Vol 2 - Cont. J. Med Res - Re

Continental J.
Medical Research 2: 1 - 5, 2007

© Wilolud Online Journals, 2007.
ANTIBIOTICS COMMONLY USED IN THE TREATMENT OF ACUTE OROFACIAL BACTERIAL

INFECTIONS IN GENERAL DENTAL PRACTICE IN DELTA STATE OF NIGERIA.
1
Okagbare T. E. and 2Emudianughe T. S.
1
Department of Preventive Dentistry and 2Department of Pharmacology and Therapeutics, College of
Health Sciences, Delta State University, Abraka, Nigeria.
ABSTRACT
Information on acute orofacial bacterial infections and the antibiotics commonly used
in their management in general dental practice in Delta State, was obtained by
reviewing a total of some 300 case records, randomly selected from five hospitals in
Delta State. The following bacterial infections: acute dento-alveolar abscess, lateral
periodontal abscess, post-extraction infection (dry socket), pericoronitis, acute
ulcerative gingivitis (AUG), cellulitis and suppurative sialadenitis were investigated;
and the estimates of the number of each type of infection in the five hospitals were
found to be similar. Four different antibiotics – ampicillin, penicillin, metronidazole
and erythromycin were mostly prescribed, in a variety of regimens for the treatment
of orofacial bacterial infections in these hospitals. Majority of patients 138-186(46-
62%) received a 5-day course of ampicillin (250-500mg, qid) for bacterial conditions
other than AUG, for which 3 days of metronidazole (200-400mg tid) was mostly
prescribed 22(91.7%). However cellulitis was treated initially or all the way with 300
to 600 mg (0.5 to 1.0 mega units) i.m. or i.v., 6 hourly benzylpenicillin, sometimes in
combination with metronidazole.
KEYWORDS: Orofacial bacterial infections, Anitbiotics, General dental practice,

Delta State.
INTRODUCTION
In the treatment of dental infections phenoxymethylpenicillin has traditionally been regarded as the
antibiotics of choice all over the world, with erythromycin as an alternative for patients with known
hypersensitivity to penicillins (Chow et al). In Delta State ampicillin is the most commonly prescribed,
contrary to the above general impression, with erythromycin also as an alternative for patients with known
hypersensitivity to penicillins. Ampicillin injection is sometimes given in a stat. dose of 0.5g followed by
oral doses. Where penicillin was prescribed, it was either benzylpenicillin i.m. or i.v. or procaine pencillin
i.m. only.
1
Okagbare T. E. and Emudianughe T. S: Continental J. Medical Research 2: 1 - 5, 2007
The aim of the present study is to obtain information about patterns of acute orofacial infection among
patients attending general dental surgeries in Delta State, and to gain information on which antibiotics are
mostly prescribed for their treatment.
Table 1 Types / number of acute orofacial infections reviewed per hospital

DSC Central Central Central Federal Medical Total
hospital hospital hospital hospital Centre Asaba
Warri Sapele Agbor
Bacterial infection
Acute dento-alveolar abscess 24 25 25 24 24 122
Pericoronitis 14 13 13 15 15 70
Lateral periodontal abscess 7 5 7 6 7 32
Post-extraction infection 5 7 6 6 5 29
Acute ulcerative gingivitis 5 4 6 4 5 24
Cellulites 4 4 2 4 3 17
Salivary gland infection 1 2 1 1 1 6
Total 60 60 60 60 60 300
MATERIALS AND METHOD

One research assistant was recruited for this study and five hospitals were involved. The hospitals are Delta
Steel Company Hospital, Orhuwhorun – Warri; Central Hosptial Warri; Central Hospital Sapele; Central
Hospital Agbor and Federal Medical Centre, Asaba all in Delta State of Nigeria. The case records of some
60 randomly selected patients treated with antibiotics for orofacial bacterial infections in each of the
hospitals over a period of two to three months were reviewed, adding up to a total of 300. The antibiotics
prescribed for the treatment of the following bacterial infections: acute dento-alveolar abscess, lateral
periodontal abscess, post-extraction infection (dry socket), pericoronitis, acute ulcerative gingivitis (AUG),
supurative sialadenitis (salivary gland infection) and cellulitis were recorded. Also recorded were the
prescribed antibiotic regimen (drug, dose and duration).
ANALYSIS
The percentage of the number patients administered with each of the antibiotics and the durations
prescribed for each antibiotic were generated and compared.
RESULTS
Four different antibiotics were commonly prescribed as the drug of first choice for the treatment of
orofacial bacterial infections-ampicillin, penicillin, metronidazole and erythromycin. A total of 300 cases of
bacterial infection were reviewed in this study. The number of cases of infection per hospital is recorded in
2
Table 1 and it shows that the estimates of the number of each type of infection were similar in all the five
hospitals. The acute conditions which appeared most frequently were dento-alveolar abscess 122 (40.7%)
and pericoronitis 70 (23.3%). Suppurative salivary gland infection was very uncommon 6 (2%). Majority
138-186 (46-62%) of the patients received ampicillin for all conditions other than AUG, for which most
22(91.7%) patients received metronidazole (Table 2). The duration of drug therapy was variable, being
either 3, 5 or 7 days (Table 2). A 5-day course was prescribed for all infections, with the exception of
AUG, for which 3 days of therapy was prescribed most frequently 11 (45.8%).
Table 2 Antibiotic of choice and duration of therapy for the treatment of acute orofacial infection
Antibiotic Prescribed, % Duration prescribed, %
Acute infection Amp Pen Metr Eryth 3 days 5 days 7days
Acute dento-alveolar abscess 69 13 9 9 5 91 4

Lateral periodontal abscess 63 11 19 7 8 89 3
Post-extraction infection 63 6 21 10 7 82 6
Pericoronitis 58 4 32 6 10 81 9
Acute ulcerative gingivitis 5 1 92 2 46 44 10
Salivary gland infection 41 10 38 11 2 88 10
Cellulitis 6 91 2 1 69 26 5
Key: ampicillin (Amp), Penicillin (Pen), metronidazole (Metr), erythromycin (Eryth)
DISCUSSION
The infections reviewed in this study have characteristic clinical presentations and diagnosis can therefore
usually be made by clinical examination and history. None of the diagnosed infections were proven
microbiologically, since it is not a normal practice in general dental situation to make use of diagnostic
microbiological laboratories. Therefore, the information reported here should be regarded as reasonable
estimates and not taken as actual incidences of each type of infection.
Some microbial studies have revealed a predominance of strict anaerobes in acute dento-alveolar abscess
(Williams et al 1983, Lewis et al 1986); a majority of which are penicillin-resistant strain of Bacteriodes
species (Heimdahl et al 1980). These findings have given rise to recommendations for the use of antibiotics
such as metronidazole (Ingham et al 1977), cephalosporins (Cumming et al 1980) or clindamycin (Schuen
et al). Clindamycin appears to be more effective against infections involving the bone or fractures,
3
although it is recommended that its usage should be restricted, unless specifically indicated by bacterial
culture, due to the possibility of inducing colitis (Mehrohof et al 1976).
Of the drugs prescribed for bacterial infection, three agents (ampicillin, penicillin and metronidazole)
accounted for the vast majority (85-97%) of first antibiotics of choice. The popularity of ampicillin here is
probably based on the fact that it is easily available, cheap and effective against the majority of bacteria
encountered in acute dental infections, and adverse reactions are rare. A high-dose of penicillin regimen
was always the treatment of choice for cases of cellulitis like Ludwig’s Angina for which 600 to 1200mg (1
to 2 mega units) benzylpenicillin i.m. or i.v. 6 hourly is commonly prescribed. Metronidazole was the most
frequently prescribe agent for AUG and second most frequently prescribed agent for the treatment
pericoronitis. This is to be expected since metronidazole, which is only effective against strict anaerobes,
has been shown to perform well in the treatment of both these conditions. The low incidence of the use of
metronidazole for the treatment of acute dento-alveolar abscess is perhaps surprising, because it has been
shown that strict anaerobes predominate and are the most likely pathogens in this infection (Lewis et al
1986, 1988). In addition, metronidazole and a closely related drug ornidazole have been shown to be
effective clinically in the treatment of acute dental abscess (Ingham et al 1977, von Konow et al 1983).
In this study, the duration of therapy varied from 3 to 7 days, with a 5-day regimen being most popular,
apart from the 3-day course of therapy employed (46%) in the management of AUG. It has been
recommendation that therapy should be continued for 2 days after resolution of infection. Historically,
these duration times may have been adopted due to the fear of encouraging the emergence of resistant
bacteria. However, it has been suggested more recently that the use of antibiotics beyond the time of
clinical improvement encourages the emergence of resistance bacterial forms rather than reducing it (Lacey
et al 1984).
The present study has revealed that these four antibiotics, in a variety of regimens, are being used
successfully in the management of acute orofacial infections in general dental practice in Delta State of
Nigeria. However, it is important that patients who failed to respond to present treatment options or present
with unusual clinical signs be recognized, since this may indicate an underlying systemic disease. This is
particularly relevant with the prevalence of patients suffering from HIV/AIDS.
ACKNOWLEDGEMENTS
We gratefully acknowledge the assistance of the medical record personnel of the five hospitals involved in
this study.
4
REFERENCES
Chow A W, Roser S M, Brandy F A, (1978). Orofacial odontogenic infections. Ann. Intern. Med; 88:392-
402.
Cumming C E, Ross P W, Smith G F, Lough H, Moyes A, (1980). The use of cefadroxil in the treatment of
acute orofacial infections. J. Dent; 127: 247-251
Heimdahl A, von Konow L, Nord C. E, (1980). Isolation of beta –lactamase producing bacteroides strains
associated with clinical failures of penicillin treatment of human orofacial infections. Arch. Oral Biol; 25:
689-692.
Ingham H R, Hood F J C, Bradburn P, Tharagonnet D, Selkon J B, (1977). Metronidazole compared with

penicillin in the treatment of acute dental infections. J. Oral Surg; 14: 264-269.
Lacey R W, (1984). Evolution of microorganisms and antibiotic resistance. Lancet; 2: 1022-1025.
Lewis M A O, MacFarlane T W, McGowan D A, (1986). Quantitative bacteriology of dentoaveolar

abscesses. J. Med. Microbiol; 21: 101-104.
Lewis M A O, MacFarlane TW, McGowan D A, MacDonald D G, (1988). Assessment of the Pathogenicity

of bacterial species isolated from acute dentoaveolar abscess. J. Med. Microbiol; 27: 109 – 116.
Mehrhof A I, (1976). Clindamycin: an evaluation of its role in dental patients. J. Oral Surg; 43: 207-215.
Schuen N J, Panzer J D, Atkinson W H, (1974). A comparison of clindamycin and penicillin in the

treatment of oral infections. J. Oral Surg; 32: 503 – 505.
von Konow L, Nord C E, (1983). Ordnidazole compared to phenoxymethylpenicillin in the treatment of

orofacial infection. J. Antimicrob. Chemother, 11: 207 – 215.
Williams B L, McCann G F, Schoenknecht F D, (1983). Bacteriology of dental abscess of endodontic

origin. J. Clin. Microbiol; 18: 770 - 77
Received for Publication: 07/11/2007

Accepted for Publication: 24/12/2007
Corresponding Author:
Dr. T. E. Okagbare
Department of Preventive Dentistry, College of Health Sciences, Delta State University, Abraka, Nigeria.
E-mail:tuweyire @yahoo.com
5
Continental J. Medical Research 2: 6 - 13, 2008
AN OVER VIEW OF THE CLINICAL RELEVANCE OF THE KNOWLEDGE OF THE ORMAL AND
ABNORMAL ANATOMY OF THE SELLA TURCICA, USING PLAIN RADIOGRAPHS
Zagga AD1 and Saidu SA2

1 2
Departments of Anatomy and Radiology. College of Health Sciences. Usmanu Danfodiyo University,
Sokoto, Nigeria.
ABSTRACT
Careful examination of the changes within the sella is far more rewarding than
measuring the dimensions of the sella. A review was composed via Medline Internet
search and literature search. Knowledge of the normal and abnormal anatomy of the
sella turcica is significant clinically in the determination of increased intracranial
pressure, the determination of direct pressure erosion of the sella from external cases
in the immediate vicinity of the sella and the detection of intrasellar expanding
lesions. It is concluded that deformity of the sella turcica is often the only clue that
abnormality exists within the cranium: hence a familiarity with its anatomy and
radiologic appearance is essential.
KEY WORDS: Sella turcica, knowledge, normal and abnormal anatomy, clinical
relevance.
INTRODUCTION
The sella turcica (‘Turkish saddle’) is the superior saddle shaped concavity on the intracranial surface of
the body of the sphenoid bone (Chummy and Sinnatamby, 2004). It contains the central hypophyseal or
pituitary fossa which lodges the hypophyses cerebri or pituitary gland. It has been shown that about 80% of
the sella is occupied by the pituitary gland and that the gland may increase in size during pregnancy
(DiChiro and Nelson, 1962). It has also been suggested that the sella increases in size with age (Israel,
1970).
The anatomy of the sella turcica is variable in size and shape. It has been classified into three types: round,
oval and flat (Jones et al., 2004). It can also be deep or shallow in both children and adults (Isadore, 1976).
In profile, the sella at times has a somewhat high concave appearance caused by what appears to be an
excavation beneath the anterior clinoids. This is frequently described in children and has no pathological
significance. The floor of the sella turcica, which in most cases is concave, may be, flat or even convex
(Bruneton et al., 1979).
Careful examination of the changes within the sella is far more rewarding than measuring the dimensions
of the sella (Jones et al., 2004).
This paper aims at looking into the relevance of the familiarity with the normal and abnormal anatomy of
the sella turcica in clinical practice, using plain radiographs.
Normal anatomy of the sella turcica.

