3-
year-olds and a second group of chil-
dren aged 8 and 9.
They included sunset yellow col-
oring, also known as E110; carmoisine,
or E122; tartrazine, or E102; ponceau
4R, or E124; the preservative sodium
benzoate, or E211; and other colors.
One of the two mixtures contained
ingredients commonly drunk by young
British children in popular drinks, they
said. They did not specify what foods
might include the additives.
Both mixtures significantly affected
the older children. The 3-year-olds were
Statin withdrawal after stroke worsens outcome
NEW YORK (Reuters Health) –
Discontinuing statin treatment after
a stroke is associated with an increased
risk of death or dependency after 90
days, according to a study in the
medical journal Neurology.
Recent reports suggest that statins,
a popular class of cholesterol-lowing
drugs, such as Zocor or Mevacor, may
protect the brain during the early
phases of an ischemic stroke, the authors
explain. An ischemic stroke, the most
common type of stroke, occurs when
the blood flow to an area of the brain is
cut off, usually by a clot, and the brain
tissue no longer receives oxygen and
begins to die. The results of clinical
studies suggest that withdrawal of
statins impair the blood vessel function
and worsens brain injury. However, oral
medications are often stopped during the
first days of a stroke because the patient
may not be able to swallow them.
Dr. Jose Castillo from Universidad
de Santiago de Compostela, Spain,
most affected by the mixture that closely
resembled the average intake for children
that age, Stevenson’s team reported.
“The implications of these results
for the regulation of food additive use
could be substantial,” the researchers
concluded.
ONGOING DEBATE
The issue of whether food additives
can affect children’s behavior has been
controversial for decades. Benjamin
Feingold, an allergist, has written books
arguing that not only did artificial colors,
flavors and preservatives affect children
but so did natural salicylate compounds
found in some fruits and vegetables.
Several studies have contradicted this
notion. Stevenson’s team made up sev-
eral batches of fruit drinks and carefully
watched the children after they drank
them. Some did not contain the additives.
The children varied in their responses
but in general reacted poorly to the
Source: REUTERS/HEALTH, Wensday, September 5, 2007
and associates investigated 89 stroke
patients who had been on statin
therapy. The patients were assigned
to have their statin stopped for the first
3 days after admission or to receive
Lipitor immediately (orally or by
nasogastric tube), regardless of prior
statin drug and dosage. On day 4, all
of the patients were put on Lipitor.
After 3 months, 27 of the 46
patients (60 percent) who had an
interruption in statin therapy were
dead or dependent, the authors report,
compared with only 16 of 43 patients
(39 percent) of the patients who did
not withdraw from statin treatment.
Even after age and severity of the
stroke were considered, statin with-
drawal was still associated with a
4.66-fold increased risk of death or
dependency.
In other findings, statin withdrawal
was associated with a 7-fold increased
risk of early neurologic deterioration,
Source: REUTERS/HEALTH, Tuesday, August 28, 2007
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
cocktails, Stevenson’s team reported.
“We have found an adverse effect
of food additives on the hyperactive
behavior of 3-year-old and 8/9-year-
old children,” they wrote.
Dr. Sue Baic, a registered dietitian
at the University of Bristol, said in a
statement: “This is a well designed
and potentially very important study.”
“It supports what dietitians have
known for a long time, that feeding
children on diets largely consisting of
heavily processed foods which may also
be high in fat, salt or sugar is not
optimal for health.”
Others disagreed.
“The paper shows some statistical
associations. It is not a demonstration
of cause and effect,” said Dr. Paul
Illing, a registered toxicologist and
safety consultant in Wirral, Britain.
as well as an increase in the area of
volume of brain injury.
The risk of adverse outcomes was
similar between patients in the statin
withdrawal group and in another group
of patients who were not on a statin at
time of their stroke, the investigators
found. Early neurologic deterioration
and stroke volume, however, were
significantly worse in the statin
withdrawal group than in patients not
previously treated with statins.
The findings suggest that after an
ischemic stroke the protective effects
of previous statin therapy on the brain
disappear if the drug is withdrawn,
which also cause deleterious effects
when compared with stroke patients
who were not protected by statin
treatment, the authors conclude.
“Our findings strongly support
that previous statin therapy should
not be interrupted during the acute
phase of ischemic stroke.”
273
 6 PRACTICA MEDICALÅ
ACTIVITATEA PREVENTIVÅ
Which lifestyle interventions
effectively lower LDL cholesterol?
ELIZABETH POWERS, MD; JOHN SAULTZ, MD; ANDREW HAMILTON, MLS
Oregon Health and Sciences University, Portland
CLINICAL COMENTARY
Consider patient preference when discussing lifestyle
modification
Vincent Lo, MD
San Joaquin Family Medicine Residency, French Camp,
Calif
Therapeutic lifestyle changes are the initial treatment of
choice for reduction of cardiac risk factors, but both patients
and physicians often see these modifications as confusing and
difficult to achieve. A recent year-long study on different diets
concluded that dietary adherence is more important than a
specific type of diet for weight loss and reduction of cardiac
risk factors (1). Another recent study reports no difference in
weight loss among diets, based on different exercise duration
and intensities over 1 year in a group of sedentary and
overweight women (2). Therefore, family physicians should
consider culture, patient preference, and practical issues such
as cost and availability, when discussing therapeutic lifestyle
modification with patients.
EVIDENCE-BASED ANSWER
Counseling, weight loss, exercise, and drinking
alcohol all effectively lower low-density lipo-
protein cholesterol (LDL-C). Specifically, one to
2 daily drinks of alcohol lowers LDL-C, if con-
sumed regularly for more than 4 weeks (strength
of recommendation [SOR]: A, based on con-
sistent results of multiple randomized controlled
trials [RCTs]).
Counseling by physicians, dieticians, or
pharmacists is effective at increasing patient
compliance with medications, thereby lowering
LDL-C (SOR: C, good evidence that intervention
274 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
lowers LDL-C, insufficient to prove that it reduces
mortality/morbidity).
Weight loss has been associated with re-
ductions in LDL-C. However, other factors –
including degree of caloric restriction, drug
intervention, and diet composition – may play a
more significant role than weight loss alone (SOR:
A, based on a meta-analysis and consistent results
of RCTs).
Exercise significantly lowers LDL-C (SOR: A,
based on meta-analyses and consistent results of
RCTs). Smoking cessation may have a beneficial
effect (SOR: B, based on inconsistent results from
RCTs that it lowers LDL-C). Exercise-based
alternative practices (yoga and tai chi) lower LDL,
and meditation may have a beneficial effect (SOR:
C, moderate evidence that intervention lowers
LDL, insufficient evidence to prove that it reduces
mortality/morbidity).
EVIDENCE SUMMARY
Elevated LDL-C is an independent risk factor
for coronary heart disease (CHD), (3) the leading
cause of death in the US (4). Lowering LDL-C by
60 mg/dL reduces CHD events by 50% after 2
years (5). Although medications successfully lower
LDL-C and decrease CHD risk, therapeutic
lifestyle changes remain the initial therapy for most
adult patients (3,6).
FAST TRACK
Weight loss lowers LDL-C, although some
studies suggest it may be short-term.
Our search located evidence about alcohol
consumption, counseling, exercise, weight loss,
alternative lifestyle measures, and smoking
 WHICH LIFESTYLE INTERVENTIONS EFFECTIVELY LOWER LDL CHOLESTEROL?
Table. A- and B-level evidence points to effectiveness of lifestyle interventions
cessation. The TABLE summarizes the evidence
for each.
1 TO 2 DRINKS DAILY REDUCED LDL-C
One 5-year-long cohort study (N=933)
showed that alcohol was associated with LDL-C
reduction in a dose-dependent manner (7). Two
crossover trials (4-6 weeks in duration) conducted
among heavy drinkers showed that LDL-C
increased when alcohol intake decreased. Two
randomized crossover trials (8-12 weeks in
duration) found a statistically significant decrease
in LDL-C with consumption of 1 to 2 drinks daily.
COUNSELING IMPROVES
MEDICATION ADHERENCE
An RCT (N=167) with 8 years of follow-up
found that patient education and counseling
effectively improved medication adherence (8).
Another RCT (N=1162) lasting 1 year, however,
found that nutrition counseling by primary care
physicians resulted in no significant change in
LDL-C compared with usual care (9).
FAST TRACK
2 clinical trials found that LDL decreased
significantly with 1 to 2 alcohol drinks per day.
Studies focused on enhancing dietary com-
pliance did not find consistent post-intervention
improvement. Greater medication adherence or
improved dietary compliance did result in
consistent significant improvements in LDL-C.
EXERCISE LOWERS LDL; WEIGHT LOSS
A FACTOR
Aerobic exercise effectively lowers LDL-C. This
reduction is enhanced by weight loss and diet
and mitigated by weight gain (10). An analysis of
4 RCTs showed that LDL-C also decreased with
resistance training.
A higher body-mass index is associated with
higher LDL-C. However, the effect of weight loss
perse on LDL-C remains unclear. Multiple short-
term studies have found that a modest amount
of weight loss (5%-10%) is associated with a
significant reduction in LDL-C (11). A meta-
analysis found a 0.8 mg/dL LDL-C decrease for
every kg of weight lost. Long-term follow-up,
however, showed that LDL-C returned to baseline
even when weight loss was maintained. Eight
clinical trials failed to demonstrate a reduction in
LDL-C postintervention with up to 10 kg of weight
loss. Studies using weight-loss drugs (Sibutramine,
Orlistat) found more significant weight loss during
treatment, along with greater decrease in LDL-C,
when compared with studies using only lifestyle
modifications.
OTHER MEASURES HAVE MIXED
RESULTS
High-quality RCTs (N=267) with yoga or tai
chi as the exercise intervention showed a
statistically significant decrease in LDL-C over 12
to 14 weeks (12). Two RCTs investigated the effect
of meditation on LDL-C with mixed results. One
(N=16) showed a significant decrease in LDL-C
over 8 weeks, while a second (N=60) showed
no difference in LDL-C. A high-quality RCT
(N=91) with a combined intervention (coun-
seling, exercise, and meditation over 1 year)
showed a significant decrease in LDL-C.
In cross-sectional surveys, LDL-C does not
appear to differ between smokers and non-
smokers. One meta-analysis found a dose-
dependent relationship between smoking and
LDL-C, with overall LDL-C 1.7% higher for
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 275
WHICH LIFESTYLE INTERVENTIONS EFFECTIVELY LOWER LDL CHOLESTEROL?

smokers compared with nonsmokers (13). Two
RCTs investigated the effect of smoking cessation
on LDL-C with mixed results. One (N=935)
showed a decrease in non fasting LDL-C while a
second (N=140) showed no difference in LDL-C.
RECOMMENDATIONS FROM OTHERS
According to ATP III guidelines, (3) all adults
with LDL-C above goal should be treated with
therapeutic lifestyle changes for primary and
secondary prevention of CHD. These include a
diet intervention, increased physical activity, and
weight loss. Physicians are encouraged to refer
patients to a nutritionist. If LDL-C is not at goal
after 6 weeks, changes are intensified; physicians
should consider pharmacologic therapy if a
patient is still unable to attain his or her goal.
ACP III guidelines recommend an office visit every
4 to 6 months to monitor adherence.
American Heart Association guidelines rec-
ommend that physicians counsel smokers at
every office visit to stop smoking. The American
College of Cardiology recommends abstinence
from alcohol for patients with suspected alcoholic
cardiomyopathy. For patients with heart failure
from any other cause, alcohol consumption is
usually limited to 1 drink per day.

REFERENCES
1. Dansinger ML, Gleason JA,
Griffith JL, et al. – Comparison of
the Atkins, Ornish, Weight Watchers,
and Zone Diets for weight loss and
heart disease risk reduction. JAMA
2005; 293:43-53
2. Jakicic JM, Marcus BH, Gallagher
KL, et al. – Effect of exercise
duration and intensity on weight loss
in overweight sedentary women.
JAMA 2003; 290:1323-1330
3. National Cholesterol Education Pro-
gram Expert Panel on Detection –
Evaluation and Treatment of High
Blood Cholesterol in Adults (ATP
III). Executive Summary. JAMA
2001; 285:2486-2497
4. Deaths – Final Data for 2003.
National Vital Statistics Report 2003;
54(13). 120pp. (PHS) 2006-1120
5. Law MR, Wald NJ, Rudnicka AR –
Quantifying effects of statins on low
density lipoprotein cholesterol,
ischaemic heart disease, and stroke:
systematic review and meta-analysis.
BMJ 2003; 326:1423
6. Grundy SM, Cleeman JI, Merz CN,
et al. – National Heart, Lung and
Blood Institute; American College of
Cardiology Foundation; American
Heart Association. Implications of
recent clinical trials for the National
Cholesterole Education Program
Adult Treatment Panel III guidelines.
Circulation 2004; 110:227-239
7. Nakanishi N, Yoshida H,
Nakamura K, et al. – Influence of
alcohol intake on risk for increased
low-density lipoprotein cholesterol in
middle-aged Japanese men. Alcohol
Clin Exp Res 2001; 25:1046-1050.
8. Rachmani R, Slavacheski I, Berla
M, et al. – Treatment of high-risk
patients with diabetes: motivation
and teaching intervention: a
randomized, prospective 8-year
follow-up study. J Am Soc Nephrol
2005; 16:S22-S26
9. Ockene IS, Hebert JR, Ockene JK,
et al. – Effect of physician-delivered
nutrition counseling training and an
office-support program on saturated
fat intake, weight, and serum lipid
measurements in a hyperlipidemic
population: Worcester Area Trial for
Counseling in Hyperlipidemia
(WATCH). Arch Intern Med 1999;
159:725-731
10. Kelley GA, Kelley KS, Tran ZV –
Exercise, lipids, and lipoproteins in
older adults: a meta-analysis. Prev
Cardiol 2005; 8:206-214
11. Poobalan A, Aucott L, Smith WC,
et al. – Effects of weight loss in
overweight/obese individuals and
long-term lipid outcomes: a
systematic review. Obesity Rev 2004;
5:43-50
12. Tsai JC, Wang WH, Chan P, et al. –
The beneficial effects of Tai Chi
Chuan on blood pressure and lipid
profile and anxiety status in a
randomized controlled trial. J Altern
Complement Med 2003; 9:747-754
13. Craig WY, Palomaki GE, Haddow
JE – Cigarette smoking and serum
lipid and lipoprotein concentrations:
an analysis of published data. Br
Med J 1989; 298:784-788
ADDITIONAL REFERENCES
ALTERNATIVE LIFESTYLE
PRACTICES
1. Bijlani RL, et al. – A brief but
comprehensive lifestyle education
program based on yoga reduces risk
factors for cardiovascular disease
and diabetes mellitus. J Alt
Complement Med 2005; 11:267-274
2. Tsai JC, et al. – The beneficial effects
of Tai Chi Chuan on blood pressure
and lipid profile and anxiety status
in a randomized controlled trial. J Alt
Complement Med 2003; 9:747-754
3. Mahajan AS, Reddy KS, Sachdeva
U – Lipid profile of coronary risk
subjects following yogic lifestyle
intervention. Indian Heart J 1999;
51:37-40
4. Carson MA – The impact of a
relaxation technique on the lipid
profile. Nurs Res 1996; 45:271-276
5. Jula A, et al. – Long-term non-
pharmacological treatment for mild
to moderate hypertension. J Intern
Med 1990; 227:413-421
6. Carson MA, et al. – The effect of a
relaxation technique on coronary risk
factors. Behav Med 1988; 14:71-77
ALCOHOL
1. Coimbra SR, et al. – The action of
red wine and purple grape juice on
vascular reactivity is independent of
plasma lipids in
hypercholesterolemic patients.
Brazilian J Med Biol Res 2005;
38:1339-1347
2. Hansen AS, et al. – Effect of red
wine and red grape extract on blood
lipids, haemostatic factors, and other
risk factors for cardiovascular
disease. Eur J Clin Nutr 2005; 59:449-
455
3. Chrysohoou C, et al. – Effects of
chronic alcohol consumption on lipid
levels, inflammatory and