The sella turcica (‘Turkish saddle’) is the superior saddle shaped concavity on the intracranial surface of
the body of the sphenoid bone (Chummy and Sinnatamby, 2004). It contains the central hypophyseal or
pituitary fossa which lodges the hypophyses cerebri or pituitary gland. Anteriorly its bony landmarks
include the planum sphenoidale, the limbus sphenoidale, the chiasmatic sulcus, and the tuberculum sellae.
Anterolateral landmarks include the optic canal, the anterior clinoid processes, and the optic strut, which
forms the floor of the optic canal. The floor of the sella is the roof of the sphenoidal air sinus. Posteriorly,
6
Zagga AD and Saidu SA: Continental J. Medical Research 2: 6 - 13, 2008
the sella is bounded by the dorsum sellae and the posterior clinoid processes; its lateral margins are the
carotid sulci, and its superior boundary is the diaphragma sellae (Newton and Potts, 1971).
The planum sphenoidale: - The planum sphenoidale is a thin well-defined plate of bone that extends from
the cribriform plate to the limbus sphenoidale. The central portion, which extends forward and articulates
with the cribriform plate, has been termed the ethmoidplate. Its lateral extensions form the roofs of the
optic canals and blend with the anterior clinoid prosseses. The planum sphenoidale has a smooth upper
surface that may be slightly concave. The width of the planum is determined by the degree of separation
between the two orbits (Newton and Potts, 1971).
The limbus sphenoidale:-The limbus sphenoidale marks the posterior boundary of the planum sphenoidale.
The appearance of the limbus varies with the shape of the chiasmatic sulcus. When the chiasmatic sulcus is
concave, the limbus sphenoidale is prominent. On the other hand, when the chiasmatic sulcus is convex the
limbus is barely discernible (Newton and Potts, 1971).
The chiasmatic sulcus: - The chiasmatic sulcus is a depression of variable depth, spanning the distance
between the cranial openings of the optic canals. Anteriorly it is bounded by the limbus sphenoidale, and
posteriorly the tuberculum sellae. The chiasmatic sulcus is usually horizontal, but it may at times be almost
vertical. The width of the chiasmatic sulcus is determined by the width of the planum sphenoidale in an
inverse relationship. Thus, a wide planum, leads to a narrow chiasmatic sulcus (Newton and Potts, 1971).
The tuberculum sellae: - The tuberculum sellae is a transverse ridge that forms the posterior margin of the
chiasmatic sulcus as well as the anterior margin of the pituitary fossa. It spans the distance between the
anterior limits of the carotid sulci. This distance is variable and determines the length of the tuberculum
sellae. The prominence of the tuberculum sellae is related to the shape of the chiasmatic sulcus (Newton
and Potts, 1971).
The anterior clinoid processes: - The anterior clinoid processes are formed by the medial prolongation of
the free posterior margin of the lesser wing of the sphenoid bone. Between the anterior clinoid processes
and the tuberculum sellae is a notch which marks the termination of the carotid groove for passage of the
internal carotid artery. Thus, the anterior clinoid processes form the anterior and lateral borders of the
carotid sulcus. The appearance, shape, and thickness of the anterior clinoid processes vary considerably.
They are frequently asymmetric, and occasionally one may be vestigial or absent. The tips of the anterior
clinoid processes are situated slightly lateral to the posterior clinoid processes (Newton and Potts, 1971).
The middle clinoid processes: -The middle clinoid processes are in constant elevations on the anterior wall
of the pituitary fossa, medial to the carotid artery. At this level the internal carotid arteries pierce the
duramater and become intradural. Ossification of the intraclinoid bridge between the anterior and middle
clinoid processes leads to the formation of the caroticoclinoid canal (Newton and Potts, 1971). This canal is
believed to be a developmental anomaly (Kier, 1968).
The floor of the sella: - For purposes of description, the floor of the sella turcica will include portions of the
anterior and the posterior walls of the pituitary fossa. The floor of the sella turcica is therefore considered
to extend from the tuberculum to the dorsum sellae. In the sagittal plane the floor usually has a rounded
appearance, but its horizontal portion may be relatively straight. In the coronal section the horizontal
portion of the floor usually has a slightly convex or flat appearance. Occasionally it has a slight downward
concavity. The sellar floor may be asymmetric, sloping downward more on one side than on the other. The
horizontal portion of the carotid sulcus forms the lateral margin of the floor. The boundary between the
floor and the carotid sulcus is normally rounded (Newton and Potts, 1971).
The carotid sulcus: - The carotid sulcus is a shallow groove along the superolateral aspect of the sphenoid
sinus that is formed by the cavernous portion of the internal carotid artery. The depth of the carotid sulcus
varies. The sulcus is usually shallow but may have a prominent inferior border (Newton and Potts, 1971).
7
The dorsum sellae: - The dorsum sellae is the vertical posterior boundary of the sella and is formed by two
lateral struts topped by a horizontal strut. It varies greatly in shape and thickness (Newton and Potts, 1971).
Mahmoud (1958) found that the thickness of the dorsum ranges from 2 to 7 mm but that only the lateral
portions are thick. The central portion is a well-defined hollow between the sturdier lateral pillars and
forms a bed for the posterior portion of the pituitary gland. The central portion is often extremely thin. It
may even be absent so that a foramen is found within the dorsum sellae (Fry and du Bouley, 1965). The
lateral aspect of the dorsum sellae may be grooved by the sixth nerve or by a persistent trigeminal artery.
The anterior wall of the dorsum sellae is smooth, whereas the posterior aspect is rough. The roughness of
the posterior aspect of the dorsum is due to the dural venous plexus in this location. The posterior clinoid
processes are the lateral and superior extensions of the dorsum sellae (Newton and Potts, 1971).
The posterior clinoid processes: - The posterior clinoid processes are the lateral and superior extensions of
the dorsum sellae. The tips of the posterior clinoid processes are usually rounded, and they project forward
and slightly laterally. Occasionally the tips are pointed and may extend forward to join with the anterior
clinoid processes (bridged sella) (Newton and Potts, 1971).
The diaphragma sellae: - The diaphragma sellae is the dural fold formed by the anterior extension of the
tentorium. It is attached anteriorly to the tuberculum, posteriorly to the dorsum, and laterally to the
interclinoid ligament, which joins the anterior and posterior clinoid processes. The diaphragma sellae has a
central opening that transmits the pituitary stalk (Newton and Potts, 1971). Busch (1951) reported that the
thickness of the diaphragma, as well as the size of the opening, varies. He examined 788 sellae turcicae and
described three main types of diaphragma sellae: (1) diaphragma forms a complete covering with only a
small opening for the pituitary stalk (41.9%); (2) the diaphragma is incomplete, with an opening for the
stalk less than 3 mm (37.6%); and (3) the diaphragma is represented by only a rim of tissue less than 2 mm
in width (20.5%). In a similar study the opening for the pituitary stalk was noted to be greater than 5 mm in
39% of the cases (Bergland, 1968). In sagittal section the diaphragma sellae usually slopes slightly
downward into the sella (Newton and Potts, 1971).
Abnormal sella.
Small sella
There is no constant relationship between the size of the sella and the size of the hypophysis. It is very
unusual for the sella to be abnormally small. The sella that appears small in the lateral projection may
nevertheless be normal because of its greater than average width (Fisher and DiChiro, 1964). A small sella
may be found in pituitary hypopituitarism (Riach, 1966), and growth hormone deficiency (Fisher and
DiChiro, 1964) if the onset of the disease is before the age of six years. Fisher & DiChiro (1964) found the
sella to be small in 56.8% of forty-four subjects with hypopituitarism. Fisher and DiChiro (1964) also
found a small sella in 13.5% of subjects with genetic dwarfism. The sella turcica was also reported to be
small in a 13½ year old boy with Cushing’s syndrome due to an adrenocortical adenoma (Steinbach et al.,
1963). A small sella was also reported in Sheehan’s syndrome (Meador and Worrel, 1959). A small sella in
lateral profile may also be found in dystrophia myotica but is not diagnostic of this condition (Caughey,
1952). The sella may be vestigial. This entity has been termed dysplasia of the sella (Lundberg and
Gemzell, 1966).
Large sella without local bone destruction

Intrasellar masses may cause enlargement of the sella with preservation of cortical bone. In these instances
there is uniform enlargement with a deepening of the floor, and thinning, as well as posterior displacement
of the dorsum. Uniform enlargement of the sella is most commonly seen in pituitary tumors, which include
chromophobe adenoma, easinophilic adenomas, basophilic adenoma, Nelson’s Syndrome,
polyadenomatosis, and carcinoma of pituitary. Others are empty sella syndrome, craniopharyngioma,
intrasellar aneurysm, hypothyroidism, hypogonadism, neurofibromatosis and oxycephaly (Bergland et al.,
1968).
Large sella with local bone destruction or erosion
8
Erosion of undersurface of anterior clinoid processes and chiasmatic sulcus

Erosion of undersurface of anterior clinoid and chiasmatic sulcus can result from glioma of optic chiasm,
optic nerve glioma, J sella, optic nerve sheath tumor, pituitary adenoma, aneurysm, dilated third ventricle,
craniopharyngioma, frontal lobe tumour, Hunter’s syndrome/mucopolysaccharidoses type 11/gargoylism,
neurofibromatosis and carotid cavernous fistula (Newton and Potts, 1971).
Erosion of upper surface of anterior clinoid processes

This condition may result from supra-sellar meningioma, increased intracranial pressure due to dilated third
ventricle, aneurysm, frontal lobe tumour, suprasellar arachnoid cysts in gargoylism (Newton and Potts,
1971).
Localized erosion of floor

Localized erosion of the sella turcica floor may be due to nasopharyngeal tumor, sphenoid sinus
mucocoele, metastases e.g. from carcinoma of the prostate, basal encephalocoele, giant cell tumor,
leiomyoma, juvenile nasopharyngeal angiofibroma and postoperative sella (Newton and Potts, 1971).
Erosion of dorsum and posterior clinoid processes

Lateral surface: - This may be affected by parasellar meningioma, neurofibroma, chordoma, aneurysm of
internal carotid artery, anomalous vessels, and miscellaneous conditions; e.g. epidermoid and subarachnoid
cysts (Newton and Potts, 1971).
Anterior surface of dorsum: - This may be eroded by intrasellar masses, including pituitary tumors (Newton
and Potts, 1971).
Upper surface of dorsum and posterior clinoid processes: - These may be eroded by the supra-sellar masses
such as craniopharyngioma, optic chiasm glioma, hypothalamic tumor, meningioma, subarachnoid cyst,
aneurysm, histiocytosis X, atypical teratoma (ectopic pinealoma), lipoma, dilated third ventricle, frontal
glioma and dermoid cyst (Newton and Potts, 1971).
Posterior surface: - The posterior surface of the dorsum sellae may be eroded by posterior fossa tumours
(e.g. astrocytoma in children), metastasis (e.g. from colloid carcinoma), arachnoid cyst and basilar artery
aneurysm (Newton and Potts, 1971).
Local bony sclerosis and change in texture