276 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007


haemostatic factors in the general
population: the ‘ATTICA’ study. Eur
J Cardiovasc Prev Rehabil 2003;
10:355-361
4. Dixon JB, Dixon ME, O’Brien PE –
Alcohol consumption in the severely
obese: relationship with the metabolic
syndrome. Obes Res 2002; 10:245-252
5. Baer DJ, et al. – Moderate alcohol
consumption lowers risk factors for
cardiovascular disease in
postmenopausal women fed a
controlled diet. Am J Clin Nutr 2002;
75:593-599
6. Nakanishi N, et al. – Influence of
alcohol intake on risk for increased
low-density lipoprotein cholesterol in
middle-aged Japanese men. Alcohol
Clin Exp Res 2001; 25:1046-1050
7. Senault C, et al. – Beneficial effects
of a moderate consumption of red
wine on cellular cholesterol efflux in
young men. Nutr Metab Cardiovasc
Dis 2000; 10:63-69
8. Rakic V, et al. – A controlled trial of
the effects of pattern of alcohol
intake on serum lipid levels in regular
drinkers. Atherosclerosis 1998;
137:243-252
9. Kiechl S, et al. – Alcohol
consumption and atherosclerosis:
what is the relation? Prospective
results from the Bruneck Study.
Stroke 1998; 29:900-907
10. Hein HO, Suadicani P, Gyntelberg
F – Alcohol consumption, serum low
density lipoprotein cholesterol
concentration, and risk of ischaemic
heart disease: six year follow up in
the Copenhagen male study. BMJ
1996; 312:736-741
11. Clevidence BA, et al. – Effects of
alcohol consumption on lipoproteins
of premenopausal women. A
controlled diet study. Arterioscler
Thromb Vasc Biol 1995; 15:179-184
12. Sharpe PC, et al. – Effect of red
wine consumption on lipoprotein (a)
and other risk factors for
atherosclerosis. QJM 1995; 88:101-
108
13. Masarei JR, et al. – Effects of
alcohol consumption on serum
lipoprotein-lipid and apolipoprotein
concentrations. Results from an
intervention study in healthy
subjects. Atherosclerosis 1986; 60:79-
87
COUNSELING
1. Ragucci KR, et al. – Effectiveness of
pharmacist-administered diabetes
mellitus education and management
services. Pharmacotherapy 2005;
25:1809-1816
2. Sallinen J, et al. – Effects of
strength training and nutritional
counseling on metabolic health
indicators in aging women. Can J
Appl Physiol 2005; 30:690-707
WHICH LIFESTYLE INTERVENTIONS EFFECTIVELY LOWER LDL CHOLESTEROL?
3. Levetan CS, et al. – Impact of
computer-generated personalized
goals on cholesterol lowering. Value
Health 2005; 8:639-646
4. Rachmani R, et al. – Treatment of
high-risk patients with diabetes:
motivation and teaching intervention:
a randomized, prospective 8-year
follow-up study. J Am Soc Nephrol
2005; 16:S22-S26
5. Burke LE, et al. – Improving
adherence to a cholesterol-lowering
diet: a behavioral intervention study.
Patient Educ Couns 2005; 57:134-142
6. Lee SS, Cheung PY, Chow MS –
Benefits of individualized counseling
by the pharmacist on the treatment
outcomes of hyperlipidemia in Hong
Kong. J Clin Pharmacol 2004; 44:632-
639
7. Simpson DR, Dixon GB, Bolli P –
Effectiveness of multidisciplinary
patient counseling in reducing
cardiovascular disease risk factors
through nonpharmacological
intervention: results from the Healthy
Heart Program. Can J Cardiol 2004;
20:177-186
8. Lichtman JH, et al. – Clinical trial of
an educational intervention to
achieve recommended cholesterol
levels in patients with coronary artery
disease. Am Heart J 2004; 147:522-
528
9. Thomas HD, Maynard C, Wagner
GS – Results from a practice-based
lipid clinic model in achieving low
density lipoprotein cholesterol goals.
N C Med J 2003; 64:263-266
10. Reid R, et al. – Dietary counseling
for dyslipidemia in primary care:
results of a randomized trial. Can J
Pract Res 2002; 63:169-175
11. Palomaki A, et al. – Effects of
preventive group education on the
resistance of LDL against oxidation
and risk factors for coronary heart
disease in bypass surgery patients.
Ann Med 2002; 34:272-283
12. Vale MJ, et al. – Coaching patients
with coronary heart disease to
achieve the target cholesterol: a
method to bridge the gap between
evidence-based medicine and the
“real world” – randomized
controlled trial. J Clin Epidemiol 2002;
55:245-252
13. Cabrera-Pivaral CE, et al. – Effects
of an educational intervention on
plasma levels of LDL cholesterol in
type 2 diabetics. Salud Publica Mex
2001; 43:556-562
14. Henkin Y, et al. – Dietary treatment
of hypercholesterolemia: do dietitians
do it better? A randomized,
controlled trial. Am J Med 2000;
109:549-555
15. Faulkner MA, et al. – Impact of
pharmacy counseling on compliance
and effectiveness of combination
lipid-lowering therapy in patients
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
undergoing coronary artery
revascularization: a randomized,
controlled trial. Pharmacotherpy 2000;
20:410-416
16. Hines L – Can low-fat/cholesterol
nutrition counseling improve food
intake habits and hyperlipidemia of
renal transplant patients? J Ren Nutr
2000; 10:30-35
17. Hebert JR, et al. – A dietitian-
delivered group nutrition program
leads to reductions in dietary fat,
serum cholesterol, and body weight:
the Worcester Area Trial for
Counseling in Hyperlipidemia
(WATCH). J Am Diet Assoc 1999;
99:544-552
18. Allison TG, et al. – Achieving
National Cholesterol Education
Program goals for low-density
lipoprotein cholesterol in cardiac
patients: importance of diet, exercise,
weight control, and drug therapy.
Mayo Clin Proc 1999; 74:466-473
19. Ockene IS, et al. – Effect of
physician-delivered nutrition
counseling training and an office-
support program on saturated fat
intake, weight, and serum lipid
measurements in a hyper-lipidemic
population: Worcester Area Trial for
Counseling in Hyperlipidemia
(WATCH). Arch Intern Med 1999;
159:725-731
20. Verges BL, et al. – Comprehensive
cardiac rehabilitation improves the
control of dyslipidemia in secondary
prevention. J Cardiopulm Rehabil 1998;
18:408-415
21. Keyserling TC, et al. – A
randomized controlled trial of a
physician-directed treatment
program for low-income patients
with high blood cholesterol: the
Southeast Cholesterol Project. Arch
Fam Med 1997; 6:135-145
22. Johnston HJ, et al. – Diet
modification in lowering plasma
cholesterol levels. A randomized trial
of three types of intervention. Med J
Aust 1995; 162:524-526
23. Anderson JW, Brinkman VL,
Hamilton CC – Weight loss and 2-
year follow-up for 80 morbidly obese
patients treated with intensive very-
low-calorie diet and an education
program. Am J Clin Nutr 1992;
56:244S-246S
24. Rabkin SW, et al. – A randomized
clinical trial comparing behavior
modification and individual
counseling in the nutritional therapy
of non-insulin-dependent diabetes
mellitus: comparison of the effect on
blood sugar, body weight, and serum
lipids. Diabetes Care 1983; 6:50-56
EXERCISE
1. Kelley GA, Kelley KS, Tran ZV –
Exercise, lipids, and lipoproteins in
277
WHICH LIFESTYLE INTERVENTIONS EFFECTIVELY LOWER LDL CHOLESTEROL?
older adults: a meta-analysis. Prev
Cardiol 2005; 8:206-214
2. Kelley GA, Kelley KS, Tran ZV –
Aerobic exercise and lipids and
lipoproteins in women: a meta-
analysis of randomized controlled
trials. J Womens Health 2004;
13:1148-1164
3. Halbert JA, et al. – Exercise training
and blood lipids in hyperlipidemic
and normolipidemic adults: a meta-
analysis of randomized, controlled
trials. Eur J Clin Nutr 1999; 53:514-
522
4. Yu-Poth S, et al. – Effects of the
National Cholesterol Education
Program’s Step I and Step II dietary
intervention programs on
cardiovascular disease risk factors: a
meta-analysis. Am J Clin Nutr 1999;
69:632-646
5. Tran ZV, Weltman A – Differential
effects of exercise on serum lipid and
lipoprotein levels seen with changes
in body weight. A meta-analysis.
JAMA 1985; 254:919-924
SMOKING
1. Allen SS, Hatsukami D, Gorsline J –
Cholesterol changes in smoking
cessation using the transdermal
nicotine system. Transdermal
Nicotine Study Group. Prev Med
1994; 23:190-196
2. Hughes K, et al. – Relationships
between cigarette smoking, blood
pressure and serum lipids in the
Singapore general population. Int J
Epidemiol 1993; 22:637-643
3. Vyssoulis GP, et al. – Dyslipidemic
effects of cigarette smoking on beta-
blocker-induced serum lipid changes
in systemic hypertension. Am J
Cardiol 1991; 67:987-992
4. Cuesta C, et al. – Effects of age and
cigarette smoking on serum
concentrations of lipids and
apolipoproteins in a male military
population. Atherosclerosis 1989;
80:33-39
5. Craig WY, Palomaki GE, Haddow
JE – Cigarette smoking and serum
lipid and lipoprotein concentrations:
an analysis of published data. BMJ
1989; 298:784-788
6. Rabkin SW – Effect of cigarette
smoking cessation on risk factors for
coronary atherosclerosis. A controlled
clinical trial. Atherosclerosis 1984;
53:173-184
7. Halfon ST, Green MS, Heiss G –
Smoking status and lipid levels in
adults of different ethnic origins: the
Jerusalem Lipid Research Clinic
Program. Int J Epidemiol 1984; 13:17-
183
8. Brischetto CS, et al. – Plasma lipid
and lipoprotein profiles of cigarette
smokers from randomly selected
families: enhancement of
278 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
hyperlipidemia and depression of
high-density lipoprotein. Am J Cardiol
1983; 52:675-680
9. Sutherland WH, et al. – Adiposity,
lipids, alcohol consumption,
smoking, and gender. Am J Clin Nutr
1980; 33:2581-2587
10. Heyden S, et al. – The combined
effect of smoking and coffee drinking
on LDL and HDL cholesterol.
Circulation 1979; 60:22-25
WEIGHT LOSS
1. Wood RJ, et al. – Carbohydrate
restriction alters lipoprotein
metabolism by modifying VLDL,
LDL, and HDL sub-fraction
distribution and size in overweight
men. J Nutr 2006; 136:384-389
2. Lofgren I, et al. – Weight loss
associated with reduced in-take of
carbohydrate reduces the
atherogenicity of LDL in
premenopausal women. Metabolism
2005; 54:1133-1141
3. LaHaye SA, et al. – Comparison
between a low glycemic load diet and
a Canada Food Guide diet in cardiac
rehabilitation patients in Ontario. Can
J Cardiol 2005; 21:489-494
4. Zemel MB, et al. – Dairy
augmentation of total and central fat
loss in obese subjects. Int J Obes
2005; 29:391-397
5. Fernandez ML, et al. – Beneficial
effects of weight loss on plasma
apolipoproteins in post-menopausal
women. J Nutr Biochem 2004; 15:717-
721
6. Zaffari D, et al. – Effectiveness of
diet in hyperlipidemia in renal
transplant patients. Transplant Proc
2004; 36:889-890
7. Erdmann J, et al. – Cholesterol
lowering effect of dietary weight loss
and orlistat treatment–efficacy and
limitations. Aliment Parmacol Ther
2004; 19:1173-1179
8. Yancy WS Jr, et al. – A low-
carbohydrate, ketogenic diet versus a
low-fat diet to treat obesity and
hyperlipidemia: a randomized,
controlled trial. Ann Int Med 2004;
140:769-777
9. Four popular diets all good for
weight loss but not equal for
reducing heart disease risk SAMJ
2004; 94:161
10. Brook RD, et al. – Effect of short-
term weight loss on the metabolic
syndrome and conduit vascular
endothelial function in overweight
adults. Am J Cardiol 2004; 93:1012-
1016
11. Poobalan A, et al. – Effects of
weight loss in overweight/obese
individuals and long-term lipid
outcomes–a systematic review. Obes
Rev 2004; 5:43-50
12. Ley SJ, et al. – Long-term effects of
a reduced fat diet intervention on
cardiovascular disease risk factors in
individuals with glucose intolerance.
Diabetes Res Clin Pract 2004; 63:103-
112
13. Lovejoy JC, et al. – Consumption of
a controlled low-fat diet containing
olestra for 9 months improves health
risk factors in conjunction with
weight loss in obese men: the Ole’
Study. Int J Obes Relat Metab Disord
2003; 27:1242-1249
14. Bergholm R, et al. – Lowering of
LDL cholesterol rather than moderate
weight loss improves endothelium-
dependent vasodilation in obese
women with previous gestational
diabetes. Diabetes Care 2003; 26:1667-
1672
15. Melanson K, et al. – Weight loss
and total lipid profile changes in
overweight women consuming beef
or chicken as the primary protein
source. Nutrition 2003; 19:409-414
16. Allison DB, et al. – A novel soy-
based meal replacement formula for
weight loss among obese individuals:
a randomized controlled clinical trial.
Eur J Clin Nutr 2003; 57:514-522
17. Lucas CP, Boldrin MN, Reaven GM –
Effect of orlistat added to diet (30%
calories from fat) on plasma lipids,
glucose, and insulin in obese patients
with hypercholesterolemia. Am J
Cardiol 2003; 91:961-964
18. Reid R, et al. – Dietary counseling
for dyslipidemia in primary care:
results of a randomized trial. Can J
Diet Pract Res 2002; 63:169-175
19. Boozer CN, et al. – Herbal ephedra/
caffeine for weight loss: a 6-month
randomized safety and efficacy trial.
Int J Obes Relat Metab Disord 2002;
26:593-604
20. Parker B, et al. – Effect of a high-
protein, high-monoun-saturated fat
weight loss diet on glycemic control
and lipid levels in type 2 diabetes.
Diabetes Care 2002; 25:425-430
21. Delahanty LM, et al. – Clinical and
cost outcomes of medical nutrition
therapy for hypercholesterolemia: a
controlled trial. J Am Diet Assoc 2001;
101:1012-1023
22. Ashley JM, et al. – Weight control in
the physician’s office. Arch Intern
Med 2001; 161:1599-1604
23. Shintani TT, et al. – The Hawaii
Diet: ad libitum high carbohydrate,
low fat multi-cultural diet for the
reduction of chronic disease risk
factors: obesity, hypertension,
hypercholesterolemia, and
hyperglycemia. Hawaii Med J 2001;
60:69-73
24. Raeini-Sarjaz M, et al. –
Comparison of the effect of dietary
fat restriction with that of energy
restriction on human lipid
metabolism. Am J Clin Nutr 2001;
73:262-267
25. Manley SE, et al. – Effects of three
months’ diet after diagnosis of Type