This may be brought about by disease conditions like fibrous dysplasia, ossifying fibroma, meningioma,
metastatic tumours to the skull, suprasellar tumors (such as craniopharyngioma, atypical teratoma),
osteochondroma, osteoma, chondroma of the skull, the clivus, the cerebello pontine angle, and the planum
(Minagi and Newton, 1969), soft tissue masses, miscellaneous conditions, such as infections (e.g.
tuberculosis, coccidioidomycosis, or pyogenic abscess), trauma (e.g. fracture of the dorsum sellae, floor of
the sella and clivus) (Engels, 1961).
Changes in sella in increased intracranial pressure

Erosion of sellar cortex:
Erosion of the cortical bone that lines the pituitary fossa is usually seen earliest at the anterior part of the
base of the dorsum. The erosion often spreads to involve most of the sellar floor but occasionally is first
recognized more anteriorly (Newton and Potts, 1971). Mahmoud (1958) showed that the process is truly an
erosion caused by osteoclasts and that the pits produced in the lamina dura tend to coalesce. In the earlier
stages optimal roentgenograms may reveal pinpoint interruptions of the white line of the lamina dura. As
erosion progresses, the roentgenographic appearance becomes more obviously abnormal. The outlines of
the sella (i.e. lamina dura) are described as rubbed out or osteoporotic (Newton and Potts, 1971).
Erosion of top of dorsum sellae:
9
Destruction of top of dorsum may include loss of those rough elements of bone that are the site of
attachment of the petroclinoid ligaments. As a result of erosion of the posterior clinoid processes, the
dorsum in the lateral view may appear as a truncated cone with a flattened top or as a thin spike. In both
cases the upper margins are poorly demarcated unless all that remains is a single flake of bone (Newton and
Potts, 1971).
Changes in anterior clinoid processes:

The anterior clinoid processes are affected late and in ways different from those of the posterior. In long
standing hydrocephalus, the entire base of the skull may be thin. The anterior clinoid processes become
thinner and sharper, and in lateral views they may be difficult to recognize. In the posteroanterior inclined
projection the anterior clinoid processes and the lesser wings of the sphenoid form frail and indistinct lines
(Newton and Potts, 1971).
Enlargement of sella
When the sella enlarges as a result of raised intracranial pressure or hydrocephalus, invariably some erosion
or alteration of shape occurs. In raised intracranial pressure the sella may become enlarged in one of three
ways: (1) the lamina dura may be destroyed so completely that it no longer has the strength to withstand
intracranial pressure as a result the sellar floor herniates downward into the sphenoid sinus; (2) coalescence
of erosions in cancellous bone, particularly at the base of the dorsum sellae, may cause the cavity of the
sella to extend downward into the clivus, this extension may be appreciated in histologic sections but the
cavity does not reach sufficient size to be recognised easily on roentgenograms; (3) enlargement may take
place by less dramatic changes in long standing conditions. Erosion is not a feature; but growth under
abnormal stimuli causes a peculiar shape of sella. The commonest of these peculiarities is seen sufficiently
often to be considered characteristic of chronic obstructive (non-communicating) hydrocephalus. It is not a
true enlargement of the sellar cavity itself. The dorsum is short, indeed sometimes extremely so. The
longest axis of the sella turcica in the lateral view is more or less in line with clivus. The reason for this
appearance is that the anterior sellar wall is elongated upward into the chiasmatic sulcus, which itself is
enlarged. Commonly the anterior clinoid processes, presumably because of unusual torsion on their
ligaments, are blunt and massive. The upper cavity, limited anteriorly by the chiasmatic sulcus, is occupied
by the dilated third ventricle. The cortex is often well formed and without erosions (Newton and Potts,
1971).
Pressure changes of some sort may be noted in about one third of patients with tumors distant from the
sella. Of these, 20% do not have papilledema, and amongst them are many who, despite short clinical
histories and the absence of other signs of raised intracranial pressure, have longstanding and operable
tumors. The earliest detectable abnormality is usually a loss of the lamina dura. Under ideal circumstances
this loss is occasionally detected within a few weeks after onset of raised pressure (Tonnis et al., 1954).
Erosion of lamina dura

As an isolated sign, without any other abnormality of the sella turcica, erosion of the lamina dura was
found in about 12% of intracranial tumours (Category I erosion) (du Bouley and El Gammal, 1966). In
about twice this number of patients with either infra- or supratentorial tumours, erosion of the lamina dura
and some additional sellar abnormality were seen. Such erosion occurs in many cases of aqueduct stenosis,
but virtually never in communicating hydrocephalus (Newton and Potts, 1971).
Erosion of top and back of dorsum sellae

Tumours of the posterior fossa cause erosion of the top and back of the dorsum sellae (category II erosion)
(du Boulay and El Gammal, 1966), about twice as often as do supratentorial tumours. Even so, however,
only 10% of posterior fossa tumours are associated with such erosion. In patients with supratentorial
tumours, category II change is usually associated with other sellar abnormalities, particularly an extensive
erosion of the lamina dura. With hydrocephalus resulting from infratentorial masses, it may be seen alone,
however. Still more commonly this type of erosion results from a suprasellar tumour (Newton and Potts,
1971).
10
Erosion of planum sphenoidale:

After many months of raised intracranial pressure, erosion of the lamina dura may have extended to the
planum sphenoidale. The usually crisp white line of that structure blurs or disappears. Nearly always
before this disappearance, the top of the dorsum has also been damaged. The combination of erosion of the
top of the dorsum sellae, of the lamina dura, and of the planum sphenoidale (category III sellar change) (du
Bouley and El Gammal, 1966) is nearly always caused by a slow growing frontal or posterior frontal tumor.
Often this tumour is glioma, sometimes a meningioma.
Differentiation between the effects of raised intracranial pressure and the effects of local tumours.
Destruction of the cortical lining of the pituitary fossa may also accompany the growth of tumours,
particularly pituitary tumours, within the sella. After thorough examination of the plain roentgenograms of
the skull, only about 3% of all pituitary tumours cause confusion regarding diagnosis. The majority of the
plain roentgenograms present fairly obvious evidence of the true nature of tumour (Newton and Potts,
1971).
Ballooning of the pituitary fossa is the most common of the additional and specific signs in pituitary
adenoma. Sclerosis of bone betrays a meningioma or occasionally a chordoma. Rarely, gliomas of the
optic chiasm cause a characteristic excavation in the anterior part of the sellar region. Craniopharyngioma
is usually suprasellar and retrosellar. Although a fair number of these tumours protrude into the cavity of
the pituitary fossa as well, half of all craniopharyngiomas cause a shortened and extremely flat dorsum.
The cortical top of the dorsum in these cases is usually preserved. The abnormality may therefore be
distinguished from that caused by frontal tumours and from those producing hydrocephalus (Newton and
Potts, 1971).
Differentiation between the changes of pressure in adults and the effect of local tumour and disease is more
difficult in the following circumstances: (1) when there is apparently complete destruction of the dorsum
sellae; in these situations one should search for displacement of fragments, away from the cavity of the
sella (intrasellar tumor), or toward it (hydrocephalus and craniopharyngioma); (2) when, occasionally,
erosion of the lamina dura by pituitary adenoma is accompanied by enlargement of the sella, which
nevertheless is not characteristically ballooned in shape; (3) rarely, when metastatic carcinoma has spread
from the pituitary fossa or the suprasellar region; destruction, or at least an obvious change in texture,
extends more deeply into the bone than is the case with raised intracranial pressure (4) when the lesion,
usually an aneurysm of the internal carotid, is truly parasellar; in these situations the lateral roentgenogram
may suggest at first glance an enlargement and osteoporosis. Careful examination of all views reveals the
true state. A faint but sharply outlined dorsum (of which as much as one lateral half may be missing),
destruction of one lateral half of the sellar floor, and destruction usually of an anterior clinoid process are
all visible (Newton and Potts, 1971).
Changes in sella in childhood.

Similar to adults, the lamina dura in children is eroded in similar situations and after a similar length of
time. Changes in sella in childhood may be over looked because diastasis of the sutures attracts the
attention of the radiologists. Destruction of the top of the dorsum results particularly from tumours of the
posterior fossa that cause hydrocephalus. Rarely destruction may be seen as a result of long-standing
frontal and fronto-parietal masses that push the base of the brain against the base of the skull (Newton and
Potts, 1971).
In children, however, opportunities for the more chronic sellar changes are fewer. Moreover, slow-growing
frontal tumours, which in adults cause many of the most severely damaged sellae, are exceptional before
the age of 30. Consequently chronic sellar changes in children tend to be restricted to those suffering from
developmental abnormalities, especially aqueduct stenosis. In infancy, changes resulting from
communicating hydrocephalus are confined to a simple elongation of the sella, which may accompany a
general expansion of the head (Newton and Potts, 1971).
11
Changes in sella with relief of raised intracranial pressure.

Roentgenograms obtained after excision of cerebral tumors and after operative procedures for the relief of
hydrocephalus have been studied. These indicated that osteoclastic resorption ceases rapidly and is
replaced by increased new bone formation. Within a few weeks the lamina dura reappeared and some
evidence of repair of the dorsum sellae and posterior clinoid processes was seen. The fact that bone (e.g.
the posterior clinoid processes) should reappear, must mean that some periosteal or osteoid tissue had not
been destroyed entirely. Total destruction and displacement, however, cannot be corrected, so the reformed
bone in advanced cases is abnormal in shape. The dorsum may be short, or the cavity of the sella enlarged
(Newton and Potts, 1971).
From observation of patients with recurrent symptoms, the susceptibility to erosion of the reformed lamina
dura appears to be much less than that of the original bone lining. A second episode of raised intracranial
pressure rarely causes erosion (Newton and Potts, 1971).
CONCLUSION
It is concluded that deformity of the sella turcica is often the only clue that abnormality exists within the
cranium: hence a familiarity with its anatomy and radiologic appearance is essential.
REFERENCES
Bergland, R.M., Ray B.S., Torack, R.M. 1968. Anatomical variations in the pituitary gland and adjacent
structures in 225 human autopsy cases. J. Neurosurg.; 28:93-99.
Bruneton, J. N., Drouilard, J.P., Sabatier, J.c., Elie, G.P and Travenir, J.F, 1979. Normal variants of the
sella turcica. Comparison of Plain radiographs and tomograms in 200 cases. Radiology;131:99-
104.
Busch, W. 1951. Die Morphologic der sella turcica und ihre Bexiehungen zur Hypophyse, Arch. Path.
Anat.; 320: 437-458.
Caughey, J. E. 1952. Bone changes in the skull in dystrophia myotonica, J. Bone Joint Surgery.; 34B, 343-
359.
Chummy S. and Sinnatamby (2004). (Editors) Last’s Anatomy: Regional and Applied; 10th edition.
Churchill Livingstone; Edinburgh, London,NewYork, Philadelphia, Sydney, Toronto.pp501-504.
DiChiro, G. and Nelson, K. B., 1962. The volume of the sella turcica. AJR Am. J. Roentgenol.; 87: 989-
1008.
du Boulay, G. H., and El Gammal, T. 1966. Classification, clinical value and mechanism of sella turcica
changes in raised intracranial pressure, Brit. J. Radiol.; 39: 422-442.
Engels, E. 1958. The roentgen appearance of the carotid sulcus of the sphenoid bone, Acta Radiol.; 49:
113-116.
Engels, E. 1961. Basal skull fractures involving the sella turcica. Clin. Radiol.; 12: 177-178.
Fisher, R. L. and DiChiro, G. 1964: The small sella turcica. Amer.Roentgenol.; 91: 996-1005.
Fry, K. I., and du Boulay, G. H. 1965. Some observations on the sella in old age and arterial hypertension,
Brit. J. Radiol.; 38: 16-22.
Isadore Meschan M.A. M.D, 1976. An Atlas of Anatomy Basic to Radiology. 1st Edition. W. B. Saunders
Company; Philadelphia, London, Toronto. pp343-349.
12
Israel, J. H, 1970. Continuing growth in sella turcica with age, AJR Am. J. Roentgenol.; 108: 516-527.
Jones, R.M., Faqir, A., Millet, D.T., Mous, K.F., McHugh, S, 2004. Bridging and Dimensions of Sella
Turcica in Subjects Treated by Surgical Orthodontics Means or Orthodontics only. The Angle
Orthodontist; 75(5): 714-718.
Kier, E.L. 1968. The infantile sella turcica. New roentgenologic and anatomic concepts based on a
developmental study of the sphenoid bone. AJR Am. J. Roentgenol.; 102:747-767.
Laschi, G. 1931. Un caso di foramen dorsi sellae, Radiol. Med.; 18: 707-712.
Lundberg, P. O. and Gemzell, C. 1966. Dysplasia of the sella turcica: Clinical and laboratory investigations
in three cases, Acta Endocrinol.; 52:478-488.
Mahmoud, M.S. 1958. The sella in health and disease: value of the radiographic study of the sella turcica
in morbid anatomical and topographic diagnosis of intracranial tumours, Brit. J. Radiol.;
Supp. 8, 1-100.
Meador, C. K. and Worrel, J.L. 1959. The sella turcica in post- partum pituitary necrosis (Sheehan’s
Syndrome). Ann. Intern. Med.;65: 252-264.
Minagi, H., and Newton, T. H. 1969. Cartilaginous tumours of the base of the skull, AJR Am. J.
Roentgenol.; 105: 308-313.
Newton, T.H. and Potts, D.G. 1971. (Editors) Radiology of the skull and brain, The Skull: Volume 1, Book
1; The CV Mosby Company; Saint Louis; pp359-405.
Riach, I.C.F. 1966. The pituitary fossa in childhood with particular reference to hypopituitarism, Brit. J.
Radiol.; 39: 241-243.
Steinbach, H. L., Noetzei, M., and Ozoof, M. B. 1963. Small pituitary fossa in Cushing’s syndrome due to
adrenal neoplasm, Neuro Eng. J. Med.; 269: 1286-1289.
Tonnis, W., Schiefer, W., and Rausch, F. J. 1954. Sella veranderungen bei gesteigerten schadelinnendruck,
Deutsch Z. Nervenheilk., 171: 351-369.

Corresponding Author:
Dr. A.D. Zagga,
Department of Anatomy, College of Health Sciences, Usmanu Danfodiyo University, PMB 2346, Sokoto,
Nigeria.
E mail:adauduzagga@yahoo.com
Fax: +234-80-231514.
13
POST PRANDIAL BLOOD PRESSURE CHANGES IN PATIENTS WITH CHRONIC RENAL

FAILURE DURING HEMODIALYSIS.
Onyemekeihia UR1, Esume CO 2, Bamgboye LE,3 Anyanwu BE4

1
Department of Medicine, Nephrology Unit, Central Hospital, Warri.
2
Department of Pharmacology and Therapeutics, Delta State University, Abraka. 3Nephrology Unit, St.
Nicholas Hospital, Lagos. 4 Department of Family Medicine, Delta State University, Abraka.
ABTRACT:
Hypotension is a recognized complication of hemodialysis (HD), and many factors
had been implicated one of which is eating before or during hemodialysis.
Postprandial hypotension (PPH) was first recognized in 1977 by Seyer Hanseen. PPH
is defined as decrease in systolic blood pressure or diastolic blood pressure of
20mmhg or more and 10mmhg or more respectively. The mechanisms of PPH are not
fully understood but factors such as Impairment of baroreflex function, Inadequate
postprandial increase in cardiac output, Impaired peripheral vasoconstriction, Insulin
induced vasodilatation and Release of vasodilatory gastrointestinal peptides with
attendant splanchnic blood pooling have been implicated. This study investigates the
effect of food on blood pressure of patients during hemodialysis, with the view of
proffering advice about meals during HD. The study was carried out over a six weeks
period in St. Nicholas hospitals, Lagos, a privately owned 50-bedded hospital with a
well developed renal transplant unit and a state of the art dialysis centre. There is also
an efficient catering unit. Sixty one subjects were studied, 31 sessions being test
session and 30 being controls. Of the 31 test sessions, 18 (58%) were males; and 13
(42%) were females while 18 (60%) of the controls were males and 12(40%) females,
with age ranging from 15-79 years. The nature of the study was explained to the
patients and consent obtained. Those who wished to eat were given a standard meal of
their choice. Before the start of HD or eating, initial BP was taken. Freizinus(R) 4008
HD machines and bicarbonate dialysate fluid were used for all patients. Blood
pressure was monitored hourly for 4 hours. The patients who took antihypertensives
before hemodialysis or had cause to take them during HD were excluded from the
study. Those who did not eat were used as controls. There was Postprandial
hypotension in 7 (23%); 6(86%) Diastolic Blood Pressure only, 1 (14%) both Systolic
blood pressure and Diastolic Blood Pressure. All the patients were monitored for
symptoms of weakness, dizziness, and chest pain.
KEYWORDS: Postprandial, blood pressure, changes, patients, chronic renal failure,

hemodialysis.
INTRODUCTION
Hypotension is a recognized and preventable complication of HD and our current understanding of
postprandial hypotension is limited by the lack of a standardized, clinically meaningful definition
(Jansen,1995). Analogous to orthostatic hypotension, postprandial hypotension is commonly defined in
the literature as a decrease in systolic blood pressure of 20mmhg or more within 2 hours of the start of a
meal (Jansen, 1995). Postprandial hypotension also develops when the absolute level of systolic blood
pressure after a meal decreases to less than 90mmhg and when the systolic
14
Onyemekeihia UR et al: Continental J. Medical Research 2: 14 - 19, 2008
blood pressure before a meal was greater than 100mmHg (Jansen 1995). After a meal, supine heart rate
and cardiac output increase, while supine diastolic blood pressure and total systemic resistance decreases
in normal healthy individuals. Food ingestion increases splanchnic and hepatic blood flow. Redistribution
of volume compromises cardiac filling, decreases cardiac output, and leads to a decrease in mean arterial
pressure.
TABLE 1: MEAN BP AT VARIOUS TIMES DURING HD
TIME(HR) TEST(MMHG) CONTROL(MMHG)
0 171 23 169 23
----- ± ----- ----- ± -----
94 14 92 18
1 168 23 168 22
------ ± ------ ---- ± ------
92 15 91 12
2 169 31 176 27
------ ± ------ ----- ± ------
94 19 95 16
3 169 28 176 26
------- ± ------ ----- ± ------
93 18 93 17
4 169 24 182 27
------ ± ------ ----- ± -----
92 19 97 15
During hemodialysis and hypovolemia, the body tries to conserve blood flow to vital organs by
vasoconstriction. Food ingestion during dialysis results in an obligatory increase in splanchnic blood flow
with sequestration of blood in the splanchnic pool and decreases venous return. Though eating during
hemodialysis sessions is a widespread practice, it may lower blood pressure, probably due to a reduction
in peripheral vascular resistance from food’s effect on alimentary tract blood flow (Barakat et al 1993).
Other factors responsible are, Impairment of baroreflex function, Inadequate postprandial increase in
cardiac output, Impaired peripheral vasoconstriction, Insulin induced vasodilatation and Release of
vasodilatory gastrointestinal peptides (Jansen 1989). Postprandial hypotension (PPH) was first
15
recognized in 1977 by Seyer-Hanseen in a patient with Parkinson’s disease (Seyer-Hanseen 1977).

Sherman et al in 1988 studied postprandial blood pressure changes during hemodialysis. In this study of 9
patients who had end stage renal disease (ESRD), but not diabetes, a standard meal was given during 62
of 125 dialysis treatments. Meals consisted of two slices of white bread, 2 ounces of turkey breast, pound
cake, and 4 ounces of cranberry juice. During dialysis, blood pressures were measured by
sphygmomanometry at 30-minute intervals prior to meals and every 15 minutes following meals.
Hypotension was defined as a 25% or greater fall in mean arterial pressure from the blood pressure
recorded immediately prior to feeding time. The investigators found that there were 13 episodes of
symptomatic hypotension in the 45-minute postprandial intradialytic period compared with two episodes
during the corresponding fasting period.
TABLE 2: BP WITH RESPECT TO SEX AT VARIOUS TIMES
0 hr 1 hr 2 hrs 3hrs 4hrs

TEST Males 167 25 165 24 163 31 166 25 167 22
± ± ± ± ±
96 14 92 17 94 20 94 19 91 16
Females 173 22 172 23 175 31 172 31 172 25
± ± ± ± ±
90 15 91 14 94 19 93 16 93 16
Males 166 23 164 25 167 25 169 22 176 26
± ± ± ± ±
94 12 92 15 93 17 93 15 98 13
females 173 23 172 29 186 29 184 30 188 28

± ± ± ± ±
CONTROL
90 16 91 19 95 16 94 19 97 17
Barakat et al in 1993 reported that food ingestion during dialysis causes hypotension primarily because of
decrease in systemic vascular resistance. Other workers have demonstrated postprandial hypotension
during Haemodialysis ( Shibagaki 1998, Zocalli 1989 and Hirakata 1987). It May result in syncope, fall,
dizziness, weakness, angina pectoris and stroke. Postprandial hypotension is distinct from and probably
more common than orthostatic hypotension (Jansen and Lipsitz 1995).
AIMS AND OBJECTIVES

To determine the effect of food on blood pressure of patients during haemodialysis, with the view of
proffering advice about feeding during haemodialysis.
MATERIALS AND METHOD

The study was carried out over a 6-weeks period in ST. Nicholas hospital, Lagos (SNH).SNH is a
privately owned 50 bedded hospital with a well developed renal transplant unit and a state of the art
dialysis centre with 7 functional dialysis machines. It also has standard and efficient catering unit.
Freizinus 4008 HD machines and bicarbonate dialysate fluid was used for all patients.
There were a total of 61 subjects all of whom were hypertensive but not diabetic with age ranging
between 15-79 years. Thirty one of them wished to eat and were given a standard meal of their choice and
used as test subjects. Thirty of them who did not eat were used as controls.
16
Patients who took antihypertensive before HD or had cause to take them while on HD were excluded.
The nature of the study was explained to patients, and consent obtained. Before the start of HD or eating,
initial BP (O HR) was taken. Blood Pressure was monitored hourly for 4 hours by Sphygmomanometry
and recorded. All the patients were monitored for symptoms of weakness, dizziness, and chest pain.
The Data was analyzed using the SPSS+PC statistical package and test of significance was done using t-
test.
RESULTS:
Sixty one sessions were studied: 31 test sessions and 30 controls and their blood pressures are as
presented in table 1. Of the 31 test sessions, 18 (58%) were males and 13 (42%) were females. Of the 30
control, 18 (60%) were males and 12 (40%) were females.
The Patients ages ranged between 15 and 79 years. All patients in the sessions had hypertension. The
172 26
Mean Blood Pressure for all patients was ± MMHG, with the males having a mean blood
99 17
167 26 177 27
pressure of ± MMHG and the Females ± MMHG. The Mean BP in the test and
94 16 93 18
169 27 174 25
control for both sexes was ± MMHG and ± MMHG respectively.
93 17 93 17
There was Postprandial hypotension in a total of 7 (23%) patients; 6 (86%)of whom had Diastolic Blood
Pressure reduction only and 1 (14%) had Systolic blood pressure and Diastolic Blood Pressure reduction.
There was no isolated Systolic Blood Pressure Postprandial hypotension.
There was increase in Blood Pressure in 9 patients (30%) of the Control. 5 of these patients (55%) had
increase in Systolic blood pressure only, 2 (22%) diastolic blood pressure only; and 2(22%) a
combination of Systolic Blood Pressure and Diastolic blood Pressure. There was 1 case (3%) of
hypotension amongst the control. Only 2 (6%) of test group complained about weakness, but was not
enough to discontinue HD.
DISCUSSSION
In this study we compared the effect of food on blood pressure of patients undergoing Hemodialysis
using 31test subjects who ate just before or during hemodialysis and 30 control subjects who were in the
fasting state during hemodialysis.
When compared to the controls, there were more significant falls in blood pressure among the test group
(P<0.05). Postprandial hypotension occurred in 7 (23%); while only 1% of the control had postprandial
hypotension.
However, there was increase in Blood Pressure in 9 (30%) Of Control; 5 (55%) Systolic blood pressure
only, 2 (22%) diastolic blood pressure only; 2 (22%) Systolic Blood Pressure and Diastolic blood
Pressure 2 (22%).
Hypotension though a complication of hemodialysis may be worsened by eating during or before