2 diabetes on plasma lipids and
lipoproteins. Diabetes Med 2000;
17:518-523
26. Cordero-MacIntyre ZR, et al. –
Weight loss is correlated with an
improved lipoprotein profile in obese
postmenopausal women. J Am Coll
Nutr 2000; 19:275-284
27. Noakes M, Clifton PM – Weight loss
and plasma lipids. Curr Opin Lipidol
2000; 11:65-70
28. Purnell JQ, et al. – Effect of weight
loss with reduction of
intraabdominal fat on lipid
metabolism in older men. J Clin
Endocrinol Metab 2000; 85:977-982
29. Zambon A, et al. – Effects of
hypocaloric dietary treatment
enriched in oleic acid on LDL and
HDL subclass distribution in mildly
obese women. J Intern Med 1999;
246:191-201
30. Di Buono M, et al. – Weight loss
due to energy restriction suppresses
cholesterol biosynthesis in
overweight, mildly
hypercholesterolemic men. J Nutr
1999; 129:1545-1548
31. Herbert JR, et al. – A dietitian-
delivered group nutrition program
leads to reductions in dietary fat,
serum cholesterol, and body weight:
the Worcester Area Trial for
Counseling in Hyperlipidemia
(WATCH). J Am Diet Assoc 1999;
99:544-552
32. Yu-Poth S, et al. – Effects of the
National Cholesterol Education
Program’s Step I and Step II dietary
intervention programs on
cardiovascular disease risk factors: a
meta-analysis. Am J Clin Nutr 1999;
69:632-646
33. Bray GA, et al. – Sibutramine
produces dose-related weight loss.
Obes Res 1999;7:189-198
34. Wadden TA, Anderson DA, Foster
GD – Two-year changes in lipids and
lipoproteins associated with the
maintenance of a 5% to 10%
reduction in initial weight: some
findings and some questions. Obes
Res 1999; 7:170-178
35. Turley ML, et al. – The effect of a
low-fat, high-carbohydrate diet on
sesrum high density lipoprotein
©2007, Dowden Health Media, Inc. All rights reserved. This article was reprinted from the original article published in the Journal of
Family Practice, June 2007, Vol. 56, No. 6, pp 483-489. A publication of Dowden Health Media, Inc.
SOCIETźII ACADEMICE
WHICH LIFESTYLE INTERVENTIONS EFFECTIVELY LOWER LDL CHOLESTEROL?
cholesterol and triglyceride. Eur J Clin
Nutr 1998; 52:728-732
36. Butowski PF, Winder AF – Usual
care dietary practice, achievement
and implications for medication in
the management of
hypercholesterolemia. Data from the
U.K. Lipid Clinics Programme. Eur
Heart J 1998; 19:1328-1333
37. Stefanick ML, et al. – Effects of diet
and exercise in men and
postmenopausal women with low
level HDL cholesterol and high levels
of LDL cholesterol. N Engl J Med
1998; 339:12-20
38. St Jeor ST, et al. – A classification
system to evaluate weight
maintainers, gainers, and losers. J Am
Diet Assoc 1997; 97:481-488
39. Muls E, et al. – Effects of initial BMI
and on-treatment weight change on
the lipid-lowering efficacy of fibrates.
Int J Obes Relat Metab Disord 1997;
21:155-158
40. McCarron DA, et al. – Nutritional
management of cardiovascular risk
factors. A randomized clinical trial.
Arch Intern Med. 1997; 157:169-177
41. Fox AA, et al. – Effects of diet and
exercise on common cardiovascular
disease risk factors in moderately
obese older women. Am J Clin Nutr
1996; 63:225-233
42. Pascale RW, et al. – Effects of a
behavioral weight loss program
stressing calorie restriction versus
calorie plus fat restriction in obese
individuals with NIDDM or a family
history of diabetes. Diabetes Care
1995; 18:1241-1248
43. Schaefer EJ, et al. – Body weight
and low-density lipoprotein
cholesterol changes after
consumption of a low-fat ad libitum
diet. JAMA 1995; 274:1450-1455
44. Andersen RE, et al. – Relation of
weight loss to changes in serum
lipids and lipoproteins in obese
women. Am J Clin Nutr 1995; 62:350-
357
45. Wing RR, Jeffery RW – Effect of
modest weight loss on changes in
cardiovascular risk factors; are there
difference between men and women
or between weight loss and
Vizita¡i site-ul
DE MEDICINÅ
www.samf.ro
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
maintenance? Int J Obes Relat Metab
Disord 1995; 19:67-73
46. Svendsen OL, Hassager C,
Christiansen C – Six months’
follow-up on exercise added to a
short-term diet in overweight
postmenopausal women–effects on
body composition, resting metabolic
rate, cardiovascular risk factors and
bone. Int J Obes Relat Metab Disord
1994; 18:692-698
47. Svendsen OL, Hassager C,
Christiansen C – Effect of an
energy-restrictive diet, with or
without exercise, on lean tissue mass,
resting metabolic rate, cardiovascular
risk factors, and bone in overweight
postmenopausal women. Am J Med
1993; 95:131-140
48. Datillo AM, Kris-Etherton PM –
Effects of weight reduction on blood
lipids and lipoproteins: a meta-
analysis. Am J Clin Nutr 1992;
56:320-328
49. Wolever TM, et al. – Beneficial effect
of low-glycemic index diet in
overweight NIDDM subjects. Diabetes
Care 1992; 15:562-564
50. Anderson JW, Brinkman VL,
Hamilton CC – Weight loss and 2-
year follow-up for 80 morbidly obese
patients treated with intensive very-
low-calorie diet and an education
program. Am J Clin Nutr 1992;
56:244S-246S
51. Williams PT, et al. – Effects of
exercise-induced weight loss on low
density lipoprotein subfractions in
healthy men. Arteriosclerosis 1989;
9:623-632
52. Wood PD, et al. – Changes in
plasma lipids and lipoproteins in
overweight men during weight loss
through dieting as compared with
exercise. N Engl J Med 1988;
319:1173-1179
53. Hagan RD, et al. – The effects of
aerobic conditioning and/or caloric
restriction in overweight men and
women. Med Sci Sports Exerc 1986;
18:87-94
54. Walsh DE, Yaghoubian V – Effect
of glucomannan on obese patients: a
clinical study. Int J Obes 1984; 8:289-
293
A FAMILIEI
279
 7 PRACTICA MEDICALÅ
ACTIVITATEA PREVENTIVÅ
Does a low-fat diet help prevent
breast cancer?
ELIZABETH STEINER, MD*; DAVID KLUBERT, MD**; MEG HAYES, MD***;
ANDREW HAMILTON, MS, MLS***
*Oregon Health and Science University, Portland
**Apogee Informatics, Portland, Oregon
***Oregon Health and Science University, Portland
CLINICAL COMENTARY
Losing weight is still a good strategy
Kathryn Kolasa, PhD, RD, LDN
East Carolina University, Greenville, NC
Women at risk for breast cancer – and cancer survivors –
want to know about lifestyle changes that can reduce their
risks for cancer or recurrence. There is growing evidence that
obesity plays a role in cancer development and promotion.
A low-fat diet has been demonstrated as a successful strategy
for weight loss. However, for most women, making these changes
can be difficult without extensive instruction, support, and
motivation. Limiting sweetened beverages, increasing
consumption of fruits and vegetables, and limiting fat intake
are 3 strategies women can use to achieve a healthy weight. If
this turns out to reduce their risk of breast cancer, so much the
better!
EVIDENCE-BASED ANSWER
No. Studies show no evidence that reducing
dietary fat decreases a woman’s risk of developing
postmenopausal breast cancer within the sub-
sequent 14 years (strength of recommendation
[SOR]: B, based on large heterogeneous
prospective cohort studies and appropriate meta-
analyses of these studies). Overall, evidence is
insufficient to recommend for or against
reduction in dietary fat to reduce risk of breast
cancer for women, although recommendations
for prudent fat intake may be justified on other
grounds.
280 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
EVIDENCE SUMMARY
Our Medline search retrieved 1114 English-
language studies published from 1960 through
October 2006. We limited this set to randomized
controlled trials and cohort studies, leaving 212
articles. We then excluded articles that had small
sample sizes, did not follow subjects for at least 5
years, did not include original data, included
men, did not give prevalence or incidence rate
of breast cancer in the subjects, or did not discuss
diet assessment tools. Of the remaining articles,
we selected the 11 best studies to include in the
review.
Early studies evaluating national average
dietary fat intake and breast cancer incidence
rates showed an almost linear relationship
between increased dietary fat and increased
breast cancer incidence. (1) However, increased
fat intake occurs primarily in industrialized
nations, providing multiple possible confounders
for increased rates of breast cancer, such as
pollutants and increased consumption of pres-
ervatives, pesticides, and other chemicals.
FAST TRACK
Reducing a woman’s dietary fat intake does
not appear to reduce her risk of breast cancer.
Case-control studies have shown some
minimally increased risk related to dietary fat
consumption, but there is concern about recall
bias in these studies. (2) Since the late 1970s, 7
large, well-designed prospective cohort studies
 DOES A LOW-FAT DIET HELP PREVENT BREAST CANCER?

have examined the possible relationship between
dietary fat and breast cancer. (1) The findings have
been somewhat contradictory, with some studies
showing statistically significant associations toward
increased risk with higher fat intake. (3-5)
Since the late 1990s, several meta-analyses,
a systematic review of these cohort studies, and
the Women’s Health Initiative Randomized
Controlled Diet Initiative have largely concluded
that there is no difference in breast cancer
incidence between women with a low-fat diet
(<20% of total calories from fat) and women
with average or high-fat diets (>40% total calories
from fat) (1,3,6,7).
The meta-analysis performed by Boyd et al
did find a statistically significant difference, with
relative risks ranging from 1.11 for overall to 1.19
for high-saturated-fat diets (8). The upper limit
of all confidence intervals was no higher than
1.35, however, suggesting a lack of clinical
significance. The best-designed studies also
evaluated dietary composition with regard to key
types of fat (saturated, mono- and poly-
unsaturated; animal vs vegetable vs marine) and
found no significant differences based on type
of fat consumed (1) .
Preliminary evidence indicates that lowering
dietary fat consumption may help with
secondary prevention of breast cancer, but no
large studies have been performed to date (9).
Recently, a nested study within the Women’s
Intervention Nutrition Study did show that
women with breast cancer who decreased their
fat intake to a median of 33 g/day had a hazard
ratio of 0.76 for relapse over 60 months
(compared with controls who ate a median of
51 g/day) (10).
FAST TRACK
The WHI showed that women with breast
cancer who reduced fat intake had a lower hazard
ratio for relapse.
RECOMMENDATIONS FROM OTHERS
There are no evidence-based or specific
recommendations for the primary prevention of
postmenopausal breast cancer for women
through dietary fat reduction. In particular,
neither the American Academy of Family
Physicians, American College of Surgeons,
National Institutes of Health, American College
of Obstetricians and Gynecologists, American
College of Physicians, US Preventive Services Task
Force, or the Centers for Disease Control and
Prevention provide any guidelines on dietary fat
restriction for primary prevention of post-
menopausal breast cancer.
The American Heart Association does have
guidelines for coronary artery disease prevention
for women, which include a low-fat diet (11).
The USPSTF has no specific guidelines regarding
dietary fat consumption for the general pop-
ulation.

REFERENCES
1. Willett WC – Diet and breast cancer.
J Intern Med 2001; 249:395-411
2. Bingham SA, Luben R, Welch A, et
al. – Are imprecise methods obscuring
a relation between fat and breast
cancer? Lancet 2003; 362:212-214
3. Mattisson I, Wirfalt E, Wallstrom P,
et al. – High fat and alcohol intakes
are risk factors of postmenopausal
breast cancer: a prospective study
from the Malmo diet and cancer
cohort. Int J Cancer 2004; 110:589-597
4. Sieri S, Krogh V, Muti P, et al. –
Fat and Protein Intake and
subsequent Breast Cancer risk in
Postmenopausal Women. Nutr Cancer
2004; 42:10-17
5. Velie E, Kulldorff M, Schairer C, et
al. – Dietary fat, fat subtypes, and
breast cancer in postmenopausal
women: a prospective cohort study. J
Natl Cancer Inst 2000; 92:833-839
6. Holmes MD, Hunter DJ, Colditz
GA, et al. – Association of dietary
intake of fat and fatty acids with risk
of breast cancer. JAMA 1999;
281:914-920
7. Low-Fat Dietary Pattern and risk of
Breast Cancer, Colorectal Cancer,
and Cardiovascular Disease – The
Women’s Health Initiative
randomized Controlled Dietary
Modification Trial. Available at:
www.whi.org/findings/dm/
dm.php. Accessed on June 14, 2007
8. Boyd NF, Stone J, Vogt KN, et al. –
Dietary fat and breast cancer risk
revisited: a meta-analysis of the
published literature. Br J Cancer 2003;
89:1672-1685
9. Rock CL – Diet and breast cancer:
can dietary factors influence
survival? J Mammary Gland Biol
Neoplasia 2003; 8:119-132
10. Rowan T, Chlebowski GL,
Blackburn CA, et al. – Dietary Fat
Reduction and Breast Cancer
Outcome: Interim Efficacy Results
From the Women’s Intervention
Nutrition Study. J Natl Cancer Inst
2006; 98:1767-1776
11. Mosca L, Appel LJ, Benjamin EJ, et
al. – Evidence-based guidelines for
cardiovascular disease prevention in
women. Circulation 2004; 109:672-
693

© 2007, Dowden Health Media, Inc. All rights reserved. This article was reprinted from the original article published in the Journal of
Family Practice, July 2007, Vol. 56, No. 7, pp 583-584. A publication of Dowden Health Media, Inc.

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 281

DOES A LOW-FAT DIET HELP PREVENT BREAST CANCER?
Revista presei medicale
Human stem cells heal the hearts of rats
WASHINGTON (Reuters) – A
nutritious cocktail helped human
embryonic stem cells thrive and repair
the damaged hearts of rats, U.S.
researchers reported on Sunday.
The experiment provides the best
evidence yet that the powerful but
controversial stem cells might be used
to repair the ravages of heart attacks
and heart failure, the researchers said.
Biotechnology company Geron
Corp said it would try to develop the
cells into a product. “We’re developing
our cardiomyocyte product, GRNCM1,
to address the large unmet need in
heart failure,” said Dr. Thomas
Okarma, president and chief executive
officer of Geron.
Stem cells are the body’s master
cell, acting as a source for the various
cells and tissues in the body. Those
taken from days-old embryos, called
embryonic stem cells, are the most
malleable and can produce all of the
cell types.
Their use is controversial because
some people oppose the destruction of
a human embryo. U.S. President
George W. Bush has kept strict limits
on federal funding of human
embryonic stem cell research. There are
no restrictions on privately funded
researchers.
SOCIETźII ACADEMICE
282 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
By MAGGIE FOX, Health and Science Editor
Okarma said embryonic stem cells
were the only human stem cells that
had been shown to form cardio-
myocytes – heart muscle cells.
Because embryonic stem cells are
so immature, it is very difficult to
control what kinds of cells they
produce, and the fear is that a tooth
could grow inside a heart, for instance.
“We got stem cells to differentiate
into mostly cardiac muscle cells, and
then got those cardiac cells to survive
and thrive in the damaged rat heart,”
said Dr. Chuck Murry of the Univ-
ersity of Washington’s Institute for
Stem Cell and Regenerative Medicine,
who worked on the study.
But the cells died when they
injected them into the hearts of the
rats, the researchers reported in the
journal Nature Biotechnology.
COMMON PROBLEM
“This problem is not unique to our
system. Death of transplanted cells is
slowing research progress in cell
therapy for diabetes, Parkinson’s
disease and muscular dystrophy,
among other diseases,” they wrote.
So the team developed what they
dubbed a “survival cocktail” that
included various proteins and other
compounds to stop the cells from
dying.
Source: REUTERS/HEALTH, Sunday, August 26, 2007
Vizita¡i site-ul
DE MEDICINÅ
www.samf.ro
It worked. When they caused heart
attacks in the rats and then injected
the new heart muscle cells, every graft
survived and integrated into the hearts
of the rats.
They beat in rhythm and improved
the heart function of the rats, they
reported.
“This is one of the most successful
attempts so far using cells to repair
solid tissues – every one of the treated
hearts had a well-developed tissue
graft,” Murry said.
This is key to treating someone
after a heart attack, known medically
as a myocardial infarction, said Dr.
Michael Laflamme, who also worked
on the study.
“This sort of treatment could help
the heart rebound from an infarction
and retain more of its function after-
wards,” Laflamme said in a statement.
An estimated 865,000 people have
heart attacks in the United States
every year and more than a third
eventually develop heart failure, a
chronic condition in which the heart
fails to pump blood properly. A third
of heart failure patients die within two
years.
A FAMILIEI