Haemodialysis. Several factors had been implicated, which could be decreased cardiac output due
17
to splanchnic sequestration or decreased vascular resistance due to splanchnic vasorelaxation (Barakat et

al, 1993). Although the mechanism is not fully understood, postprandial blood pressure reduction seems
to be related to glucose related factors, since blood pressure only falls after oral glucose loading, but not
after oral fructose, fat or protein loading. Vasoactive gastrointestinal hormones may play a role in the
glucose induced vasodilation of splanchnic vasculature, but attempts to identify such hormones were
unsuccessful (Jansen and Hoefnagels, 1989).It has been suggested that interference of insulin with a
sympathetic response diminished by age or disease to splanchnic vasodilation, may be responsible for the
postprandial fall in blood pressure in the elderly. However, vasodilator effects of insulin or a baroreflex
response diminished by insulin do not seem to be involved (Jansen and Hoefnagels, 1989, 1990). The
immediate cause of hypotension during dialysis is intravascular hypovolaemia which is related to the
procedure itself (Shibagaki et al, 1998). To analyze the effects of food intake during hemodialysis on
blood volume of the large vessels quantitatively, Shibagaki et al, (1998) monitored Hematocrit of the
arteriovenous shunt blood continuously in the patients treated with hemodialysis regularly and estimated
blood volume. They reported that food intake during hemodialysis decreases blood volume of the large
vessels transiently but significantly. Blood pressure is dependent on blood volume especially in black
subjects in whom hypertension is volume dependent. From our results, Diastolic Blood pressure seems to
be mostly affected in postprandial hypotension during haemodialysis which is in consonance with work
done by Sherman et al (1998). Males seem to be more affected by postprandial hypotension though the
difference is not significant (P>0.05, Table 2). This may imply a sex difference in the pathophysiology of
postprandial hypotension and requires further investigation. The hypotension is more marked the longer
the patients stay on the dialysis machine as our results showed more significant difference in systolic
blood pressure during the fourth hour (Table 1). Patients may be symptomatic of postprandial
hypotension. Hypotension during dialysis may induce minor but troublesome side effects in the patient,
such as nausea, vomiting, and dizziness, but may also lead to more serious complications, such as cardiac
or cerebral ischemia. There are dialysis patients who hardly suffer from hypotensive episodes. However,
HD-associated hypotension is especially frequent in elderly people and in those patients with a
compromised cardiovascular system. Particularly the latter group, hypotension may have serious
consequences (Reed and Devous, 1985). In our study, only 2 (6%) of test group complained about
weakness, but was not enough to discontinue HD.
Eating has adverse effects on the hemodynamics of circulation during hemodialysis and should be
avoided in patients with intradialytic hypotension. (Zocalli et al, 1989). All physicians caring for chronic
renal failure patients should be aware of the hypotensive effects of food ingestion during haemodialysis.
Postprandial hypotension should be considered in the evaluation of syncope, falls, dizziness and other
cerebral ischaemic symptoms. Consumption of meal during haemodialysis should be avoided in patients
at risk of hypotension during treatment. Further studies needs to be carried out to determine the effects of
sex, Body Mass Index, age, aetiology of Chronic Renal Failure, blood flow rate, type and quantity of
food on Blood Pressure during hemodialysis. The limitations in the study were non uniformity in timing
of meals, the type and quantity of food and blood flow rate.
AKNOWLEDGEMENT
The authors wish to express their gratitude to the management of Saint Nicholas Hospital, Lagos for
allowing them to conduct this research with their health facility. Our gratitude also goes to all staff of the
renal dialysis (SNH) unit for their meticulous and relentless efforts towards the success of this work.
REFERENCES
Barakat, M.M.; Nawab, Z.M.; Yu, A.W.; Lau A.H; Lng, T.S; Daugirdas, J.T (1993): Hemolytic effects of
intradialytic food ingestion and the effects of caffeine. J Am Soc Nephrol.;(11):1813-8
18
Hirakata, H; Onoyama, K; Hori, K; Fujimi, S; Fujishima, M (1987): The hemodynamic and humoral
responses to tilting in diabetic patients on chronic hemodialysis treatment. Clin Nephrol.; 27(6):298-303.
Jansen R.W. and Hoefnagels, W.H.(1989): Postprandial reduction in blood pressure after meals in the
elderly. A review article. Trijdschr Gerontal Geriatr.20 (4):141-6
Jansen, R.W. and Hoefnagels,W.H.(1990):Postprandial blood pressure reduction. Neth J Med.; 37(1-2):80-
8.
Jansen, R.W and Lipsitz, LA. (1995): Postprandial Hypotension: Epidemiology, Pathophysiology, and
Clinical Management. Annals of Internal Medicine. 122(4)286-95.
Reed, G and Devous M. (1985): Cerebral blood flow autoregulation and hypertension. Am. J Med
Sci.;285:37-44
Seyer-Hansen K. (1977): Postprandial hypotension. Br Med. J. 2:1262
Sherman R.A. Torres F. and Cody RP. (1988): Postprandial blood pressure changes during hemodialysis.
Am J Kidney Dis .12(1):37-9.
Shibagaki, .Y. and Takaichi,. K. (1998): Significant reduction of the large-vessel blood volume by food
intake during hemodialysis. Clin Nephrol. 49(1):49-54.
Zoccali, C; Ciccarelli, M; and Maggiore, Q. (1989): Postprandial alterations in arterial pressure control
during hemodialysis in uremic patients. Clin Nephrol. 31(6):323-6.

Corresponding Author
C.O. Esume,
Department of Pharmacology and Therapeutics, Delta State University, Abraka
Email: esumec@yahoo.co.uk
19
AN EPIDEMIOLOGICAL STUDY OF ADDICTION AND PSYCHOSOCIAL BEHAVIOUR AND RISK

OF OBESITY IN URBAN POPULATION
Khalid U Khayyam1, Sazina Muzammil2, Mohd Yunus1, Zulfia Khan1

1
Department of Community Medicine, Jawaherlal Nehru Medical College, Aligarh Muslim University, Aligarh,
UP, India 2Department of Physiology, Jawaherlal Nehru Medical College, Aligarh Muslim University,
Aligarh, UP, India
ABSTRACT
Objective: To study addiction and psychosocial behaviour in relation to obesity in
urban population.
Method: A prospective study in an urban health training center of

Department of Community Medicine, Jawaherlal Nehru Medical College, Aligarh
Muslim University, Aligarh, Utter Pradesh, INDIA through predesign and pretested
questionnaire base.
Results: Individuals addicted to alcohol (2%) and pan (10.7%) were found to be more
obese as compared to individuals addicted to tobacco (1.3%), pan masala (2.4%) and
cigarettes (2.6%).The prevalence of obesity was more in individuals having
abnormal psychosocial behaviour like withdrawn (3%), self conscious (51.1%),
loneliness (5%), anxiety (14%) and depression (12%).
Conclusion: The addiction of alcohol, pan and abnormal psychosocial behaviour

play a role in development of obesity.
KEY WORDS: Obesity, Addiction, Psychosocial behaviours, Urban population,

prevalence, Body mass index.
INTRODUCTION
Obesity is a very complex disorder in which multiple causative factors are potentially operative1. Any
factor (eg. genetic, metabolic, psychological, social or environmental) which increase energy uptake or
decreases energy expenditure can lead to positive energy balance and hence obesity. The body has
excellent physiological defenses against the depletion of body energy stores, but it has weak defense
against the accumulation of excess energy stores. Studies have shown that addiction to a particular
substance like tobacco, alcohol, etc. and psychosocial behaviour can contribute to obesity. Some alcoholic
beverages such as beer and wines are carbohydrates and they increase calories uptake2. Suter et al3 point
out that as an energy source, unlike other sources of energy, alcohol cannot be stored in body and appears
to have absolute priority in metabolism. This takes place at expense of other metabolic pathways, including
the suppression of lipid oxidation, which appears to be a critical factor in the development of positive
energy balance.
Cigarettes smokers tend to have less weight as compared to non-smokers and ex-smokers. Studies have
shown that ex-smokers tend to gain weight after quiting smoking4,5,6,7.
The obese have a high incidence of body image problems and disturbances in perception and conceptual
organization of certain physiological states8. A reduction in psychological stress and improvement in self-
esteem are noted in obese when they loose weight. As a consequence of
20
Khalid U Khayyam et al: Continental J. Medical Research 2: 20 - 23, 2008
overweight many persons experienced job discrimination, public redicule, embarrassment, withdrawn, fear
or worry.9,10,11,12
This prospective study was aimed to determine the association of addiction and psychosocial behaviour
with obesity in urban population.
Table 1: Distribution of Obesity According to Addiction
Alcohol Tobacco Smoking Pan-Masala Pan Drug None

Subjects
Obese 9 6 12 11 49 0 371
(n=458) (2.0) (1.3) (2.6) (2.4) (10.7) (0) (81.0)
Non 27 184 177 169 254 0 2724
Obese (0.8) (5.2) (5.0) (4.8) (7.2) (0) (77.0)
(n=3535)
Chi square 7.08 13.8 5.37 5.62 6.84 0 3.61
1 d. f
P 0.01 0.001 0.05 0.02 0.01 0 0.10
Figure in bracket indicates percentage of the value above it.
MATERIAL AND METHODS

This prospective study was carried out in and around urban health training center of Department of
Community Medicine, Jawaherlal Nehru Medical College, Aligarh Muslim University, Aligarh, Utter
Pradesh, INDIA.
At screening, weight and height were measured, and Body Mass index (BMI) calculated as weight/ height2
(kg/m2) was used as an index of relative weight. Persons with BMI>30 kg/m2 were considered obese and
those with BMI between 20-24.9kg/m2 were considered non obese. Total persons screened were 3993, out
of which 458 were obese and 3535 were found non- obese. Information on lifestyle characteristics and
psychosocial behavior was received by pre-designed questionnaire.
Addiction:
Alcohol/ tobacco chewing/ smoking/ pan masala/ pan/ drugs/ none
Psycho- social behaviour:

Withdrawn/self-conscious/ loneliness/ emotional deprivement/ anxiety/ depression/ none. Data were
analysed using percentage and chi-square test.
RESULTS
Table 1 shows that distribution of obese and non-obese in accordance with the addiction. Obesity was more
prevalent in individuals who were less addicted to tobacco (1.3%), smoking (2.6%) and pan masala (2.4%).
Addiction to alcohol (2%) and pan (10.7%) was more prevalent among obese as compared to non-obese.
Table 2 shows the distribution of obese and non-obese subjects in accordance with psychosocial
behaviours. The prevalence of obesity was more in individuals having abnormal psychosocial behaviours
like withdrawn (3%), self conscious (51.1%), loneliness (5%), anxiety (14%) and depression (12%) as
compared to non-obese.
21
DISCUSSION
In the present study we found that obesity was more prevalent in those consuming alcohol and pan as
compared to those addicted to tobacco and smoking .The findings are similar to other studies. Garrow et
al4, James6, Garrison7 , Glanser et al5 found that people who smoke cigarettes tend to be less in weight than
non-smoker and ex-smoker tend to gain weight. Goya and Gerald13 demonstrated a positive relation
between alcohol consumption and body weight irrespective of type of drink consumed. In prospective
analysis, heavy drinking was associated with increased weight gain, and this was most apparent in men
who had never smoked. In individuals who already have hypertension, even moderate consumption of
alcohol readily increases serum triglyceride leading to obesity14.
Table 2: Distribution of Obesity According to Psycho- Social Behaviour

Withdrawn Self Loneliness Emotional Anxiety Depression None
Subjects consious deprivement
Obese 14 234 23 9 64 55 59
(n=458) (3.0) (51.1) (5.0) (2.0) (14.0) (12.0) (12.9)
Non Obese 61 424 141 70 353 389 2097
(n=3535) (1.7) (12.0) (4.0) (2.0) (10.0) (11.0) (59.3)
Chi square 1 3.19 455.0 0.98 0.0 6.72 0.38 350.83
d. f
P 0.1 0.001 0.5 N.S. 0.01 N.S. 0.001