What we really need to do to
reduce cardiovascular events in
hypertensive patients
Consultant Cardiologist, HT Ong Heart Clinic, Penang, Malaysia
FORGET ABOUT A SILVER BULLET
Researchers have conducted numerous trials
over the last decade to find an antihypertensive
drug that best reduces cardiovascular events while
reducing blood pressure. However, this objective
review of 13 comparative antihypertensive drug
trials over the past decade involving more than
168,000 patients reveals no great differences in
the cardiovascular protective effects of diuretics,
beta-blockers, calcium channel blockers, angio-
tensin receptor blockers (ARBs), and angiotensin-
converting enzyme (ACE) inhibitors.
In fact, this review indicates that there were
no significant differences in the primary cardio-
vascular endpoints in more than 90% of the
patients studied. Where a difference in secondary
clinical outcome was demonstrated, fewer events
consistently occurred in the regimen that reached
the lower blood pressure level.
This assessment will likely fly in the face of the
way that many would view this body of research.
That’s understandable. At first glance, it would
appear that these 13 trials, with different meth-
odology and endpoints, have produced con-
flicting conclusions with the confusion worsened
by pharmaceutical companies seeking to interpret
the results to best suit their marketing needs. (1-
3)
It is not the quality of the data, however, that
is in question; the controversy lies in the
interpretation. Subjecting the studies to further
statistical analysis would simply obscure the
information.
By reviewing the data impartially and
objectively as a whole, though, and interpreting
individual studies in light of similar studies, it
becomes evident that there is more consensus
than conflict. The studies support the notion that
we should concentrate on getting patients to goal,
PRACTICA MEDICALÅ
ACTIVITATEA PREVENTIVÅ 8
HT ONG, FRCP (Glas, Edin), FACC, FESC
In this article:
• Review of 13 comparative antihypertensive drug trials
• Where to begin when there are coexisting conditions
• Report takes aim at poor medication adherence
Practice recommendations
• In your efforts to reduce cardiovascular events in
hypertensive patients, concentrate on getting patients to
goal, rather than on which drugs to use to get them
there (A).
• Beta-blockers – especially atenolol – should not be the
drug of first choice when treating older patients with
hypertension (A).
• Multiple drugs are required for adequate blood pressure
control in most patients (A).
Strength of recommendation (SOR)
A. Good quality patient-oriented evidence
B. Inconsistent or limited-quality patient-oriented evidence
Consensus, usual practice, opinion, disease-oriented evidence,
case series
rather than focusing on which drugs we’ll use to
get them there.
METHODS
I performed a PubMed search of the last 10
years using the keywords hypertension,
comparative, drug trials. I supplemented my
search with references from the JNC 7, WHO,
BHS/NICE, and European hypertension guide-
lines. For this review, I included only randomized
controlled trials with clinical cardiovascular
primary endpoints. The studies had to have
enrolled at least 500 patients and followed them
for at least 3 years. Thirteen trials satisfied these
criteria. (4-17) All 13 are summarized in the Table,
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 283
WHAT WE REALLY NEED TO DO TO REDUCE CARDIOVASCULAR EVENTS IN HYPERTENSIVE PATIENTS
but I will review 5 of the more recent trials here.
They are:
• ASCOT-BPLA – Anglo-Scandinavian
Cardiac Outcomes Trial-Blood Pressure
Lowering Arm
• ALLHAT – Antihypertensive and Lipid-
Lowering Treatment to Prevent Heart
Attack Trial
• ANBP2 – Second Australian National
Blood Pressure Study
• LIFE – Losartan Intervention For Endpoint
reduction
• VALUE – Valsartan Antihypertensive Long-
term Use Evaluation.
Calcium channel blockers vs beta-blockers
ASCOT-BPLA studied 19,257 high-risk
hypertensive patients on amlodipine (Norvasc),
adding perindopril, or atenolol (Tenormin),
adding bendroflumethiazide. (17) After 5.5 years,
the primary end-point of nonfatal myocardial
infarction (MI) and cardiovascular death was
similar (relative risk [RR]=0.90; 95% confidence
interval [CI], 0.79–1.02; P=.1052).
FAST TRACK
More than 60% of the patients in one trial
required 2 or more drugs for good blood pressure
control.
Total coronary endpoint, stroke, and mortality
were all lower on amlodipine. Blood pressure was
significantly lower on amlodipine compared with
atenolol, with an average difference of 2.7/1.9
mm Hg over the trial duration (18).
At the end of the trial, patients on amlodipine
also had a significantly higher HDL cholesterol,
and lower body mass index, triglyceride, creatin-
ine, and glucose levels. However, when
researchers made a multivariate adjustment for
all of these risk factors, cardiovascular event rate
differences between the 2 groups disappeared,
underscoring the importance of controlling for
all risk factors in reducing clinical cardiovascular
events (18,19).
A careful reading of ASCOT-BPLA, then,
makes it clear that this study does not support
the notion that newer antihypertensives (calcium
channel blockers and ACE inhibitors) are superior
to older ones (beta-blockers and diuretics)
(20,21). This study actually demonstrates that
while blood pressure reduction is vital, the
differences between regimens are less important.
LARGEST HYPERTENSIVE TRIAL EVER
STUDIED 4 DRUGS
ALLHAT, the largest hypertensive trial ever
conducted, randomized 15,255 patients to
284 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
chlorthalidone, 9061 to doxazosin (Cardura), 9048
to amlodipine, and 9054 to lisinopril (Prinivil/
Zestril) (10,11). (The arm involving doxazosin was
terminated after 3.2 years) (11,12).
Compared with the beta-blocker, more
patients achieved target blood pressure control
on chlorthalidone (63% vs 58%), and systolic
blood pressure was about 2 mm Hg lower.
Although the primary outcome of fatal coronary
heart disease and nonfatal MI was equal in both
groups (doxazosin=7.91%; chlorthalidone=
7.76%; RR=1.03 [95% CI, 0.93–1.15]; P=.62),
the doxazosin arm had more stroke, heart failure,
and combined cardiovascular events.
Patients on amlodipine and lisinopril had a
longer follow-up of 4.9 years. Systolic blood
pressure was higher on amlodipine (0.8 mm Hg,
P=.03) and lisinopril (2 mm Hg, P<.001) than
on chlorthalidone. The primary endpoint (fatal
coronary heart disease and nonfatal MI) was
similar on the diuretic (11.5%), calcium channel
blocker (11.3%; RR=0.98 [95% CI, 0.90–1.07];
P=.65), and ACE inhibitor (11.4%; RR=0.99
[95% CI, 0.91–1.08]; P=.81). Compared with
the diuretic arm, the calcium channel blocker arm
had a higher incidence of heart failure, while the
ACE inhibitor arm had a higher incidence of heart
failure, stroke, and combined cardiovascular
disease. The results were similar whatever the initial
glycemic state, renal function status, and racial
makeup of the patients studied (23-26). More than
60% of patients in ALLHAT required 2 or more
drugs for good blood pressure control (27).
“Diuretics first” for patients with or without
diabetes?
In ALLHAT, although diabetes occurred more
frequently and fasting glucose rose in patients on
diuretics, these metabolic abnormalities did not
result in more cardiovascular events. Even among
patients with diabetes, heart failure was more
common on doxazosin, amlodipine, and lisinopril
compared with those on chlorthalidone (23,24).
Given that the ultimate aim of hypertensive
therapy is to reduce clinical disease – not just to
improve laboratory profiles – ALLHAT should put
to rest any apprehension physicians have about
diuretic use. These findings have even led to
suggestions that diuretics be the first line anti-
hypertensive agent, in both diabetic and non-
diabetic patients (28-30).
ACE INHIBITOR VS DIURETIC
ANBP2 randomized hypertensive patients to
initial treatment with an ACE inhibitor (n=3044)
or a diuretic (n=3039) (12). With similar blood
 WHAT WE REALLY NEED TO DO TO REDUCE CARDIOVASCULAR EVENTS IN HYPERTENSIVE PATIENTS

Table. More consensus than conflict among 13 comparative antihypertensive drug trials with
cardiovascular primary endpoints
ACE I, angiotensin-converting enzyme inhibitor; CCB, calcium channel blocker; CHD, coronary heart
disease; CI, confidence interval; CV, cardiovascular; HF, heart failure; MI, myocardial infarction.
*Defined as coronary events including MI, heart failure, acute occlusion of artery, dissecting or
ruptured aortic aneurysm, and cerebrovascular events including stroke and transient ischemic
attacks.
† Defined as cardiac death, hospitalized heart failure, nonfatal MI, and emergency procedures to
prevent MI.
‡ Defined as cardiac death or sudden death, MI, angina pectoris requiring hospitalization, heart
failure requiring hospitalization, serious arrhythmia, and coronary interventions.

pressure reduction in both arms (26/12 mm Hg), FAST TRACK

treatment with the ACE inhibitor resulted in a
lower incidence of the composite primary end-
point of cardiovascular events or total death that
was of borderline significance (ACE inhibitor
=22.8%; diuretic=24.2%; RR=0.89 [95% CI,
0.79–1.00]; P=.05).
There is evidence that beta-blockers are less
useful in the older hypertensive patient.
Among women, there was no difference
between the ACE inhibitor and diuretic groups.
In the overall population, there was also no

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 285

WHAT WE REALLY NEED TO DO TO REDUCE CARDIOVASCULAR EVENTS IN HYPERTENSIVE PATIENTS
difference individually of total mortality or
incidence of first cardiovascular event or death.
Thus ANBP2 actually confirms the results from
ALLHAT by showing that ACE inhibitors and
diuretics are equivalent in reducing cardiovascular
events in hypertension (31).
LOSARTAN VS ATENOLOL
In the LIFE study, 9193 hypertensive patients
with left ventricular hypertrophy were ran-
domized to either losartan (Cozaar) or atenolol.
(9) Losartan treatment resulted in a marked
reduction in stroke incidence, which produced a
significant reduction in the composite primary
end-point of death, MI, or stroke (11% vs 13%;
RR=0.87 [95% CI, 0.77–0.98]; P=.021).
When only the 1195 patients with diabetes
were assessed, there was a significant reduction
not only in the primary endpoint but also in
cardiovascular and total mortality (32). Sur-
prisingly, the reduction of stroke incidence did
not reach statistical significance in this diabetic
population (RR=0.79 [95% CI, 0.55–1.14];
P=.204).
A word of caution, though: The results of LIFE
should be taken together with data from other
trials. No other study has demonstrated a special
benefit from the renin-angiotensin antagonists in
preventing stroke. In fact, ACE inhibitors were
weaker than the comparator drugs in preventing
stroke in both CAPPP (Table) and ALLHAT (5,10).
Various reviews have suggested that among
antihypertensive drugs, it is the diuretics and
calcium channel blockers that may be more useful
in stroke reduction (33,34).
CHALK THE BENEFIT UP TO THE
DROP IN BLOOD PRESSURE
In the LIFE study, the treated mean systolic
blood pressure was lower with losartan in the
overall (1.1 mm Hg; P=.017) and diabetic (2 mm
Hg; P value not stated) populations, and thus the
clinical benefit could possibly have been from the
better blood pressure reduction on losartan.
Furthermore, there is evidence that beta-blockers
are less useful in the older hypertensive patient,
and are especially weak in preventing stroke
incidence (35,36).
Rather than showing the superiority of the
ARB, it is fair to say that LIFE actually confirms
the importance of blood pressure reduction, and
reveals the weaker cardiovascular protective effect
of atenolol in older hypertensive patients.
286 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
VALSARTAN, AMLODIPINE IN HIGH-
RISK PATIENTS
VALUE randomized 15,245 high-risk hyper-
tensive patients to valsartan (Diovan) and amlo-
dipine (15,37). Trial researchers sought to study
the difference – for the same level of blood pressure
reduction – between the 2 regimens in the
incidence of cardiac events defined as sudden
cardiac death, hospitalized heart failure, nonfatal
MI, and emergency procedures to prevent MI. That
said, the attained blood pressure was lower on
the calcium channel blocker: 4.0/2.1 mm Hg at 1
month and 2.1/1.7 mm Hg at the end of study.
After 4.2 years, there was no significant
difference in the primary endpoint of first cardiac
event (10.6% valsartan/10.4% amlodipine;
RR=1.04 [95% CI, 0.94–1.15]; P=.49). Diabetes
was lower, but the rate of MI was higher on
valsartan. After correction for the blood pressure
difference, the composite of cardiac events,
stroke, death, or MI was similar in the 2 groups.
VALUE patients reaching adequate blood
pressure control by 6 months fared better,
regardless of drug type used. Thus demonstrating
that the benefit from good blood pressure control
was more important than the subtle differences
between antihypertensive drugs. The better
metabolic profile in the angiotensin receptor
blocker arm did not translate into a reduction in
adverse clinical disease.
The VALUE trial suggests (as did ALLHAT) that
drugs targeting the reninangiotensin system do not
provide special cardiovascular protection (10,15).
WHERE TO BEGIN WHERE ARE
COEXISTING CONDITIONS
Choosing an antihypertensive drug according
to the clinical disease and target organ most at
risk of damage is logical and in keeping with
numerous guidelines (42-45). Thus, you’ll want
to treat hypertensive patients with these
conditions as follows:
• Angina pectoris. Therapy should include
a beta-blocker or calcium channel blocker,
given their definite antianginal and possible
anti-atherosclerotic effects (16,46,47).
• Prior MI. Start the patient on a beta-
blocker (47).
• Poor left ventricular function. Start the
patient on a diuretic, and then add an
ACE inhibitor and beta-blocker, as needed
(10,49,50).
• Prior stroke (or a patient at special risk
of stroke). Begin therapy with a calcium
channel blocker or a diuretic (33,34).
 WHAT WE REALLY NEED TO DO TO REDUCE CARDIOVASCULAR EVENTS IN HYPERTENSIVE PATIENTS
Diabetic proteinuria. An ARB or an ACE
inhibitor is best suited to prevent and delay
nephropathy (51-54).
CONSENSUS EMERGES FROM
STUDIES SPANNING 10 YEARS
This objective review of the comparative
hypertension drug trials shows that there are no
great differences in the cardiovascular protective
efficacy of the diuretics, beta-blockers, calcium
channel blockers, ARBs, and ACE inhibitors.
There was no significant difference in the
cardiovascular primary endpoint in 11 of the 13
trials reviewed, involving 91% of the randomized
168,593 patients (Table) (4-8,10,11,13-17). Of
the remaining 2 trials, the difference in ANBP2
just reached a P value of .05, while the result in
LIFE was driven by a lower stroke incidence on
ARB treatment that is not noted in any of the
other studies involving an ARB or ACE inhibitor
(4-6,10,12-15).
FAST TRACK
Focus on how best to reach adequate blood
pressure control by combining several antihyper-
tensive drugs.
FOCUS ON CONTROLLING BLOOD
PRESSURE WITH COMBINATION OF
DRUGS
Given the very large number of patients
studied in these well-conducted trials, if there
were any especially useful, or detrimental,
cardiovascular effect of a particular class of
antihypertensive drug , it would have been
obvious by now. Since most patients will require
multiple drugs, the equivalent protective efficacy
of different antihypertensive drugs is reassuring
and suggests that physicians should not worry
too much about which drug to start the patient
on (28). Rather, the emphasis should be on how
best to reach adequate blood pressure control
by combining several antihypertensive drugs.
FAST TRACK
Treating patients to goal hinges on medication
adherence. See related story on page 734.
SMALL BLOOD PRESSURE
DIFFERENCES, BIG IMPACT
In LIFE (losartan vs atenolol), ALLHAT (doxa-
zosin, amlodipine, lisinopril vs chlorthalidone),
VALUE (amlodipine vs valsartan), and ASCOT
(amlodipine vs atenolol), where a secondary
cardiovascular endpoint was lower in one of the
treatment arms, it was always the arm with the
lower achieved blood pressure that had the better
clinical outcome (9-11,15,17).
REPORT TAKES AIM AT AMERICA’S
OTHER DRUG PROBLEMS: POOR
ADHERENCE
MARYA OSTROWSKI, JFP Editor
With only 50% of patients typically taking their
medications as prescribed and the cost of poor
adherence reaching an estimated $177 billion
annually in direct and indirect health care costs,
one medication safety group is saying enough is
enough.
The National Council on Patient Information
and Education (NCPIE), a nonprofit coalition that
includes health professional associations, government
agencies, and pharmaceutical companies, issued a
report this summer detailing a 10-step action plan
for reducing the adverse health and economic
consequences of poor medication adherence.
The plan, developed by a panel of experts that
NCPIE convened, calls on the government and
health care community to, among other things:
• address the barriers to patient adherence for
patients with low health literacy.
• develop a curriculum on medication
adherence for use in medical schools.
• mount a unified national education
campaign to make patient adherence a
national health priority.
“Medication adherence is America’s new drug
problem,” said Carolyn M. Clancy, MD, director
of the Agency for Healthcare Research and Quality.
AHRQ has been working with NCPIE, the FDA,
and the National Consumers League to develop a
public education campaign on medication adherence,
according to Clancy. The NCPIE report helps to
bolster those ongoing efforts, she said.
On the heels of the report, NCPIE is planning
on releasing videos that will teach seniors about
properly taking their medications, according to Ray
Bullman, NCPIE’s executive vice president.
To learn more about NCPIE’s initiatives, or for
a copy of the report, Enhancing Prescription
Medicine Adherence: A National Action Plan,
point your browser to: www. talkabouttrx.org.
These achieved blood pressure differences
although small, were significant. Small overall
mean blood pressure differences could mask
much larger blood pressure differences in the
individual patient. Consider, for instance, the
HOPE (Heart Outcomes Prevention Evaluation)
trial, where a reported overall blood pressure
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 287
WHAT WE REALLY NEED TO DO TO REDUCE CARDIOVASCULAR EVENTS IN HYPERTENSIVE PATIENTS

difference of only 3/1 mm Hg between the 2
treatment arms masked a difference of 10/4 mm
Hg in 24-hour ambulatory blood pressure and a
difference of 17/8 mm Hg in night-time blood
pressure (39,40).
Thus, instead of trying to work out why anti-
hypertensive drugs could exert apparently
different cardiovascular protective efficacy in
different trials, the simple and consistent message
is that the lower the achieved blood pressure,
the lower the adverse clinical cardiovascular
outcome.
WHAT MAKES SENSE FOR YOUR
PATIENT?
In selecting antihypertensive drugs, physicians
should be guided by data supporting a particular
drug in coexisting clinical conditions. (See “Where
to begin when there are coexisting conditions”)
In the hypertensive patient who is free of clinical
disease, a case can be made for a diuretic as the
first-line drug, although calcium channel blockers,
ARBs, and ACE inhibitors can also claim evidence
to support their use. In the older patient, beta-
blockers –especially atenolol – should not be the
drug of first choice (35,36,41).
FAST TRACK
The lower the achieved blood pressure, the lower
the adverse clinical cardiovascular outcome.
As this review of comparative hypertension
drug trials shows, multiple drugs are required for
adequate blood pressure control in most patients.
Thus, physicians should not be too preoccupied
about how to initiate treatment, but remember
to add drugs until adequate control is achieved.
FAST TRACK
“Medication adherence is America’s new drug
problem.” Carolyn M. Clancy, MD, AHRQ
director

Disclosure
No potential conflict of interest relevant to this article was reported.

REFERENCES
1. Psaty BM, Weiss NS, Furberg CD –
Recent trials in hypertension.
Compelling science or commercial
speech? JAMA 2006; 295:1704-1706
2. Abramson J, Starfield B – The effect
of conflict of interest on biomedical
research and clinical practice
guidelines: Can we trust the evidence
in evidence-based medicine? J Am
Board Fam Pract 2005; 18:414-418
3. Lexchin J, Bero LA, Djulbegovic B,
et al. – Pharmaceutical industry
sponsorship and research outcome
and quality: systematic review. BMJ
2003; 326:1167-1170
4. UK Prospective Diabetes Study
Group – Efficacy of Atenolol and
Captopril in Reducing Risk of
Macrovascular and Microvascular
Complications in Type 2 Diabetes:
UKPDS 39. BMJ 1998; 317:713-720
5. Hansson L, Lindholm LH,
Niskanen L, et al. – Effect of ACE
inhibition compared with
conventional therapy on
cardiovascular morbidity and
mortality in hypertension: The
Captopril Prevention Project
(CAPPP). Lancet 1999; 353:611-616
6. Hansson L, Lindholm LH, Ekbom
T, et al. – Randomized trial of old
and new antihypertensive drugs in
elderly patients: cardiovascular
mortality and morbidity the Swedish
Trial in Old Patients with
Hypertension 2 (STOP-Hypertension
2) study. Lancet 1999; 354:1751-1756
7. Brown MJ, Palmer CR, Castaigne
A, et al. – Morbidity and mortality in
patients randomized to double-blind
treatment with a long-acting
calcium-channel blocker or diuretic in
the International Nifedipine GITS
study: Intervention as a Goal in
Hypertension Treatment (INSIGHT).
Lancet 2000; 356:366-372
8. Hansson L, Hedner T, Lund-
Johansen P, et al. – For the NORDIL
Study Group. Randomised trial of
effects of calcium antagonists
compared with diuretics and beta-
blockers on cardiovascular morbidity
and mortality in hypertension: the
Nordic Diltiazem (NORDIL) Study.
Lancet 2000; 356:359-365
9. Dahlof B, Devereux RB, Kjeldsen
SE, et al. – For the LIFE study
group. Cardiovascular morbidity
and mortality in the Losartan
Intervention For Endpoint reduction
in hypertension study (LIFE): a
randomized trial against atenolol.
Lancet 2002; 359:995-1003
10. The ALLHAT Officers and
Coordinators for the ALLHAT
Collaborative Research Group. Major
outcomes in high-risk hypertensive
patients randomized to angiotensin-
converting enzyme inhibitor or
calcium channel blocker vs diuretic:
the Antihypertensive and Lipid-
Lowering Treatment to prevent Heart
Attack trial (ALLHAT). JAMA 2002;
288:2981-2997
11. ALLHAT officers and Coordinators
for the ALLHAT Collaborative
research Group. Diuretic versus
alpha-blocker as first-step
antihypertensive therapy: final
results from the Antihypertensive
and lipidlowering treatment to
prevent Heart Attack trial
(ALLHAT). Hypertension 2003;
42:239-246
12. Wing LMH, Reid CM, Ryan P, et
al. – For the Second Australian
National blood pressure Study
Group. A comparison of outcomes
with angiotensin converting enzyme
inhibitors and diuretics for
hypertension in the elderly. N Engl J
Med 2003; 348:583-592
13. Black HR, Elliott WJ, Grandits G,
et al. – For the CONVINCE research
Group. Principal results of the
Controlled ONset Verapamil
INvestigation of Cardiovascular End

288 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007

 WHAT WE REALLY NEED TO DO TO REDUCE CARDIOVASCULAR EVENTS IN HYPERTENSIVE PATIENTS
points (CONVINCE) trial. JAMA
2003; 289:2073-2082
14. Pepine CJ, Handberg EM, Cooper-
DeHoff RM, et al. – For the INVEST
Investigators. A calcium antagonist
vs a non-calcium antagonist
hypertension treatment strategy for
patients with coronary artery disease.
The International Verapamil-
Trandolapril Study (INVEST): A
randomized controlled trial. JAMA
2003; 290:2805-2816
15. Julius S, Kjeldsen SE, Weber M –
For the VALUE trial group.
Outcomes in hypertensive patients at
high cardiovascular risk treated with
regimens based on valsartan or
amlodipine: the VALUE randomized
trial. Lancet 2004; 363:2022-2031
16. Yui Y, Sumiyoshi T, Kodama K, et
al. – Comparison of nifedipine retard
with angiotensin-converting enzyme
inhibitors in Japanese hypertensive
patients with coronary artery disease:
the Japan multicenter Investigation
for Cardiovascular Diseases-B
(JMIC-B) randomized trial. Hypertens
Res 2004; 27:181-191
17. Dahlof B, Sever PS, Poulter NR –
For the ASCOT investigators.
Prevention of cardiovascular events
with an antihypertensive regimen of
amlodipine adding perindopril as
required versus atenolol adding
bendroflumethiazide as required, in
the Anglo-Scandinavian Cardiac
outcomes trial-blood pressure
lowering Arm (ASCOT-BPLA): a
multicentre randomized controlled
trial. Lancet 2005; 366:895-906
18. Poulter NR, Wedel H, Dahlof B –
For the ASCOT investigators. Role of
blood pressure and other variables in
the differential cardiovascular event
rates noted in the Anglo-
Scandinavian Cardiac outcomes
trial-blood pressure lowering Arm
(ASCOT-BPLA). Lancet 2005;
366:907-913
19. Daviglus ML, Liu K – Today’s
Agenda. We must focus on achieving
favorable levels of all risk factors
simultaneously. Arch Intern Med
2004; 164:2086-2087
20. Duerden M – ASCOT-BPLA. Lancet
2006; 367:206
21. Cave JA – ASCOT: A tale of two
treatment regimes. Is ASCOT all it’s
cracked up to be? BMJ 2005;
331:1023
22. The ALLHAT officers and
Coordinators for the AllHAt
Collaborative research Group. Major
cardiovascular events in hypertensive
patients randomized to doxazosin vs
chlorthalidone: the Antihypertensive
and Lipid-Lowering Treatment to
Prevent Heart Attack Trial (ALLHAT).
JAMA 2000; 283:1967-1975
23. Barzilay JI, Davis BR, Bettencourt J,
et al. – For the ALLHAT
Collaborative research Group.
Cardiovascular outcomes using
doxazosin vs chlorthalidone for the
treatment of hypertension in older
adults with and without glucose
disorders: a report from the
ALLHAT Study. J Clin Hypertens
2004; 6:116-125
24. Whelton PK, Barzilay J, Cushman
WC, et al. – For the ALLHAT
Collaborative research group. Clinical
outcomes in antihypertensive
treatment of type 2 diabetes,
impaired fasting glucose
concentration, and normoglycemia.
Antihypertensive and Lipid-
Lowering Treatment to Prevent Heart
Attack Trial (ALLHAT). Arch Intern
Med 2005; 165:1401-1409
25. Rahman M, Pressel S, Davis BR, et
al. – For the ALLHAT Collaborative
research Group. Renal outcomes in
high-risk hypertensive patients
treated with an angiotensin-
converting enzyme inhibitor or a
calcium channel blocker vs a diuretic:
a report from the ALLHAT Study.
Arch Inten Med 2005; 165:936-946
26. Wright JT, Dunn JK, Cutler JA, et
al. – For the ALLHAT Collaborative
research Group. outcomes in hyper-
tensive black and nonblack patients
treated with chlorthalidone,
amlodipine, and lisinopril. JAMA
2005; 293:1595-1607
27. Cushman WC, Ford CE, Cutler JA,
et al. – Success and predictors of
blood pressure control in diverse
North American settings: the
Antihypertensive and Lipid-
Lowering Treatment to Prevent Heart
Attack Trial (ALLHAT). J Clin
Hypertens 2002; 4:393-504
28. Williams B – Drug treatment for
hypertension: most patients will need
a treatment cocktail -including a
thiazide diuretic. BMJ 2003;326:61-
62
29. Appel LJ – The verdict from
ALLHAT—thiazide diuretics are the
preferred initial therapy for
hypertension. JAMA 2002; 288:3039-
3042
30. Salvetti A, Ghiadoni L – Guidelines
for antihypertensive treatment: An
update after the ALLHAT study. J
Am Soc Nephrol 2004; 15:S51-S54
31. Frohlich ED – Treating hypertension-
what are we to believe? N Engl J Med
2003; 348:639-641
32. Lindholm LH, Ibsen H, Dahlof B,
et al. – For the LIFE study group.
Cardiovascular morbidity and
mortality in patients with diabetes in
the losartan Intervention For
Endpoint reduction in hypertension
study (LIFE): a randomized trial
against atenolol. Lancet 2002;
359:1004-1010
33. Messerli FH, Grossman E, Lever AF –
Do thiazide diuretics confer specific
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
protection against strokes? Arch
Intern Med 2003; 163:2557-2560
34. Opie LH, Schall R – Evidence-based
evaluation of calcium channel
blockers for hypertension. J Am Coll
Cardiol 2002; 39:315-322
35. Carlberg B, Samuelsson O,
Lindholm LH – Atenolol in
hypertension: is it a wise choice?
Lancet 2004; 364:1684-1689
36. Khan N, McAlister FA – Re-
examining the efficacy of beta-
blockers for the treatment of
hypertension: a meta-analysis. CMAJ
2006; 174:1737-1742
37. Kjeldsen SE, Julius S, Brunner H,
et al. – for the VALUE Trial Group.
Characteristics of 15314 hypertensive
patients at high coronary risk. the
VALUE trial. Blood Press 2001; 10:83-
91
38. Weber MA, Julius S, Kjeldsen SE,
et al. – Blood pressure dependent
and independent effects of
antihypertensive treatment on clinical
events in the VALUE trial. Lancet
2004; 363:2049-2051
39. The Heart outcomes prevention
evaluation Study Investigators.
Effects of an angiotensin-converting
enzyme inhibitor, ramipril, on
cardiovascular events in high-risk
patients. N Engl J Med 2000;
342:145-153
40. Svensson P, De Faire U, Sleight P,
et al. – Comparative effects of
ramipril on ambulatory and office
blood pressures: a Hope substudy.
Hypertension 2001; 38:28-32
41. Ong HT – Beta-blockers in
hypertension and cardiovascular
disease. BMJ 2007; 334:946-949
42. Chobanian AV, Bakris GL, Black
HR, et al. – The National High blood
pressure education program
Coordinating Committee. The
Seventh report of the Joint National
Committee on prevention, Detection,
evaluation, and treatment of High
blood pressure. the JNC 7 report.
JAMA 2003; 289:2560-2572
43. Guidelines Committee. 2003
european Society of Hypertension-
european Society of Cardiology
guidelines for the management of
arterial hypertension. J Hypertens
2003; 21:1011-1053
44. World Health Organization.
International Society of Hypertension
Writing Group. 2003 World Health
Organisation (WHO)/International
Society of Hypertension (ISH)
statement on management of
hypertension. J Hypertens 2003;
21:1983-1992
45. Williams B, Poulter NR, Brown MJ,
et al. – Guidelines for management
of hypertension: report of the fourth
working party of the british
Hypertension Society, 2004 – BHS
289
WHAT WE REALLY NEED TO DO TO REDUCE CARDIOVASCULAR EVENTS IN HYPERTENSIVE PATIENTS

IV. J Hum Hypertens 2004; 18:139-
185
46. Nissen SE, Tuzcu EM, Libby P –
For the CAMELOT investigators.
Effect of antihypertensive agents on
cardiovascular events in patients
with coronary disease and normal
blood pressure. the CAMELOT
Study: a randomized controlled trial.
JAMA 2004; 292:2217-2226
47. Hedblad B, Wikstrand J, Janzon L,
et al. – Low dose Metoprolol CR/XL
and Fluvastatin slow progression of
carotid intima-media thickness: main
results from the beta-blocker
Cholesterol-lowering Asymptomatic
plaque Study (BCAPS). Circulation
2001; 103:1721-1726
48. Freemantle N, Cleland J, Young P,
et al. – Beta-blockade after
myocardial infarction: systematic
review and meta regression analysis.
BMJ 1999; 318:1730-1737
49. The SOLVD Investigators. Effect of
enalapril on mortality and the
development of heart failure in
asymptomatic patients with reduced
left ventricular ejection fractions. N
Engl J Med 1992; 372:685-691
50. MERIT-HF Study Group. Effect of
metoprolol CR/XL in chronic heart
failure: metoprolol CR/XL
randomised Intervention trial in
Congestive Heart Failure (MERIT-
HF). Lancet 1999; 353:2001-2006
51. Lewis EJ, Hunsicker LG, Clarke
WR, et al. – Renoprotective effect of
the angiotensin-receptor antagonist
irbesartan in patients with
nephropathy due to type 2 diabetes.
N Engl J Med 2001; 345:851-860
52. Parving HH, Lehnert H, Mortensen
JB, et al. – The effect of irbesartan on
the development of diabetic
nephropathy in patients with type 2
diabetes. N Engl J Med 2001;
345:870-878
53. Brenner BM, Cooper ME, Zeeuw D
de, et al. – Effects of losartan on
renal and cardiovascular outcomes in
patients with type 2 diabetes and
nephropathy. N Engl J Med 2001;
345:861-869
54. Wright JT, Bakris G, Greene T, et
al. – For the African American Study
of Kidney Disease and Hypertension
Study Group. Effect of blood
pressure lowering and
antihypertensive drug class on
progression of hypertensive kidney
disease: results from the AASK trial.
JAMA 2002; 288:2421-2431

Correspondence H T Ong, FRCP, FACC, FESC, H T Ong Heart Clinic, 251C Burma Road, Penang 10350, Malaysia; htyl@pd.jaring.my
©2007, Dowden Health Media, Inc. All rights reserved. This article was reprinted from the original article published in the Journal of Family
Practice, September 2007, Vol. 56, No. 9, pp 727-734. A publication of Dowden Health Media, Inc.

Revista presei medicale

Elve¡ia: cancerul învins cu ajutorul
luminii ¿i metalelor
Switzerland: cancer was depleated with the help
of light and metals
Chimi¿ti elve¡ieni de la Universi- acestuia într-un comunicat. Primele
tatea din Neuchatel, Ecole Polytechnique teste biologice desfå¿urate la EPFL ¿i
Federale din Lausanne (EPFL) ¿i de la Spitalul Universitar din Lausanne
la Spitalul Universitar din acela¿i ora¿ au dus la ob¡inerea unor „rezultate
au pus la punct o nouå armå îm- excelente“ în lupta cu celulele tumo-
potriva cancerului. Ei au combinat rale din melanom.
un medicament care måre¿te sensi- Moleculele pe baza de metale, în
bilitatea celulelor canceroase fa¡å de special cele cu platinå, sunt între-
luminå cu o serie de compu¿i chimici buin¡ate pe scarå largå în terapiile
ai ruteniului, un metal tranzi¡ional anticanceroase, dar prezintå un incon-
în tabelul periodic al lui Mendeleev. venient major, ¿i anume efectele
Substan¡ele au fost sintetizate la secundare. Ruteniul, care face parte
Institutul de Chimie al Universitå¡ii din familia metalelor platinice, pare
din Neuchatel, a precizat conducerea så fie solu¡ia salvatoare, afirmå cer-
ALIC MIRZA, 01.11.2007
cetåtorii, un poten¡ial confirmat de
altfel în urma studiilor clinice.
Cât despre luminå, în general o
razå laser distruge celulele canceroase
sensibilizate cu un medicament fa¡å
de ac¡iunea sa. Brevetat, noul plan de
atac apårut în laboratoarele Univer-
sitå¡ii din Neuchatel ¿i care combinå
lumina cu compu¿ii organo-metalici
laså så se întrevadå „speran¡a cå aceste
produse vor fi administrate paci-
en¡ilor într-un termen cât mai scurt“,
se mai afirmå în comunicat.