Figure in bracket indicates percentage of the value above it.
NS = not significant
Carl9, Hammer10, Bruch 11, David12 and Judith15 also observed that obese individuals experienced more
tension and anxiety over their body image, and psychosocial stress decreases when they loose weight. No
difference was found between mental health score of overweight and normal weight persons, but anxiety
had a definite role in those people who were trying to loose weight.
REFERENCES
Anderson L, Dibble MV, Turkki PR, Mitchell HS, Rynbergen HJ.(1982): Weight control. Nutrition
in health and disease, 17th Edn : 407- 482.
Bruch M.(1973): The Psychological handicaps of the obese. Obesity in perspective. Washington DC,
2 (2), V.S. Govt. Printing Office .
Carl C, Seltzer and Jean Mayer.(1971): Body build (somatotype) distinctiveness in obese women.
Journal Am. Dietetic Ass. 55 (5): 454-458.
David Heber, Elizabeth Somar.(1986): The health risk of obesity. Weight loss and nutrition. Health
Media of American Editorial Board. 53-58.
Garrow JS, James WPT, and Ann Ralph.(1993): Obesity: Human nutrition and dietetics. Churchill
Livingstone. 9th Edn : 465- 479.
Gassison RJ, Feinleib M, Castelliw P, Mc Nammara PM.(1983): Cigarettes smoking as a confounder

of relationship between relative weight and long term mortality, JAMA, 249:2199-2203.
Glanser SC,Glauser EM, Reidenberg MM, Rusy BF, Tallaride RJ.(1970): Metabolic changes
associated with the cessation of cigarettes smoking. Arch. Environment Health, 20 : 377.
22
Hammar SL, Campbell C, Campbell V, Woolley J.(1971): Treating adolescent obesity. Long range
evaluation of previous therapy. Clin. Pedia. 10 : 46.
James WPT. In Weatherall DJ, Ledingham JGG, Warrel DA. (1987): Obesity oxford textbook of
medicine, London Oxford. 8 : 35-51.
Jonathan J Braunstein. (1971): Management of the obese patient. Medical Clinic of North America,
55 (2) : 391-401.
Judith Rodin.(1993): Cultural and psychosocial determinants of weight concern. Ann. Intern.
Med,119 (7) Part 2: 643-645.
Mayer Mendelson. (1964): Psychological aspects of obesity. Med. Clin. North America. 48: 1373
1385.
Nestel PJ, Simons LA, Homma Y.(1976): Effect of ethanol on bile acid and cholesterol metabolism.
Am. J. Clin. Nutr. 29 : 1007.
S Goya Wannamethee and A Gerald Shaper.(2003): Alcohol, body weight and weight gain in middle
aged men. Am. J. Clin. Nutrition. 77 (5) : 1312-1317.
Suter PM, Hasler E, Vetter W. (1997): Effect of alcohol on energy metabolism and body weight
regulation: Is alcohol a risk factor for obesity? Nutr Rev, 55 : 157-71.

Dr. Khalid U Khayyam
HOD, Epidemiology and Public Health, LRS Institute of TB & Resp. Diseases,
Sri Aurobindo Marg New Delhi-110030. India
E-mail: dr.khalidukhayyam@yahoo.co.in
23
DIETARY GUIDELINES FOR GOOD HEALTH
Francis Olawale Abulude

Department of General Studies. Federal College of Agriculture, Akure 340001, Ondo State. Nigeria.
(Email: wilolud@yahoo.com)
ABSTRACT
The risk of developing obesity, diabetes, high blood pressure, alcoholism and heart
disease is on the increase in Nigeria, the main cause could be the eating behavior of
the populace. Varieties of private and government organizations (WHO, Cancer
Society, Heart Associations, Academy of Sciences and Ministries of Health) world
over have recommended dietary guidelines which are not difficult to implement and
inexpensive. This paper discussed the dietary guidelines which would encourage
people to modify their eating behavior in ways that are both healthful and pleasurable.
KEYWORDS: WHO, Heart Association, Food and Nutrition Board, Diet, High blood
pressure, Stroke
INTRODUCTION
The dietary guideline is known to be a total intake over a day or week, not to a single meal or certain foods.
These are designed to promote adequate carbohydrate, vitamin, protein and mineral intake. It also
emphasizes changes that will reduce the risk of cirrhosis of the liver, obesity, hypertension, stroke, heart
disease, alcoholism, arteriosclerosis and diabetes. In Nigeria, it is unfortunate the economic situation has
not permitted the populace to eat adequate and nutritious foods and lack of good guide did not make people
to consider their state of health.
Dietary guidelines have been set by a variety of private and government organizations. These guidelines are
designed to reduce the risk of developing certain diseases. One of the regulating bodies, Food and Nutrition
Board of the Nation Academy of Sciences, USA recommended intakes of nutrients that meet the needs of
almost all healthy people of similar age and gender. The recommended dietary allowances (RDA) have
become the premier nutrients standard in both the United States (U.S) and the World.
More than 40 countries now have their own RDA, but many other countries use the US RDA. These RDA
are just allowances and not requirements some people need less or more than the amount of nutrients. They
are updated about 4-5years (Table 1).
The RDA has got many uses which include, food labeling, food and nutrition information and education,
clinical dietetics, nutrient supplements and special dietary food, sample diet for food programs, guide for
food selection programs, planning and obtaining food supplies for groups, evaluation of dietary survey data
and other scientific research, developing new or modified food products just to mention a few. The RDA
outlined in Table1 is provided with ranges to allow people to determine their unique requirements. This
paper is aimed highlight the RDA intakes of nutrients that meet the needs of healthy people.
THE DIETARY GUIDELINES

A close look at each of the summarized guidelines would aid diet planning.
1. Eat a variety of foods
It is ideal to consume a variety of foods and one way to balance ones diet is to select from these
five major groups everyday. The groups are:
i. Fruit
24
Francis Olawale Abulude: Continental J. Medical Research 2: 24 - 27, 2008
ii. Vegetable
iii. Bread, Cereal, Rice and Paste
iv. Milk, yogurt and cheese
v. Meat, poultry, fish, dry-beans, eggs and nuts.
Women and adolescent girls need to eat more calcium rich and iron-rich foods. A meal consisting of beans
with gari accompanied by a glass of milk or cheese and an orange cover all groups. Fats, oils, and sugar/
sweets can be added to the diet in moderation just to increase its flavor and help deliver some nutrients.
2. Eat a diet low in fat, saturated fat and cholesterol

It is advisable to choose a low fat option among foods to leave room for the recommended servings from
the five groups. Meat, milk and its products are source of saturated fats in most diet, while dietary
cholesterol is derivable from animal sources. It is recommended that fats, oils, sweet should be used
sparingly. Intake of yogurt, milk and cheese should be encouraged. If one prefers whole milk or low-fat or
non-fat milk, one should cut or reduce the fat elsewhere in meals. “Moderation” should be the watch than
“elimination” of some groups.
3. Balance food intake with physical activity- maintains or improves your weight
It is advisable to do 30 minutes or more of moderate physical activity daily such as walking, bicycle riding,
rope skipping, jumping, just to mention a few. Less time should be devoted to sedentary activities such as
sitting. High-fat foods contain more energy per serving than other foods and may increase the likelihood of
weight gain. Generally, the more the weights gain for ones height, the higher the weight - related risk. It is
recommended that when weight loss is needed, this must be done slowly. A visit to the gymnasium for
physical exercise would be ideal.
4. Eat a diet moderate in sugars

Maintaining a nutritious diet and a healthy weight is crucial and so sugars should be eaten in moderation by
most healthy people and sparingly by people with low energy needs. Both sugars and starches can promote
tooth decay, the more they are consumed and the longer they reside in the mouth the greater the risk for
tooth decay. It is advisable to wash and rinse the mouth after each meal.
5. Eat plenty of grain products, vegetables and fruits

Most fruits and vegetables are naturally low in fat and provide many essential nutrients. Eat more of these
along with more grain products. (Bread, cereals, rice etc). A high carbohydrate diet is based largely on
plant foods that contain starch. The only plant exception is fruit which contains glucose, fructose, sucrose,
as well as pectin. From the health point of view a high carbohydrate diet consisting largely of plant foods is
a diet that is rich in fiber, nutrients, vitamins, saponin and essential fatty acids.
6. Eat a diet moderate in salt and sodium

Salt and other sodium containing ingredients are often used in food processing. Many dietary and lifestyle
choices influence blood pressure. There is no way at present to tell who might develop hypertension from
eating too much sodium. Consumption of less salt or sodium is not harmful and is recommended for the
healthy normal adult.
7. Drink alcoholic beverages in moderation

Alcoholic beverages are known to supply energy, but few or no nutrients. They are the third contributor to
energy intake for adults in the United State. Moderate intake is associated with a reduce risk of certain
forms of heart disease, stroke, cancer, liver and pancreases disease, accidents, birth defects, death by other
causes, risk for hypertension, heart failure. A moderate intake consists of two or fewer servings of 12 once
of beer, 5 ounces of wine and 1½ once of distilled spirits per day. It is advisable to drink alcohol with
meals. People with certain medications, children, pregnant women and those who plan to take part in
activities that require special attention or skill like driving should not drink. People with alcoholism usually
25
have unbalanced diets, which can impair absorption of vitamins and minerals from the gastrointestinal
tract. An associated problem
Table1. Recommended Dietary Allowance (Per day)

Nutrient Unit People above 4 years Old
Vit A Retinol equivalents 800-1000
Vit D International Units 200-400
Vit E International Units 8-30
Vit K mg 60-80
Vit C mg 60
Folate mg 0.4
Thiamin mg 1.1-1.5
Riboflavin mg 1.1-1.7
Niacin mg 14-20
Vit B-6 mg 1.3-20
Vit B-12 µg 2.4-6.0
Biotin mg 0.03-0.3
Pantothenic acid mg 5-10
Calcium g 1.0
Phosphorus g 0.7-10
Iodide µg 150
Iron mg 10 -18
Sodium mg 500
Magnesium mg 310 - 420
Copper mg 1.5 – 3.0
Fluoride mg 3.1 – 3.8
Zinc mg 12 - 15
Chloride mg 750 - 3400
Manganese mg 2.0-50
Potassium mg 2000
Selenium mg 55-70
Chromium mg 50-200
Molybdenum mg 75-250
Carbohydrate g 50-100
Fats/oils g No RDA but min of 4% of total energy intake
Fiber g 20-35
Protein g 44-56
Sugar g 70-80
Water ml 1ml/Kcal expended a day
Source: Wardlaw (1999).
is poor metabolism. Alcohol consumption decreases the absorption of many B vitamins, such as thiamin,
riboflavin, niacin and folate. All of these vitamins are important in maintaining proper metabolic and
nervous system function
FOOD LABELS TO PLAN HEALTHY DIETS.