Articol din BANII NOªTRI/6 Noiembrie 2007

290 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007

 PRACTICA MEDICALÅ
PREVENºIA ÎN MF 9
BNP ca factor predictiv al
morbiditå¡ii ¿i mortalitå¡ii
cordului pulmonar acut
BNP as predictive factor of morbidity
Prof. Dr. Aurel LAZÅR
and mortality in acute pulmonary
heart disease
Prof. Dr. AUREL LAZÅR, Prof. Dr. LIVIU LAZÅR, Dr. MARIUS RUS
Facultatea de Medicinå, Universitatea din Oradea

REZUMAT
Dacå se cunoa¿te deja valoarea peptidului natriuretic cerebral (BNP) în evaluarea ¿i prognosticul pacien¡ilor
cu insuficien¡å cardiacå stângå, în schimb concordan¡a între evolu¡ia pacien¡ilor cu insuficien¡å cardiacå
dreaptå ¿i valorile BNP a fost mult mai pu¡in investigatå.
Lucrarea de fa¡å î¿i propune så evalueze evolu¡ia pacien¡ilor cu tromembolism pulmonar, cu sau fårå insuficien¡å
dreaptå în corela¡ie cu valorile BNP.
În acest scop, am luat în studiu to¡i pacien¡ii cu tromembolism pulmonar, interna¡i în clinica de Cardiologie
Oradea, în perioada 1.01.2005-1.01.2007. A fost vorba de 60 de pacien¡i, cu vârsta medie de 57±19 ani, dintre
care 36 (60%) au fost bårba¡i ¿i 24 (40%) au fost femei.
Ace¿ti pacien¡i au fost urmåri¡i pe parcursul internårii. Evaluarea insuficien¡ei cardiace drepte s-a fåcut
clinic, la internare ¿i ecocardiografic la 2-7 zile de la internare. 40 (66,67%) de pacien¡i au prezentat insuficien¡å
ventricularå dreaptå, manifesta clinic în momentul internårii.
Am dozat BNP la to¡i pacien¡ii, la internare. În lotul pacien¡ilor cu trombembolism pulmonar ¿i insuficien¡å
cardiacå dreaptå (IVD), BNP a fost crescut la 34 (85%) de pacien¡i; în cel de-al doilea lot, 7 (35%) au prezentat
valori crescute ale BNP.
Dintre pacien¡ii cu IVD, 21 (52.5%) au necesitat resuscitare cardiorespiratorie sau au decedat pe parcursul
spitalizårii, iar din cel de-al doilea lot, 9 (45%) au prezentat complica¡iile amintite mai sus. To¡i pacien¡ii din
primul lot ¿i 7 din cel de al doilea, care au prezentat o evolu¡ie negativå, au avut concomitent ¿i valori crescute
ale BNP la internare.
La pacien¡ii cu IVD ¿i TEP valoarea diagnosticå a BNP s-a dovedit reduså, poate din cauza cut off-ului ales,
350 pmol/ml, dar valoarea prognosticå cåtre evolu¡ie nefavorabilå, respectiv stop cardiorespirator sau deces a
aråtat un risc de 1.6 ori mai mare la pacien¡ii cu valori crescute ale BNP.
La pacien¡ii fårå IVD valoarea predictivå negativå a BNP a fost foarte bunå, BNP scåzut putând fi folosit
pentru excluderea IVD. Riscul cåtre evolu¡ie nefavorabilå a fost de 6,7 ori mai mare la pacien¡ii cu BNP crescut
fa¡å de cei cu BNP normal în acest lot.
În ambele loturi, valoarea diagnosticå a BNP a fost moderatå, dar valoarea predictivå cåtre evolu¡ie nefavorabilå
a fost bunå, rezultatele aråtând un risc de 3 ori mai mare la cei cu BNP crescut. De asemenea, în lotul pacien¡ilor
fårå IVD valoarea predictivå a BNP este de 4,2 ori mai mare decât la cei cu IVD.
În concluzie, luând în considerare un cut-off ridicat al BNP, 350 pmol/ml valoarea diagnosticå a acestuia este
scåzutå în cazul pacien¡ilor cu IVD, dar este util în excluderea IVD la pacien¡ii fårå semne clinice de IVD, dar
la aceastå valoarea a cut-offului BNP are o importan¡å deosebitå în predic¡ia complica¡iilor, în ambele situa¡ii,
dar mai semnificativ la pacien¡ii fårå IVD.

Cuvinte cheie: BNP, tromembolism pulmonar, insuficien¡å cardiacå dreaptå

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 291

BNP CA FACTOR PREDICTIV AL MORBIDITźII ªI MORTALITźII CORDULUI PULMONAR ACUT

ABSTRACT
BNP as predictive factor of morbidity and mortality in accute pulmonary heart disease
The aim of our study was to check the predictive value of BNP in morbidity and mortality on patients with
pulmonary embolia, with or without right heart failure (RHF).
We set the cut off point for BNP values highest than is usually used to determine left heart failure, because we
expect a greater increase of BNP in that heart failures which drive to a morbid complication. The value of BNP
cut off point was 350 pmol/ml. The right ventricle has a lower mass comparing with left ventricle, that’s why,
in congestive heart failure we don’t expect a greatly increase in BNP values.
We studied 60 consecutive patients with pulmonary embolia admitted in our clinic during last 2 years. The
diagnostics of pulmonary embolia was established based on clinical criteria, X ray, computer tomography with
contrast and echocardiography. The diagnostic of RHF was based on clinical criteria and echocardiography.
We used Doppler echocardiography for diagnostic of peripheral deep venous thrombosis. Unfortunately in our
clinic ventilation/perfusion check is not available.
In 40 (66,67%) cases were established, at admission, the diagnostic of pulmonary emboli with RHF. 34
(85%) of these patients had BNP value above 350 pool/ml (mean 512 pool/ml) and 7 (35%) out of 20 patients
without RHF had BNP value above normal range (mean 439pmol/ml).
Among patients with RHF 21 (52.5%) out of 40 needed card-pulmonary resuscitation or died during
admission, and 9 (45%) of patients without RHF suffered same poor evolution. All patients with RHF and 7 of
these without RHF had BNP values above our cut off point (mean 537pmol/ml).
The diagnostic value of BNP in the case of patients with RHF was low, as the Youden index = 0.11, show off.
Instead of that, the predictive value for morbid complication show off that, on these patients the risk for a poor
evolution was 1.6 times higher in patients with high values of BNP. We presume that the diagnostic value of
BNP was low because we set a high cut off point.
Among patients without RHF the Youden index = 0.78 show off a good diagnostic values, which allows us,
actually to negate the RHF among patients without any other characteristic of right ventricle failure. The
predictive value in these case was even greater that in case of patients without RHF, and is also consequence of
the high cut off which allow us to distinguish between patients with a poor prognostic in the absence of the RHF.
Patients without RHF but with high values of BNP have a 6.7 time greater risk to have a poor outcome, cardio-
respiratory failure or to die.
Our statistics show a 4.2 times better predictive value for negative outcome on patients without RHF comparing
with that with right heart failure.
In conclusion we may say that BNP is important to predict the outcome of patients with pulmonary
thrombembolia. His accuracy is even greater in the absence of the RHF.

Key words: BNP, pulmonary thrombembolia, right heart failure

INTRODUCERE În prezent, cele mai multe protocoale recomandå

N
ivelul plasmatic al petidului natriuretic
cerebral (BNP) este crescut la pacien¡ii
cu insuficien¡å cardiacå stângå.
La pacien¡ii cu tromboemolism pulmonar
mortalitatea este crescutå, mai ales în cazul
insuficien¡ei ventriculare drepte. Existå în prezent
pu¡ine studii referitoare la cre¿terea BNP la
pacien¡ii cu insuficien¡å cardiacå dreaptå acutå.
Identificarea disfunc¡iei de inimå dreaptå este
importantå, tratamentul acesteia, în special
reducerea postsarcinii prin trombolizå, poate
duce la ameliorarea prognosticului în cazul
pacien¡ilor cu tromboembolism pulmonar (TEP).
ecocardiografia la patul bolnavului, la pacien¡ii
cu TEP pentru identificarea insuficien¡ei cardiace
drepte ¿i a gradului acesteia. Se ¿tie cå cu cât este
mai gravå disfunc¡ia inimii drepte, cu atât este
mai sumbru prognosticul acestor pacien¡i.
Un test biochimic, care så permitå evaluarea
disfunc¡iei cardiace drepte ar aduce îmbunåtå¡iri
semnificative în managementul acestor pacien¡i.
Pânå acum se ¿tie cå BNP evalueazå ¿i prezice
cu acurate¡e evolu¡ia frac¡iei de ejec¡ie a ventri-
culului stâng, capacitatea de efort, morbiditatea
¿i mortalitatea la ace¿ti pacien¡i. Date din literaturå
semnaleazå cre¿terea valorilor BNP la pacien¡ii

292 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007

 BNP CA FACTOR PREDICTIV AL MORBIDITźII ªI MORTALITźII CORDULUI PULMONAR ACUT
cu hipertensiune arterialå cronicå, respectiv la
pacien¡ii cu insuficien¡å cardiacå congestivå cronicå.
Scopul lucrårii de fa¡å este så determine dacå
valorile BNP sunt influen¡ate de TEP, cu sau fårå
insuficien¡å cardiacå dreaptå ¿i så evalueze
valoarea lui prognosticå. ‰
MATERIAL ªI METODÅ
În acest scop am evaluat to¡i pacien¡ii interna¡i
în Clinica de Cardiologie Oradea cu TEP confirmat,
pe o perioadå de doi ani, între 1.01.2005-
1.01.2007. Pacien¡ii diagnostica¡i la mai mult de
trei zile de la debutul simptomatologiei au fost
exclu¿i din studiu. Nici unul dintre pacien¡i nu era
cunoscut anterior cu disfunc¡ie de ventricul stâng.
În absen¡a insuficien¡ei cardiace drepte am
luat în considerare ca ¿i criterii de diagnostic
semnele clinice (debutul brusc al dispneei, tahip-
neea, durerea toracicå de tip pleuritic, sincopa,
hipotensiunea sau ¿ocul), diagnosticul a fost con-
firmat prin efectuarea probei Astrup pentru gaze
sanguine, aspectul ECK de tip SI, QIII, blocul de
ramurå dreaptå, unda T inversatå în precordi-
alele inimii drepte.
Din påcate, metodele noastre de diagnostic
sunt limitate de lipsa angiografiei pulmonare, a
scintigrafiei pulmonare ¿i a posibilitå¡ii de dozare
a D-dimerului. Ca ¿i criteriu de diagnostic am
utilizat ¿i prezen¡a factorilor de risc pentru TEP.
La to¡i pacien¡ii, BNP a fost recoltat la inter-
nare. Am utilizat pentru dozare teste ELISA (Bio-
medica Gruppe Wien)
Pe baza criteriilor ecocardiografice, pacien¡ii
au fost impår¡i¡i în 3 grupe dupå cum urmeazå:
• TEP masiv, pacien¡ii cu hipotensiune arte-
rialå persistentå sau ¿oc cardiogen ¿i insu-
ficien¡å ventricularå dreaptå (IVD);
• TEP mediu, pacien¡ii cu tensiune arterialå
în limite normale ¿i IVD medie;
• TEP minor, pacien¡ii fårå hipotensiune sau
IVD.
• Astfel, grupul pacien¡ilor cu TEP masiv sau
moderat a inclus pacien¡ii cu IVD, iar grupul
FIGURA 2. Pacien¡ii care au prezentat TEP asociat cu IVD comparativ cu cei fårå IVD
pacien¡ilor cu TEP minor a inclus pacien¡ii
fårå IVD.
Ca ¿i criterii ecocardiografice de apreciere a
insuficien¡ei ventriculare drepte s-au luat în consi-
derare: dilatarea de ventricul drept (diametrul
diastolic peste 30 mm), hipokinezia ventriculului
drept, mi¿carea paradoxalå a septului inter-
ventricular sau regurgitarea tricuspidianå masivå.
Nici unul dintre pacien¡i nu prezenta hipertrofie
ventricularå dreaptå. Ecocardiografia s-a efectuat
la 2-7 zile în evolu¡ie ¿i a fost interpretatå de medici
care nu cuno¿teau valorile BNP determinate la
ace¿ti pacien¡i.
REZULTATE
Am luat în studiu 60 de pacien¡i, cu vârsta
medie de 57±19 ani, interna¡i în Clinica de
Cardiologie Oradea cu TEP confirmat, pe o pe-
rioadå de doi ani, între 1.01.2005-1.01.2007.
Dintre ace¿tia, 36 (60%) au fost bårba¡i ¿i 24
(40%) femei, (Figura 1).
Dintre cei 60 de pacien¡i, 9 (15 %) au fost
diagnostica¡i cu TEP masiv, 31 (51,67%) de
pacien¡i au fost diagnostica¡i cu TEP mediu, iar
20 (33,33%) cu TEP minor. În concluzie, 66,67%
dintre pacien¡i au prezentat IVD asociatå TEP, iar
33,33% au prezentat TEP fårå IVD. Pe baza
acestui criterii am împår¡it pacien¡ii în douå
grupuri, grupul A, cei cu insuficien¡å ventricularå
dreaptå ¿i grupul B, cei fårå IVD (Figura 2).
FIGURA 1. Reparti¡ia pe sex a pacien¡ilor din lotul studiat
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 293
BNP CA FACTOR PREDICTIV AL MORBIDITźII ªI MORTALITźII CORDULUI PULMONAR ACUT
Simptomele principale au fost: dispneea în 52
(86,66%) dintre cazuri, durerea toracicå în 35
(58,33%) dintre cazuri ¿i sincopa în 9 (15%) dintre
cazuri (Figura 3).
Factorii de risc au fost: interven¡iile ginecologice
pe micul bazin în 18 (30%) cazuri, fracturile în 5
(8,33%) cazuri, în ambele situa¡ii mai recente de
2 såptåmâni; antecedente de trombozå venoaså
profundå în 12 (20%) cazuri, neoplaziile în 12
(20%) cazuri, tulburåri de coagulare peripartum
în 3 (5%) cazuri ¿i abuzul de anticoncep¡ionale
în 10 (16.67%) cazuri (Figura 4).
To¡i pacien¡ii au primit tratament cu heparinå
intravenos, dozele au fost administrate în a¿a fel
încât så se atingå valori duble ale timpului par¡ial
de tromboplastinå (APTT) ini¡ial. 6 (66,67%)
pacien¡i cu TEP masiv, 11 (35,48%) cu TEP mediu
¿i 2 (10%) cu TEP minor au primit tratament
trombolitic cu streptokinazå.
FIGURA 3. Simtom atologia de debut la pacien¡ii din lotul
studiat
FIGURA 4. Factorii de risc ai TEP la pacien¡ii din studiu
294 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
S-a recoltat BNP de la to¡i pacien¡ii la inter-
nare. Între pacien¡ii din grupul A, cu insuficien¡å
ventricularå dreaptå, dintre cei 40, 34 (85%) au
avut valori ale BNP peste 359 pmol/ml, iar 6
(15%) au avut BNP sub valoarea maximå conside-
ratå normalå.
Între pacien¡ii grupului B, dintre cei 20 de pa-
cien¡i, 7 (35%) au avut valori ale BNP peste valoa-
rea normalå, iar 13 (65%) au avut valori sub 350
pmol/ml (Figura 5).
Se observå, din analiza graficului de mai sus,
cå în lotul pacien¡ilor cu IVD, un procent sem-
nificativ dintre pacien¡i au avut valori crescute ale
BNP; în acela¿i timp, în lotul pacien¡ilor care nu
au prezentat IVD, conform criteriilor ecocar-
diografice, valorile BNP au fost crescute la un
numår mai mic de pacien¡i.
În timpul spitalizårii, dintre cei 40 de pacien¡i
ai lotului A, 21 (52,5%) au decedat, ori au ne-
cesitat resuscitare cardiorespiratorie-cerebralå în
urma stopului cardiorespirator. 19 (90,48%)
dintre ace¿tia au prezentat valori crescute ale BNP
la internare. Din grupul B, 9 (45%) pacien¡i au
prezentat stop cardiorespirator ¿i au fost resus-
cita¡i, dintre ace¿tia, 7 au fost cei cu BNP crescut
la internare (Figura 6).
Se poate remarca în ambele grupuri o inci-
den¡å crescutå a stopului cardiorespirator soldat
sau nu cu deces, ca ¿i complica¡ie a insuficien¡ei
ventriculare drepte.
A¿a cum era de a¿teptat, procentul a fost
considerabil mai mare în lotul pacien¡ilor cu TEP
masive sau moderate. De asemenea, remarcåm
cå to¡i pacien¡ii din lotul A care au prezentat
complica¡ii au avut BNP crescut la internare, ¿i 7
dintre cei 9 din lotul B au avut, de asemenea,
 BNP CA FACTOR PREDICTIV AL MORBIDITźII ªI MORTALITźII CORDULUI PULMONAR ACUT

FIGURA 5. Valorile BNP comparativ în cele douå loturi

FIGURA 6. Inciden¡a deceselor ¿i a stopului cardiorespirator în cele douå grupuri

BNP crescut la internare. Pacien¡ii cu valori CONCLUZII

normale ale BNP, la internare, au avut o evolu¡ie
mult mai bunå decât cei cu valori patologice.
Pacien¡ii cu TEP masiv ¿i mediu, trata¡i cu
streptokinazå, de¿i au avut valori crescute ale BNP
la internare, au avut o evolu¡ie bunå, nici unul
dintre pacien¡ii cu TEP mediu trombolizat ne-
fåcând parte dintre pacien¡ii cu complica¡iile mo-
nitorizate de noi, ¿i doar 1 dintre pacien¡ii cu
TEP masiv trombolizat a decedat. Aceea¿i evolu¡ie
bunå au avut ¿i pacien¡ii cu TEP minor, care au
primit tratament trombolitic, dar ace¿tia nici nu
au avut valori crescute ale BNP la internare. ‰
În concluzie, putem certifica valoarea de-
osebitå pe care BNP o are pentru diagnosticul
IVD asociat TEP, ecocardiografia a fost efectuatå
mult mai târziu ¿i nu poate aprecia corect în toate
cazurile prezen¡a IVD.
O valoare deosebitå o are dozarea BNP, mai
ales pentru predic¡ia evolu¡iei infauste la pacien¡ii
cu TEP, dintre cei 30 de pacien¡i care au decedat
sau au necesitat resuscitarea cardirespiratorie
cerebralå, 28 (93,33%) au avut valori crescute
ale BNP la internare, asociate sau nu cu IVD. ‰

PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 295

BNP CA FACTOR PREDICTIV AL MORBIDITźII ªI MORTALITźII CORDULUI PULMONAR ACUT
BIBLIOGRAFIE
1. Goldhaber SZ, Visani L,
De Rosa M – Acute pulmonary
embolism: clinical outcomes in the
International Cooperative Pulmonary
Embolism Registry (ICOPER). Lancet
1999; 353:1386-1389
2. Ribeiro A, Lindmarker P, Juhlin-
Dannfelt A, et al. –
Echocardiography Doppler in
pulmonary embolism: right
ventricular dysfunction as a
predictor of mortality rate. Am Heart
J 1997; 134:479-487
3. Kasper W, Konstantinides S,
Geibel A, et al. – Prognostic
significance of right ventricular
afterload stress detected by
echocardiography in patients with
clinically suspected pulmonary
embolism. Heart 1997; 77:346-349
4. Tsutamoto T, Wada A, Maeda K,
et al. – Plasma brain natriuretic
peptide level as a biochemical marker
of morbidity and mortality in
patients with asymptomatic or
minimally symptomatic left
ventricular dysfunction: comparison
with plasma angiotensin II and
endothelin-1. Eur Heart J 1999;
20:1799-1807
5. Cheng V, Kazanagra R, Garcia A,
et al. – A rapid bedside test for
Revista presei medicale
NEW YORK (Reuters Health) –
Young children who watch more than
a couple of hours of television a day
are more likely to have attention
problems as adolescents, researchers
from New Zealand have found.
“The two-hour point is very, very
clear with our data, very consistent with
what the American Academy of Pe-
diatrics recommends,” Carl Erik Land-
huis of the Dunedin School of Medicine
at the University of Otago, the study’s
first author, told Reuters Health.
“We’re not saying don’t watch
TV, just don’t watch too much TV,”
he added.
While there is a widespread percep-
tion that TV can contribute to at-
tention problems, there is actually
very little data on the issue, Landhuis
noted in an interview. To investigate,
he and his colleagues looked at 1,037
296 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
B-type peptide predicts treatment
outcomes in patients admitted for
decompensated heart failure: a pilot
study. J Am Coll Cardiol 2001;
37:386-391
6. Dao Q, Krishnaswamy P,
Kazanagra R, et al. – Utility of
B-type natriuretic peptide in the
diagnosis of congestive heart failure
in an urgent care setting. J Am Coll
Cardiol 2001; 37:379-385
7. Fischer Y, Filzmaier K, Stiegler H,
et al. – Evaluation of a new rapid
bedside test for quantitative
determination of B-type natriuretic
peptide. Clin Chem 2001; 47:591-594
8. Muders F, Kromer EP, Griese DP,
et al. – Evaluation of plasma
natriuretic peptides as markers for
left ventricular dysfunction. Am
Heart J 1997; 134:442-449
9. Stanek B, Frey B, Hulsmann M,
et al. – Prognostic evaluation of
neurohumoral plasma levels before
and during beta-blocker therapy in
advanced left ventricular
dysfunction. J Am Coll Cardiol 2001;
38:436-442
10. Kriiger S, Graf J, Kunz D, et al. –
Brain natriuretic peptide levels
predict functional capacity in
patients with chronic heart failure. J
Am Coll Cardiol 2002; 40:718-722
Too much TV ups kids’ risk
of attention problems
boys and girls born in 1972 and 1973,
following them from age 5 to 15.
On average, kids watched about 2
hours of TV daily when they were 5 to
11 years old, but were watching 3.13
hours on weekdays by age 13 to 15.
Study participants who had watched
more than 2 hours of TV in early
childhood were more likely to have
attention problems as young teens, the
researchers found. Those who watched
more than 3 hours were at even greater
risk.
The researchers used statistical
techniques to control for the effects of
attention problems in early childhood
and other factors that could influence
both TV watching and later attention
difficulties. They found that TV
watching, both in early childhood and
in adolescence, independently in-
fluenced the risk of these problems in
adolescence.
Source: REUTERS/HEALTH, Friday, September 7, 2007
11. Nagaya N, Nishikimi T,
Uematsu M, et al. – Plasma brain
natriuretic peptide as a prognostic
indicator in patients with primary
pulmonary hypertension. Circulation
2000; 102:865-870
12. Tulevski II, Groenink M,
van der Wall EE, et al. – Increased
brain and atrial natriuretic peptides
in patients with chronic right
ventricular pressure overload:
correlation between plasma
neurohormones and right ventricular
dysfunction. Heart 2001; 86:27-30
13. The PIOPED Investigators – Value
of the ventilation/perfusion scan in
acute pulmonary embolism: results
of the prospective investigation of
pulmonary embolism diagnosis
(PIOPED). JAMA 1990; 263:2753-
2759
14. Maisel AS, Koon J,
Krishnaswamy R, et al. – Utility of
B-natriuretic peptide as a rapid,
point-of-care test for screening
patients undergoing
echocardiography to determine left
ventricular dysfunction. Am Heart J
2001
ANNE HARDING
“Although it doesn’t prove cau-
sation, it certainly provides evidence
that the causal link is in that direc-
tion,” Landhuis said.
He and his colleagues suggest that
kids who get used to watching lots of
attention-grabbing TV may find
ordinary life situations – like the clas-
sroom – boring. It’s also possible, they
add, that TV may simply crowd out time
spent doing other activities that can build
attention and concentration skills, such
as reading and playing games.
It’s likely, Landhuis said, that kids
today watch much more TV than the
participants in his study, who had
only 2 channels to choose from in the
late 1970s.
 PRACTICA MEDICALÅ
PREVENºIA ÎN MF 10
Riscul cardiovascular
la pacien¡ii cu diabet zaharat
¿i hipertensiune arterialå
Cardiovascular risk of patients with
diabetes mellitus and hypertension
Prof. Dr. AFILON JOMPAN*, ªef Lucr. Dr. CONSTANTIN CÂRSTEA** Prof. Dr. Afilon JOMPAN

*Facultatea de Medicinå, Universitatea de Vest „Vasile Goldi¿“ Arad

**Facultatea de Medicinå, Universitatea „Transilvania“ Bra¿ov

REZUMAT
Diabetul zaharat ¿i hipertensiunea arterialå reprezintå factori de risc importan¡i în calculul riscului
cardiovascular, de evolu¡ie spre accidente ¿i complica¡ii majore.
Hipertensiunea arterialå reprezintå un factor de risc major prezentând o prevalen¡å crescutå în rândul
popula¡iei adulte studiate (29,70%).
Diabetul zaharat, cu o prevalen¡å reduså (3,03%) la scåderea toleran¡ei la glucide (5,18%), asociazå o
multitudine de al¡i factori de risc (hiperlipidemii, obezitate etc.) ce dau un caracter de gravitate în evolu¡ie.
Prevalen¡a hipertensiunii arteriale la persoanele cu diabet zaharat cre¿te de aproape 3 ori (71,05%), iar
prevalen¡a diabetului zaharat în rândul popula¡iei hipertensive se dubleazå (6,34%).
Excesul ponderal ¿i obezitatea au, de asemenea, cre¿teri importante atât la persoanele hipertensive, cât ¿i la
persoanele diabetice.
Persoanele ce asociazå diabet zaharat si hipertensune arterialå necesitå o permanentå monitorizare în asisiten¡a
medicalå primarå, un tratament non-farmacologic ¿i medicamentos adecvat.

ABSTRACT
Diabetes and high blood pressure are two very important factors in the risk of the cardiovascular disease,
often evolving towards accidents and major complications.
High blood pressure is a very dangerous risk factor with a high prevalence in the adult studied population
(29.70%).
Diabetes though not so often encountered (3.03%), when the tolerance for glucose lowers (5.18%), it begins
to be associated with lots of factors of risk (hyperlipidemias, obesity etc.) which become more and more dangerous
as the disease evolves.
The prevalence of the high blood pressure among the persons with diabetes grows almost three times (71.05%)
and the prevalence of diabetes among the hypertensive population doubles (6.34%).
Overweight, problems and obesity also present important grows both among the hypertensive persons and
the diabetic ones.
Persons that associate diabetes with high blood pressure need a permanent surveillance in primary medical
assistance, an adequate non-pharmaceutical and medicamental treatment.

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RISCUL CARDIOVASCULAR LA PACIENºII CU DIABET ZAHARAT ªI HIPERTENSIUNE ARTERIALÅ

1. IMPORTANºA PROBLEMEI
Diabetul zaharat de tip 2, precum ¿i scåderea
toleran¡ei la glucide, ca tulburåri ale metabo-
lismului glucidic, reprezintå pentru pacien¡ii
hipertensivi o asociere ce imprimå o evolu¡ie cu
risc foarte ridicat, confirmatå prin numeroase
trialuri medicale u¿or de eviden¡iat.
Deci stabilirea prevalen¡ei DZ tip 2 la pacien¡ii
hipertensivi, precum ¿i stabilirea prevalen¡ei
hipertensiunii arteriale la pacien¡ii cu DZ tip 2
reprezintå pa¿i importan¡i în monitorizarea
pacien¡ilor din asisten¡a medicalå primarå. Graficul 1. Distribu¡ia lotului pe sexe – procente
Depistarea formelor asimptomatice, în mod
activ prin examen de bilan¡ anual sau screening Remarcåm o u¿oarå prevalen¡å a popula¡iei
popula¡ional reprezintå ac¡iuni de preven¡ie se- vârstnice reunind toate grupele peste 70 de ani.
cundarå specifice activitå¡ii medicului de medicina
familiei, iar investigarea asocierii unor factori de
risc constituie premisa unei preven¡ii primare
eficiente. ‰

2. METODOLOGIA LUCRÅRII ªI LOTUL

STUDIAT
A fost luat în studiu un lot compus din 1252
de persoane dintre care 840 de femei ¿i 612
bårba¡i de vârstå adultå de peste 30 de ani, care
au fost investiga¡i prin chestionar, examen clinic
¿i de laborator.
Au fost investigate valorile glicemiei à jeun, iar
la cele superioare (90-100 mg%) a fost efectuat
¿i testul de toleran¡å la glucozå (TTG) cu 75 gr
glucozå la 2 ore, test efectuat ¿i la grupele
popula¡ionale de risc.
Au fost investigate valorile indicelui de maså
corporalå, TA sistolicå ¿i diastolicå, colesterolemia
totalå, HDL-colesterolul, trigliceridemia, uricemia, Graficul 2. Distribu¡ia popula¡iei lotului pe grupe de vârstå
fumatul ¿i consumul exagerat de alcool (declarativ).
Examinårile de laborator s-au efectuat cu Popula¡ia de tip „îmbåtrânit“, în care grupa de
acela¿i analizator ¿i procesor LABSYSTZEMS-EP vârstå de 70 de ani ¿i peste, are valoarea cea mai
în condi¡ii standard. ridicatå. Prevalen¡a hipertensiunii arteriale înregis-
Au fost luate în calcul valorile conform cri- treazå valori de 29,70% în rândul întregului lot.
teriilor ADA – 2005 pentru stabilizarea de DZ
tip 2:
Pentru glicemie à jeun:
– val. normale pânå la 110 mg%
– val. modificate (STG) 110-125 mg%
– val patologice (DZ) >126 mg %,
iar pentru TTC (testul de toleran¡a la glucozå)
– glicemia normalå la 2 ore <140 mg%
– glicemia modificatå (STG) 140-199 mg%
– glicemia patologicå (DZ) > 200 mg% ‰

3. REZULTATE
Lotul a fost alcåtuit din 1252 persoane de
peste 30 de ani, dintre care 612 bårba¡i ¿i 640
femei. Graficul 3. Prevalen¡a hipertensiunii arteriale la întregul lot

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 RISCUL CARDIOVASCULAR LA PACIENºII CU DIABET ZAHARAT ªI HIPERTENSIUNE ARTERIALÅ

Prevalen¡a hipertensiunii arteriale în rândul Dacå facem o evaluare în rândul persoanelor

lotului cre¿te odatå cu vârsta (aceasta fiind un
factor de risc suplimentar).
cu HTA (284) remarcåm o prevalen¡å a diabetului
la aceastå categorie de 6,34%.
Valorile prevalen¡ei sunt mai ridicate la hiper-
tensivi.
Comparând aceastå prevalen¡å cu valorile
lotului aceasta este dublå.

Graficul 4. Distribu¡ia prevalen¡ei HTA pe grupe de vârstå la

popula¡ia lotului

Astfel încât la 50 de ani, 1 persoanå din 3 este

hipertensiv, la 60 de ani mai mult de jumåtate,
iar peste 70 de ani 2 persoane din 3 are HTA.
O clasificare a hipertensiunii arteriale la nivelul Graficul 6. Prevalen¡a DZ, STG la popula¡ia
lotului în func¡ie de valorile TA sistolice sau TA lotului ¿i la persoanele hipertensive
diastolice are importan¡å în stabilirea riscului, dar
¿i a monitorizårii pacientului ¿i a administrårii
Referindu-se la prevalen¡a hipertensiunii în
tratamentului.
rândul popula¡iei diabetice ¿i cu scåderea
toleran¡ei la glucide, aceasta atinge valori foarte
ridicate. Asocierea HTA la popula¡ia cu tulburåri
ale metabolismului glucidic în care rolul insulino-
rezisten¡ei ca verigå patogenicå comunå este bine
recunoscut. Comparativ cu valorile întâlnite la
nivelul lotului, acestea sunt aproape duble ca
prevalen¡å la persoanele cu scåderea toleran¡ei
la glucide ¿i triple la cei cu DZ tip 2.
Desigur, aceste prevalen¡e sunt ¿i ele influen-
¡ate de vârsta pacien¡ilor de perioada de evolu¡ie

Graficul 5. Distribu¡ia popula¡iei hipertensive a lotului

în func¡ie de stadiul de evolu¡ie

Prevalen¡a DZ tip 2 la nivelul popula¡iei lotului

înregistreazå valori de 3.03%, dar apar valori
crescute ale prevalen¡ei scåderii toleran¡ei la
glucide (STG).
Totalul persoanelor cu tulburåri ale metabo-
lismului glucidic înregistreazå 8,22% din popula¡ia
lotului, deci 103 persoane ce necesitå monito- Graficul 7. Prevalen¡a HTA comparatå la nivelul
rizare permanentå. lotului ¿i la persoanele cu STG ¿i DZ tip 2.

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a DZ sau a hiperglicemiilor cu STG. Dar HTA ¿i Consumul de alcool în cantitå¡i mici ¿i mode-
diabetul zaharat au factor de risc comun insulino- rate are rol protector contra mortalitå¡ii corona-
rezisten¡a, iar obezitatea si excesul ponderal fac riene, prin înjumåtå¡irea valorilor colesterolemiei
ca prevalen¡a HTA la aceste grupe popula¡ionale totale ¿i a cre¿terii HDL colesterolului, reducerea
så fie mai crescutå. Distribu¡ia popula¡iei lotului factorilor procoagulan¡i ¿i a insulinorezisten¡ei.
în func¡ie de valorile indicelui de maså corporalå
(IMC) indicå urmåtoarele aspecte
La nivelul persoanelor cu HTA prevalen¡a
obezilor ¿i a hiperponderalilor este mai crescutå.
Obezitatea atinge peste una din patru persoa-
ne hipertensive. Excesul ponderal ¿i obezitatea
constituie, de asemenea, un factor de risc, des
asociat diabetului zaharat tip 2. Remarcåm o
prevalen¡å crescutå a obezitå¡ii ce atinge 1 din 3
persoane. Comparând valorile excesului ponderal,
hiperponderalilor ¿i obezilor la cele 3 loturi remar-
cåm o prevalen¡å crescutå la pacien¡ii cu DZ.
Obezitatea ca prevalen¡å cre¿te cu 70% fa¡å
de lot la pacien¡ii cu DZ tip 2. Graficul 10. Prevalen¡a consumatorilor de
alcool în exces

O prevalen¡å mai crescutå în rândul persoa-

nelor cu HTA. Fumatul constituie un factor de
risc major pentru bolile cardiovasculare ¿i nu
numai. Dar la pacien¡ii cu DZ ¿i HTA, fumatul,
prin nicotinå, cre¿te eliberarea de adrenalinå, dar
cre¿te ¿i rezisten¡a la insulinå.

Graficul 8. Prevalen¡a excesului ponderal,

hiperponderalilor ¿i obezilor la pacien¡ii lotului,
hipertensivilor ¿i diabeticilor

Sedentarismul constituie un factor de risc în

dezvoltarea HTA ¿i a DZ.

Graficul 11. Prevalen¡a fumatului pe cele 3

loturi de pacien¡i

Hipertensivii prezintå o prevalen¡å mai cres-

Graficul 9. Distribu¡ia sedentarismului
recunoscut de pacien¡i ca prevalen¡å la lot ¿i
persoane hipertensive ¿i diabetice
cutå.
Hiperuricemia este prezentå în propor¡ie micå,
constituind un factor de risc prezent în HTA.
Remarcåm o prevalen¡å crescutå a hiperuri-
cemiei la persoanele hipertensive.
Hipertensiunea ca factor de risc major, dia-
betul zaharat tip 2 ¿i excesul ponderal, obezitatea
ca factori de risc asocia¡i modificabili prin trata-
ment î¿i multiplicå riscul.

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 RISCUL CARDIOVASCULAR LA PACIENºII CU DIABET ZAHARAT ªI HIPERTENSIUNE ARTERIALÅ

Graficul 12. Prevalen¡a hiperuricemiei la
popula¡ia lotului hipertensivå ¿i diabeticå
Graficul 13. Compararea distribu¡iei unui factor de risc major
¿i a doi factori de risc asocia¡i în multiplicarea riscului.
Dar la ace¿ti 3 factori de risc se mai asociazå în studiu ¿i al¡i
factori de risc cu prevalen¡e semnificative, fumat, consum de alcool
în exces, hiperuricemii ¿i al¡ii nemodificabili: vârstå, sex. ‰
CONCLUZII
1. Hipertensiunea arterialå înregistreazå
valori de 29,70% la nivelul lotului, mai
crescut ca prevalen¡å la femei ¿i cre¿te
odatå cu vârsta.
2. Prevalen¡a DZ tip 2 înregistreazå 3,03%,
iar STG 5,19%.
3. Prevalen¡a DZ tip 2 în rândul
hipertensivilor cunoa¿te o cre¿tere
importantå, de 6,34%. Toate valorile se
dubleazå.
4. Prevalen¡a hipertensiunii arteriale la
persoanele cu diabet zaharat tip 2 cre¿te
de aproape 3 ori, ajungând la 71,05%.
5. Excesul ponderal ¿i obezitatea au cre¿teri
importante la persoanele hipertensive fa¡å
de lot (58,85%).
6. Excesul ponderal cre¿te ca prevalen¡å la
persoanele diabetice la 31,05%, iar
obezitatea la 34,21%.
7. Sedentarismul constituie un factor de risc
gåsit la 16,19% dintre hipertensivi ¿i la
21,05% dintre pacien¡ii cu DZ.
8. Consumul de alcool ¿i fumatul nu prezintå
diferen¡e semnificative statistic.
9. Hiperuricemia este semnificativ mai
crescutå la persoanele hipertensive
(26,40%).
10. Persoanele ce asociazå DZ tip 2 ¿i HTA au
risc crescut, cele douå afec¡iuni
multiplicându-¿i riscul. ‰

BIBLIOGRAFIE
1. Balkau B, Eschwege E – The
Diagnosis and Classification of
Diabetes and Impaired Glucose
Regulation. In Pickup JC, Wiliams G,
Textbook of Diabetes, IIPded.,
Blackwell Science, 2003; 2.1-2.13
2. Braunwald E – Heart Disease –
tratat de boli cardiovasculare, Vol. II,
Editia a 5-a, M.A.S.T.
3. Expert Committee of the Diagnosis
and Classification of Diabetis
Mellitus. Report of the Expert
Committee of the Diagnosis and
Classification of Diabetis Mellitus.
Diabetes Care, 2000; 23:S4-S19
4. Gerasim L – Medicina Internå, Vol.
II, Bolile cardiovasculare ¿i
metabolice, Editura Medicalå,
Bucure¿ti, 1996
5. Hancu N.D. – Diabetul zaharat,
nutri¡ia ¿i bolile metabolice, Manual
Universitar, „Vasile Goldi¿“
University Press, Arad, 2001
6. Jomapan A – Riscograma pacien¡ilor
hipertensivi. Revista Practica
Medicalå, Vol. I, nr. 3-4/2006, p 143-
149
7. Jompan A ¿i colab. – Tradi¡ional
nutrition an cardiovascular risck.
Revista Central European jurnal od
ocupational end environment
Medicine, Budapesta, nr, 6/2000, p
161-165
8. Jompan A – Analizele de laborator în
practica Asisten¡ei Medicale Primare
Ed. Eurostampa Timi¿oara, 2006
9. Jompan A., Timar R., Chiri¡a Livia –
Pacien¡ii hipertensivi ¿i riscul
cardiovascular asociat la nivelul
comunitar – Rev. Medicina Familiei
Nr. 52/2004, pg. 4-11
10. ªerban V., Timar R., Vlad A –
Diabetul zaharat ¿i hipertensiunea
arterialå Ed. Brumar – Timi¿oara,
2004
11. Timar R, ªerban V, Jompan A,
et al. – Diagnosticul ¿i clasificarea
diabetului zaharat în Revista
Medicina Familiei nr. 50, an 11/2004;
p. 15-18
12. Timar R., ªerban V., Jompan A.,
Diaconul Laura – Diagnosticul ¿i
clasificarea diabetului zaharat – Rev.
Medicina Familiei Nr. 50, an 11/
2004; pg.15-18

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11 PRACTICA MEDICALÅ
PREVENºIA ÎN MF

Postul ¿i beneficiile lui

pentru sånåtate
The health benefits of fasting
Conf. Dr. FLOAREA DAMASCHIN
Facultatea de Medicinå, Constan¡a

Din vremuri stråvechi, în¡elep¡ii au observat cå, atunci când oamenii acordå prea
multå aten¡ie plåcerii de a mânca, dincolo de necesitatea strictå de a se hråni pentru a
face fa¡å eforturilor zilnice ¿i ajungând la excese periculoase, ei se expun riscurilor de
îmbolnåvire! Ba mai mult, o alimenta¡ie neechilibratå, în care predominå doar anumite
alimente, poate produce nu numai modificåri organice, ci ¿i comportamentale.

E
ste din ce în ce mai evident cå, de fapt,
cele mai multe dintre bolile existente
sunt rezultatul unei „supradozåri ali-
mentare ¿i a unei gândiri deviate de la
sensul normal al vie¡ii!“ Dupå ce ani în
¿ir, prin mijloacele media, s-a sus¡inut ce bine e
så månânci cårnuri ¿i legume congelate, con-
servate, aditivate, organoleptizate, så-¡i rezolvi
nevoile gastronomice prin fast-fooduri, dupa ce
unul din cinci copii europeni este supraponderal
sau obez, dupå ce nu mai avem puterea de a
numåra pacien¡ii... medicii, o parte dintre ei... se
trezesc – parcå în maså ¿i impun regimurilor
politice analiza situa¡iei. De fapt, mi-e greu så cred
cå ei fac acest demers ¿i cred mai degrabå cå el
este rezultatul analizei economice: raportul dintre
fondurile consumate ¿i starea de sånåtate a
popula¡iei.
Cu uimire ¿i cu mare bucurie am primit primul
mesaj de educa¡ie spre sånåtate pe care-l difu-
zeazå televiziunea în ultimele luni. Din nefericire,
atâta timp cât alte reclame difuzeazå mesaje,
foarte bine prelucrate, care împing consumatorul
la un exces... e greu de acceptat cå tot mai mul¡i
oameni se vor trezi ¿i vor fi mult mai aten¡i la
alimenta¡ie. Obiceiurile alimentare odatå fixate
comportamental nu sunt mai pu¡in vicioase decât
fumatul ¿i alcoolismul. Medicii au un rol deter-
minant în evolu¡ia, spre bine, a pacien¡ilor care
au astfel de probleme. Tot mai mult trebuie pus
accentul pe påstrarea greutå¡ii, pe consumul
alimentelor care au toate gusturile ¿i toate culorile
...în fiecare zi, dar ¿i în ziua de post negru ¿i
surorile ei... zilele de post – fa¡å de alimentele
de origine animalå.
Vechii preo¡i, indiferent de religie, din timpuri
imemoriale, au hotårât ca, în func¡ie de clima
specificå regiunii în care tråiau coreligionarii lor,
cât ¿i de riscurile de îmbolnåvire existente, så
impunå, prin intermediul preceptelor religioase,
perioade de regim alimentar. Acesta era un regim
de dezintoxicare, de „curå¡are“ a organismului.
În plus, marii în¡elep¡i au constatat cå postul
negru prelungit – cu durata de 9, 21 sau 40 de
zile – poate asigura condi¡iile ideale pentru
marile revela¡ii, adicå descoperirea råspunsurilor
la întrebåri fundamentale despre via¡å, sånåtate
¿i progres spiritual. În religia cre¿tinå, posturile

302 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007


reprezintå perioade în care credincio¿ii au ocazia
så se debaraseze de excesul de proteine animale,
gråsimi, glucide. Aceasta asigurå o stare fizicå
foarte bunå, permi¡ând credinciosului så aibå ¿i
o atitudine mai potrivitå fa¡å de actul religios.
Renun¡area la plåcerile gastronomice este un mic
act de smerenie, care reaminte¿te fiecåruia despre
modestie, ab¡inere în fa¡a tenta¡iilor nesånåtoase.
Pe de altå parte, este constatat faptul cå excesul
de carne în alimenta¡ie cre¿te semnificativ agresi-
vitatea ¿i cruzimea consumatorului, îndepår-
tându-l de sentimentele de iubire, toleran¡å ¿i
întrajutorare.
Dar, aten¡ie! Postul nu presupune doar o
alimenta¡ie lipsitå de „dulce“, adicå de produse
animale, ci ¿i o dietå bine echilibratå. În concep¡ia
tradi¡ionalå chinezå, o dietå echilibratå presu-
pune combinarea, la fiecare maså, a alimentelor
acre, amårui, dulci, picante ¿i sårate. Trebuie su-
bliniat cå fiecare dintre aceste tipuri de alimente
are un rol benefic fa¡å de sånåtate, dar, în acela¿i
timp, pot fi dåunåtoare dacå sunt consumate în
exces.
Astfel, excesul de alimente:
– acre poate afecta splina, stomacul, mus-
culatura sau cavitatea bucalå (stomatite,
afte);
– amare poate tulbura aparatul respirator,
intestinul gros (diaree), pielea ¿i cre¿terea
pårului;
– dulci poate provoca boli ale rinichilor, vezicii
urinare sau ale sistemului osteo-articular;
– picante poate afecta ficatul, colecistul, ochii
sau tendoanele;
– sårate va ataca sistemul cardio-vascular ¿i
intestinul sub¡ire.
Existå înså ¿i alimente care nu au nici unul
dintre gusturile enun¡ate mai sus, dar care au
BIBLIOGRAFIE
1. Gabriela Radulian – „No¡iuni de nutri¡ie ¿i igiena alimenta¡iei“, Editura Universitarå „Carol Davila“,
Bucure¿ti, 2005
2. Dr. Floarea Damaschin – „Ecologie. Igiena“, Editura Syrinxmed, Constan¡a, 1998
3. G. Bouwenot, B. Devulder – „Nefrologie. Cancerologie. Nutri¡ie“, Editura Institutul European, 1998
4. Prof. Dr. Yusuf Al-Qaradawi – „Permis ¿i interzis în islam“
POSTUL ªI BENEFICIILE LUI PENTRU SÅNÅTATE
acelea¿i efecte asupra sånåtå¡ii. De aceea, ele se
încadreazå în denumirea de miresme.
Pe de altå parte, con¡inutul de energie al
alimentelor este deosebit de important pentru
men¡inerea sau recuperarea sånåtå¡ii. Sunt
catalogate cinci ståri energetice ale alimentelor:
caldå, fierbinte, neutrå, råcoroaså ¿i rece. Acestea
se recunosc dupå senza¡iile pe care le provoacå
dupå digerare. Dacå, de pildå, o persoanå cu
reumatism aflatå în plinå crizå va consuma
alimente (chiar ¿i numai vegetale!) care au energie
rece sau råcoroaså, nu va fi de mirare cå durerile
se vor înte¡i. Invers, atunci când se instaleazå febra
sau erup¡iile cutanate, alimentele råcoroase ¿i reci
vor fi de mare ajutor.
Acum, este mult mai u¿or de în¡eles de ce
mul¡i credincio¿i habotnici, care respectå cu
stricte¡e perioadele de post religios, pot avea mari
probleme de sånåtate dupå terminarea restric-
¡iilor: organismul lor intrå într-un dezechilibru
major ¿i nu mai poate face fa¡å unei alimenta¡ii
abundente în preparate din carne, ouå ¿i lactate.
Este cert cå avem multe de învå¡at de la chinezi
pentru a ne face alimenta¡ia mai sånåtoaså ¿i mai
echilibratå, fie în timpul posturilor, fie în cadrul
unor diete cu rol de terapie. A¿a vom putea så
evitåm obezitatea, a¿a vom putea så facem
dintr-o perioadå de post o ocazie de a fi mai
sånåto¿i fizic ¿i spiritual. A¿adar, postul poate fi
extrem de benefic asupra sånåtå¡ii, dar numai
dacå se cunosc bine principiile de mai sus.
Mul¡i scriitori de renume, arti¿ti, oameni de
¿tiin¡å, filosofi ¿i personalitå¡i eminente au fost
vegetarieni sau consumatori de carne. Buddha,
Iisus Hristos, Vergilius, Platon, Shakespeare,
Socrate, Drawin, Albert Einstein, Prin¡esa Diana,
Madonna, Paul Newman – to¡i ¿i mul¡i al¡ii au
îmbrå¡i¿at, cu entuziasm, alimenta¡ia fårå carne. ‰
PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007 303
POSTUL ªI BENEFICIILE LUI PENTRU SÅNÅTATE
Revista presei medicale
Ministrul Sånåtå¡ii, Eugen Nico-
laescu, nu îndråzne¿te så ieftineascå
medicamentele de teama companiilor
farmaceutice. Spune calm cå se teme
ca farmaci¿tii, distribuitorii ¿i produ-
cåtorii ar putea bloca furnizarea de
medicamente ¿i cå preferå så continue
negocierile pentru ca oamenii så nu
sufere din lipsa produselor.
„Mi-e greu så vå spun dacå vom
reu¿i så ieftinim medicamentele a¿a
cum am promis pentru cå distribuitorii
de medicamente ¿i producåtorii nu vor
¿i au o pârghie de ¿antaj foarte im-
portantå, aceea cå ar putea opri pro-
duc¡ia ¿i distribu¡ia, de aceea preferåm
så continuåm negocierile“, a spus
Nicolaescu la finele lui octombrie. Încå
din varå, ministrul anun¡ase cå va lua
SOCIETźII ACADEMICE
304 PRACTICA MEDICALÅ – VOL. 2, NR. 4(8), AN 2007
View publication stats
Santaj?!?
A blackmail?!?
toate måsurile ca, de la 1 noiembrie,
medicamentele så se ieftineascå în
medie cu 15%, motivul fiind unul de
bun-sim¡: så aibå ¿i oamenii bani de
tratamente. Acum înså Nicolaescu
face pasul cumva tipic: o då cotitå.
Scuza e relativ bizarå, mai ales venind
de la un ministru. E ca ¿i cum ar spune
cå statul român e complet lipsit de
apårare în fa¡a ¿antajului orchestrat
de priva¡i. Sunå balcanic ¿i tragic, dar
explica¡ia pre¿edintelui Colegiului
Farmaci¿tilor din România, Dumitru
Lupuliasa, face un pic de luminå
occidentalå.
„Reducerea pre¡urilor la medica-
mente ar trebui sus¡inutå din fon-
durile statului ¿i så se facå prin
reducerea TVA. În caz contrar vor
Acest articol poate fi gåsit ¿i în numårul 256 al revistei „Banii No¿tri“
Vizita¡i site-ul
DE MEDICINÅ
www.samf.ro
DENISA MÅRUNºOIU
06.11.2007
exista consecin¡e negative ¿i pentru
cetå¡eni pentru cå la raft nu vor mai
exista medicamente“, a spus Lupuliasa,
explicând cå distribuitorii vor prefera
så vândå medicamentele în alte ¡åri
care au pre¡uri mai mari. Adicå o
explica¡ie destul de logicå în capi-
talism ¿i pe o pia¡å liberå.
E pu¡in probabil ca Nicolaescu
så-¿i fi bazat afirma¡iile legate de redu-
cerea pre¡urilor pe ideea cå producåtorii
¿i distribuitorii vor sus¡ine acest pro-
ces cu banii lor de buzunar. Probabil
cå spera så ob¡inå ni¿te bani de la
bugetul de stat. ªi la fel de probabil cå
nu i-a ob¡inut. Caz în care nu ¿tiu
cine pe cine ¿antajeazå.
A FAMILIEI