Nutrition labeling is intended to give information concerning the energy, protein, fat, carbohydrate,
minerals and vitamins contained in a given amount of food and consumers have more nutrition information
in food labels. It is possible to determine which foods are healthful, a consumer can know how a particular
food fits into their daily nutrition needs. On the labels, important information like fat, cholesterol, saturated
fat and sodium are highlighted. It is advisable to use them to make wise choices among foods. It is
26
recommended that regulatory bodes like National Agency for Food and Drug Administration and Control
(NAFDAC) should enforce the use of labels on food packages in Nigeria.
Nutrient Density Guide in Food Choice

Nutrient density is the ratio formed by dividing a food’s contribution to nutrient needs by its contribution to
energy needs. When its contribution to nutrient needs exceeds its energy contribution the foods are
considered to have a favorable nutrient density.
To determine the nutrient density of a food, this is simply by comparing its vitamin or mineral content with
the amount of energy it provides. A food is said to be nutrient dense if it provides a high amount of a
nutrient for a relatively small amount of kcals. The higher a food’s nutrient density the better it is as a
nutrient source. Generally, nutrient density is assessed with respect to individual nutrients, for example;
many fruits and vegetables have high content of vitamin C compare with their modest energy content.
(They are nutrient dense foods for vitamin C), nonfat milk is much nutrient dense than sugared soft drink
for many nutrients. Nonfat milk has more protein, vitamin A, thiamin, riboflavin and calcium than soft
drink. Nutrient dense foods, such as nonfat and low-fat milk, lean meat beans, oranges, carrots, whole
bread and whole-grain breakfast cereals do help balance less nutrient dense foods such as cookies and
potato that many people like to eat. Eating nutrient dense foods can aid diet planning for people who tend
to consume little food including some older people and those following weight-loss diets.
CONCLUSION
This paper has highlighted the RDA intakes of nutrients that meet the needs of healthy people, but do not
take into account special needs that may require individual adaptation (physical activity, climate, aging and
clinical problems). However, it is important to follow the dietary guidelines in order to promote the
relationship between nutrient intake and high wellness, longevity and chronic disease prevention.
REFERENCE
Atherton H.V and Newlander J.A (1987). Chemistry and testing of diary products. 4th ed. CBS Publishers
and Distribution. Indiana. Pp 376.
Christie J.S. (1991). Food for vitality. Bantam ed. Transworld Publisher Ltd. London. Pp.35-76.
Fellows P. (1997). Traditional foods-processing for profits. Intermediate Technology Publishers. UK. Pp
27-193.
Food and Nutrition Board (1981). National Academy of Sciences – National Research Council:
Recommended dietary allowances, Revised, Washington, DC.
McBean L (1996). The dietary guidelines: change and implications. Dairy council Digest.67:7
Nieman D.C. Butteworth D.E and Nieman C.N (1992). Nutrition. 1st ed. Wm. C. Brown publishers USA.
Pp. 45-50
Revised Nuffield Advance Science Chemistry (1984). Teacher’s guide to food science. A special study.
Published for Nuffield-Chelsea Curriculum Trust. Longman Group, UK. Ltd.pp.16-17
Trust well A.S (1987). Evolution of dietary recommendations, goals and guidelines. American Journal of
Clinical Nutrition. 45:1060-72
Wardlaw G.M (1999). Perspectives in nutrition. 4th ed. International edition. WCB-McGraw-Hill
Companies Inc, USA. Pp 51-532.
27
CORRELATION OF SERUM URIC ACID WITH MATERNAL AGE, PARITY AND SEVERITY OF
BLOOD PRESSURE IN PRE–ECLAMPTIC PREGNANCIES
Sazina Muzammil1, Khalid Umer Khayyam2, Nayyar Parvez3

1
Department of Physiology,Hamdard Institute of Medical Science, Jamia Hamdard,Hamdard Nagar,New
Delhi-110062,INDIA. 2Department of Epidemiology and Public Health,Lala Ram Institute of Tuberculosis
and Respiratory Diseases,Sri Aurobindo Marg, New Delhi-110030,INDIA. 3Department of Pharmaceutics,
Advance Institute of Phamacy,MD University. Rohtak,Faridabad,Haryana,INDIA.
ABSTRACT
Maternal serum uric acid was determined in 30 pre- eclamptic and 20 normal
pregnant females in their third trimester. Serum uric acid was 3.52± 0.75 in normal
pregnancies and 6.03 ± 1.67 in pre- eclamptic pregnancies. This increase in serum
uric acid was highly significant (P<0.001). There was no influence of parity and
maternal age on serum uric acid. Serum uric acid levels increased significantly from
5.05±0.89 to 7.49±1.50 with increase in mean arterial pressure above 115 mmHg in
pre –eclamptic pregnancies. (P<0.01)
KEYWORDS: Serum uric acid,Eclampsia, Pre-eclampsia,Hyperuricaemia, Maternal

age, Parity, Mean arterial pressure.
INTRODUCTION
Possible biochemical indices of pre-eclampsia have been sought for many years. Amongst the many
markers which have been investigated, perhaps serum uric acid has been considered the most reliable. The
relationship between hyperuricaemia and pre-eclampsia was first noted (Slemons and Bogert 1917) and it
is now principally agreed that hyperuricaemia is a characteristic of pre-eclampsia (Hill et al 1978). Serum
uric acid is also a reliable index of foetal welfare when pregnancy is complicated by pre-eclampsia,
prognosis of foetus is poor irrespective of level of blood pressure (Verma 1982).
Serum uric acid is one of the parameter used in early diagnosis of pregnancy induced hypertension, and a
level of 5.5mg% or more can be taken as a warning sign of pregnancy induced hypertension and is
associated with increased perinatal morbidity and mortality (Ranjan et al 1996; Lim et al 1998).
Various studies have demonstrated a correlation between serum uric acid and pre-edampsia (Voto et al
1988; Koike et al 1997; Garrone et al 1997 and D’ Anna et al 2000) but information about the influence of
maternal age, parity and mean arterial pressure on serum uric acid in pre-eclamptic pregnancies is scanty.
The present study has examined the serum uric acid concentration in pre-eclamptic and normal pregnant
females in the third trimester of pregnancy. The influence of maternal age, parity and mean arterial
pressure on uric acid is studied.
MATERIALS AND METHODS

The present study was conducted on proven cases of pre-eclampsia. Thirty pre-eclamptic females in third
trimester of pregnancy were selected from Inpatient and Outpatient Department of Obstetrics and
Gynaecology, Jawaherlal Nehru Medical College,Aligarh Muslim University, Aligarh, Uttar Pradesh,
INDIA, in a period of one year ( March 2002 to February 2003). Exclusion criteria were
28
Sazina Muzammil et al: Continental J. Medical Research 2: 24 - 34, 2008
associated renal/hepatic/cardiac disorder; metabolic disorders; concomitant severe complications of

pregnancy, pregnancy less than 28 wks or more than 41 weeks, multiple pregnancy and any medication
during pregnancy except vitamins, iron and calcium (Farah et al 1993).
Previously healthy normotensive females were considered to have pre-eclampsia if their blood pressure
after 20 weeks of pregnancy was raised to >140/90 mmHg or had mean arterial pressure
(Diastolic pressure + 1/3 pulse pressure) of more than 110mmHg. The increase in blood pressure had to be
present on at least two occasions 6 hours apart along with proteinuria of more than 300mg/day or
100mg/dl.
Twenty females with normal pregnancies in third trimester were matched on an individual basis for same
parameters and were taken as controls.
Table 1. Serum uric acid (mg/100ml) in normal and pre-eclamptic pregnancies:

Normal pregnancy (n=20) Pre- eclampsia
(n=30)
Uric acid (mg/100ml) 3.52±0.75 6.03±1.67*
Age
<25 yrs 3.48±0.64 5.58±1.07
>25 yrs 3.56±0.81 6.4±1.97
Parity
Primipara 3.78±0.63 5.73±1.49
Multipara 3.26±0.8 6.32±1.85
MAP
110-115 - 5.05±0.89**
mmHg
- 7.49±1.5
>115 mmHg
* P<0.001 ** P<0
All females were between 20-40years of age (mean age 25.53±3.9 years).
Estimations of serum Uric acid: Phosphotungstate Method (Brown 1945 and Martinek 1970)
Test principle
Uric acid in alkaline medium reduces phosphotungstic acid to “Tungsten Blue” a blue coloured complex
which is measured calorimetrically.
Procedure
Preparation of working solution:
0.5 ml of stock uric acid standard was diluted to 50 ml with distilled water and mixed well.
Step A : Deproteinization of sample
29
I ml of serum and 8 ml of distilled water was taken in clean, dry test tube to which 0.5 ml sulphuric acid,
2/3 N (Reagent 1) 0.5 ml sodium tungstate and 10% W/N (reagent 2) was added, mixed well and allowed to
stand for 10 minutes and then centrifuged.
Step B :
Three dry and clean test tubes serving as blank ‘B’, standard ‘S’ and test ‘T’ were taken. 1 ml of sodium
carbonate, 14% W/N (Reagent 3) and phosphotungstate (Reagent 4) were added to three test tubes. Then 3
ml of supernatant filtrate (from step A) was added in test ‘T’ test tube, 3 ml of working reagent was added
in standard ‘S’ test tube and 3 ml distilled water in blank ‘B’ test tube. Contents of all three test tubes were
mixed and allowed to stand in dark for 15 minutes. Optical density (OD) of blank (B), standard (S) and test
(T) were measured against distilled water on colorimeter using red filter or at 710 nm wave length.
10
Uric acid (mg/100 ml)
0
Normal pregnancy (n=20) Pre-eclamptic pregnancy
(n=30)
Figure 1 : Serum uric acid in normal and pre-eclamptic pregnancies
Calculation
Serum uric acid (mg/100ml) =
O.D test – O.D. Blank
------------------------------------- X 10
O.D. standard – O.D. blank
Statistical Analysis
Values were expressed as mean ± SD. Statistical analysis was done using student ‘t’ test. Results were
considered significant if ‘p’ valve was <0.05. Correlation between serum uric acid and mean arterial
pressure was determined by co-efficient of correlation (r).
RESULTS
The comparison of serum uric acid in normal and pre – eclamptic pregnancies is shown in Table 1 ( Fig –
1). There was a highly significant increase in serum uric acid from 3.52±0.75 in normal to 6.03 ± 1.67 in
pre- eclamptic pregnancies (p<0.001).
Serum uric acid in two age group (below 25 years and above 25 years) in normal and pre-eclamptic
pregnancies is shown in Table 1. There was no significant changes in two age group (P>0.05) both in
normal and pre- eclamptic pregnancies.
Uric acid levels were studied in two parity groups i.e. primiparous and multiparous. No significant change
(P>0.05) was seen in two parity groups.
30
Pre – eclamptic females were divided into two groups according to (MAP) mean arterial pressure (i) MAP
110-115 mmHg (ii) MAP> 115 mmHg. The normal pregnant females had mean arterial pressure below 110
mmHg. Uric acid levels increased significantly from 5.05 ± 0.89 to 7.49 ± 1.50 with increase in mean
arterial pressure above 115 mmHg (P<0.01) (Table 1, Fig 2)
Fig 3 is showing the correlation between mean arterial pressure and serum uric acid. There was a direct
positive association between serum uric acid and mean arterial pressure (r= 0.8, P<0.001) which was highly
significant.
DISCUSSION
The present study demonstrated that serum uric acid levels were significantly elevated in pre-eclamptic
pregnant females as compared to normal pregnant females. There was no effect of maternal age and parity
in both groups on uric acid levels. But uric acid levels increased significantly in pre-eclamptics with rise in
mean arterial pressure more 115 mmHg. Strong positive correlation was seen between serum uric acid and
mean arterial pressure.
10
Uric acid (mg/100ml)
9
8
7
Figure III : Correlatio
6
5
4
3
2
1
0
MAP 110-115 mmHg (n=18) MAP >115 mmHg (n=12)
Figure 2: Comparison of serum uric acid in pre-eclamptic women with 2 levels of mean artesial pressure
(MAP)
It has been more than 60 years since association between hyperuricaemia and toxemia was first noted1
During that time the theories advanced to explain this relationship have included, placental production of
uric acid (Fadel et al 1969) starvation (Diekmann 1952) lactic acidosis (Handler 1960), excessive muscle
exertion (Crowford 1941) hepatic damage (Cadden and Stander 1939) decreased glomerular filtration rate
(Schaffer et al 1943) and renal cellular damage (Treadwell and Dixon 1961).
In normal pregnancy glomerular filtration rate increases in first trimester and then remains stable until term.
The clearance of uric acid, however continues to change as pregnancy advances. Upto 16 weeks of
gestation there is decline in serum uric acid concentration and increase in execration of uric acid. From 16th
–36th weeks serum uric acid increases whereas excretion remains constant (Hytten and Lind 1973).
In pregnancy induced hypertension there was impaired glomerular filtration rate and an increased tubular
reabsorption of uric acid, leading to impaired uric acid clearance and thereby increasing serum uric acid
concentration. Although both glomerular filtration rate and clearance of uric acid were shown to decrease
in pre-eclampsia, there was no direct correlation between glomerular filtration and renal handling of uric
acid (Chesley and Williams 1945).
31
Increased oxidative stress and formation of reactive oxygen species had been proposed as another
contributing source of hyperuricaemia noted in pre- eclampsia (Many et al 1996).
Although hyperuricaemia is an acknowledged characteristic of pre- eclamptic toxaemia, (Plass 1924) did
not consider the level of uric acid to be an index of severity of disease (Pitchard and Stone 1967) found no
evidence to suggest that those with highest serum uric acid were more seriously ill.
According to some worker increased accumulation of lactic acid might lead to decrease excretion of uric
acid and thereby resulting hyperuricaemia associated with pre – eclampsia (Stander and Cadden 1934;
Quick 1932).
It was demonstrated that a significant but week correlation between serum uric acid levels and blood
pressure (Lim et al 1998) but another study showed a highly significant positive correlation as was also
shown in this study (Hickman et al 1982).
Blood Pressure (BP)
Figure 3 : Correlation of mean arterial pressure with uric acid
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Varma TR,(1982): Serum uric acid levels as an index of fetal prognosis in pregnancies complicated
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Sazina Muzammil,
Department of Physiology, Hamdard Institute of Medical Science, Jamia Hamdard,Hamdard Nagar, New
Delhi – 110002, INDIA.
34
THE VIRULENCE OF PLASMODIUM FALCIPARUM INFECTION IN HUMAN HOST
Anyanwu, E.B. 1, Onyesom, I2., Okperi, B3., Awusi, V.O. 3, Mabiaku, T.O3. Umukoro D.O.3
1
Department of Family Medicine, 3Department of Paediatrics Faculty of Clinical Medicine, 2Department of
Medical Biochemistry, Faculty of Basic Sciences, Delta State University. Abraka, Nigeria.
ABSTRACT
Malaria causes an acute febrile illness which may be characterized by periods of
fibrile paroxysms. The severity and course of an attack of malaria depends on species
and strains of the infecting parasite. Mankind is infected by four species of the genus
Plasmodium but Plasmodium falciparum is associated with the highest degree of
parasitaema due to high yields of merozoites per schizonts. The malignancy of
Plasmodium falciparum is peculiar to that species. This review highlights some of the
reasons why infection by Plasmodium falciparum may be malignant and more
virulent than the other plasmodia species.
KEYWORDS: malaria parasite, virulence, merozoite, sequestration.
INTRODUCTION
Malaria is the most important parasitic disease of man. The human disease is a protozoa infection of red
blood cells which is transmitted by the bite of blood-feeding female anopheles mosquito (White, 1996)
Malaria is found throughout the tropical region of the world, most of the Sub – Saharan Africa, South
America, South East Asia and the Western Pacific Areas (Lucas, and Gilles, (1987), Gilles, (1993a).
Malaria transmission occurs in more than 100 countries of the world. More than one billion inhabitants of
these countries are exposed to risks of malaria infection. The estimated annual global incidence of malaria
is over two million cases (White, (1996), Strickland, (1991).
Malaria is highly endemic in Nigeria and is one of the major causes of ill- health and deaths. The risk of
malaria exists throughout the country but is greater in the rural areas. Malaria leads to about 10 percent
deaths in children under five years of age and similarly, it causes about five percent of death in Uganda
(National Malaria and Vector Control Division , (1991), Bitawaha et al, 1997).
The causative agent of this parasitic disease is Plasmodium. In nature, malaria is transmitted from man to
man by a female anopheles mosquito while taking a blood meal. About 60 species of anopheles mosquitos
are important vectors and are found most frequently in tropical and sub – tropical regions.
About 40 species have been identified in Nigeria, but the major vectors of human malaria are Anopheles
gambiae, Anopheles arabiense, Anopheles funestus, and Anopheles melas. Out of the six zoo-geographical
regions of the world, the most important vector in the Afro – Tropical zone including Nigeria is the
Anopheles gambiae (Service, 1993).
Mankind is infected by four species of the genus Plasmodium. These are Plasmodium falciparun,
Plasmodium ovale, Plasmodium vivax and plasmodium malaria.
Plasmodium ovale has been reported predominantly from East and West Africa. It is uncommon outside
Africa.
Plasmodium vivax is the major species in the temperate zones, Central America, and the Indian sub-
continent. But Plasmodium falciparum has increased in India over the last decades. This is due to the
transfer of anopheles mosquitoes on board of aircraft during stop – over’s in endemic zones. This is why
35
Anyanwu, E.B et al: Continental J. Medical Research 2: 35 - 38, 2008
International regulations sanctions the spraying of planes with insecticides in malaria zones before take off
(Bouree et al, 1993).
Plasmodium malaria is less common but is found in most areas especially in West and Central Africa.
Plasmodium falciparum predominates in the Sub – Saharan Africa, Papua New Guinea and Haiti
(Isselbacher et al, 1994)
The severity and course of an attack of malaria depends on the species of infecting parasite, on the age of
the patient, state of immunity, general health and nutritional status of the patient.
Falciparum malaria is responsible for almost the entire 2 million deaths attributed to malaria each year
worldwide. Of all the species of plasmodia, Plasmodium falciparum is the most highly pathogenic, and is
associated with malignant type of malaria. It is the chief infection in areas of endemic malaria in Africa,
and in a non- immune patient, it usually runs an acute course. Such course could be fatal unless promptly
treated with specific drugs. Plasmodium falciparum is associated with the heaviest degree of parasitaemia.
Infection with human malaria begins when the feeding female anopheline mosquito inoculates plasmodial
sporozoites into the human host (Table 1). These migrate into the liver cells and the process of asexual
reproduction called pre – erythrocytic schizogony starts.
This process result into schizonts which enlarge, while the nucleus and cytoplasm divides to form
thousands of merozoites, which eventually leads to the rupturing of the liver cells. This process librates
thousands of merozoites into the circulation to penetrate red blood cells.
The sporozoites of Plasmodium falciparum yields about 30,000 – 40,000 merozoites per sporozoite, while
the merozoites yield per sporozoite is lower in the other species (Gilles,1993b).
Also, the nuclear division is faster in the Plasmodium falciparum species.
Table 1: Some comparative character of sporogonic and schizogonic stages of four species of human
plasmodium
Species Duration of Duration of pre – Hypnozoite Number of
sporogony in erythrocytic stage in human merozoite in pre-
anopheles (at erythrocytic
280C) schizont
P. vivax 8-10 days 6-8days + 10, 000
P. malaria 14-16days 14-16days 0 15, 000
P. ovale 12-14days 9days + 15, 000
P.falciparum 9-10days 5½ – 7days 0 30, 000
Source: Gilles, (1993b)
The malignancy of falciparum malaria is peculiar to that species. The merozoite emerging from the liver
are considerably more numerous than those of the other species.
Also, the merozoites of Plasmodium falciparum appear to enter the erythrocytes more efficiently than the
merozoites of the other malaria parasites.
Plasmodium falciparum is the only human malaria parasite that is found in equal numbers in erythrocyte of
all ages. Plasmodium vivax for example, invades primary the reticulocytes, while Plasmodium malariae
seems to prefer the older, natural red blood cells (Gilles, 1993b).
Again, the severity of malaria infection caused by Plasmodium falciparum is made even worse by the
increasing resistance to commonly used anti-malaria drugs. Resistance to chloroquine has been documented
in most countries with falciparum transmission over the last two decades and resistance to other alternate
36
anti-malarial drugs has followed in many counties of the world (Olatunde, (1977), Eke, (1979), Salako,
and Fedeke-Aderounmu, (1987), Oduola (1992), Hagos (1993).
Some prior treatment is extremely common, particularly in developing countries where drugs such as
chloroquine are sold across the counter for treatment of fevers and suspected malaria. This action has
helped in a very large way in spreading resistant strains of falciparum malaria.
Another factor that aids the virulence or malignancy of Plasmodium falciparum is the process of
sequestration of parasitized red blood cells. At about 24-26 hours of development of the parasite in the
human host, the falciparum parasite which has infected red blood cells disappears from the circulation by
attachment or cycle-adherence to the wall of venules and capillaries in vital organs vis-a-vis, brain heart,
placenta, spleen, intestine and bone marrow (Gilles , 1993). It has been demonstrated that sequestration of
red blood cells containing mature forms of the parasites in capillaries and post-capillaries venules appears
to be a constant feature of severe falciparum malaria (Macpherson et al, 1985). Most of the fatal cases
show blocking or occlusion of the capillaries by clumps of red blood cells harbouring developing parasite,
huge number of which can be seen in smears and sections of post-mortem materials.
This process of sequestration leads to reduction in the supply of oxygen and other nutrients to the affected
organs. Notably, sequestration is not seen in the other relatively bargain human malaria.
REFERENCES
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(1997). Herbal Treatment of Malaria-four cases reports from Rukararewe Partnership Workshop for rural
development (Uganda). Tropical Doctor ; 27 (Suppl 1): 17-19.
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Eke, R.A (1979). Possible Chloroquine Resistant Plasmodium Falciparium in Nigeria. A J Trop Med Hyg;
28 (6); 1074-1075.
Gilles. H.M (1993a). Epidemiology of Malaria. In: Gilles, H.M. and Warrel, D.A (Eds). Bruce-Chwatts
Essential Malariology. 3rd edition. Great Britain, Edward Arnold (Publisher);. pp. 124-164.
Gilles, H.M (1993b). The Malaria Parasite, In: Gilles H.M., and Warrel, D.A (eds). Bruce- Chwatt’s
Essential Malariology. Great Britain, Edwin Arnold (Publisher),. pp. 12-34
Hagos, B., Khan, B., Ofulla, A.V.O., Kariuki, D., and Martin, S.K (1993). Responses of Falciparum
malaria to Chloroquine and three-second line antimalaria Drugs in a Kenya Coastal School Age
Population. East Afr Med J.; 70 (10); 620-623.
Isselbacher, K.J., Braunwald, E., Wilson, J.D., Martin, J.B., Fauci, A.S., and Kasper, D.L. (1994) (Eds).
Protozoal infection: Malaria. In: Harrison’s Principles of Internal Medicine. 13th edition. McGraw – Hill
Inc. USA;. pp. 307 – 310
Lucas, A.O., and Gilles, H.M (1987). The Protozoal Disease, Malaria. In: Luca, A.O., and Gilles, H.M.
(Eds). A Short Textbook of Preventive Medicine for the Tropics. 2nd edition. ELBS;. pp. 189-196.
Macpherson, G.G., Warrel, M.J., White N.J., Looareesuwan, S., and Warrel, D.A (1985). Human Cerebral
Malaria. A quantitative ultrastructure analaysis of parasitized erythrocyte sequestration. AJP , 119 (3); 385
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FMOH (1991). Malaria in Nigeria: Epidemiology and Control. Nig. Bull Epidemiol .; pp. 2-19.
Oduola, A.M.J., Sowunmi, A., Milhouse, W.K., Kyle, D.E., Markin, R.K., Walker, O (1992). Innate
Resistant to new Antimalarial Drugs in Plasmodium Falciparum from Nigeria. Trans Roy Soc Tropl Med
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Olatunde, A (1977). Chloroquine Resistance Plasmodium Falciparum and Malaria in Africa. Trans Roy
Soc Tropl Med Hyg, 71 (1) , 80-81
Salako, L.O., and Fedeke-Aderounmu, A (1987). In-vitro Chloroquine and Mefloquine Resistant
Plasmodium Falciparum in Nigeria. The Lancet,; pp. 572-573.
Service, M.W (1993). The Anopheles Vector. In: Gilles, H.M., and Warrel, D.A. (Eds) Bruce-Chwatt’s
Essential Malariolgy. 3rd edition. Great Britain, Edward Arnold (Publisher);. PP. 96-123.
Strickland, G.T (1991). Infections of the Blood and Reticuloendothelial system Malaria. In: Strickland,
G.T. (Ed), Hunter’s Tropical Medicine. 7th edition. Philadelphia; W.B. Saunder’s Company;. pp. 584-614.
White, N.J (1996). Malaria. In: Cook, G.C. (Ed); Manson’s Tropical Disease. 20th edition. London; WB
Saunder’s Company;.

Anyanwu, E.B.
Department of Family Medicine, Faculty of Clinical Medicine, Delta State University. Abraka, Nigeria.
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Continental J.

Medical Research 2: 1 - 5, 2007

ANTIBIOTICS COMMONLY USED IN THE TREATMENT OF ACUTE OROFACIAL BACTERIAL

KEYWORDS: Orofacial bacterial infections, Anitbiotics, General dental practice,

Table 1 Types / number of acute orofacial infections reviewed per hospital

MATERIALS AND METHOD

Antibiotic Prescribed, % Duration prescribed, %

Acute infection Amp Pen Metr Eryth 3 days 5 days 7days

Acute dento-alveolar abscess 69 13 9 9 5 91 4

Key: ampicillin (Amp), Penicillin (Pen), metronidazole (Metr), erythromycin (Eryth)

Ingham H R, Hood F J C, Bradburn P, Tharagonnet D, Selkon J B, (1977). Metronidazole compared with

Lacey R W, (1984). Evolution of microorganisms and antibiotic resistance. Lancet; 2: 1022-1025.

Lewis M A O, MacFarlane T W, McGowan D A, (1986). Quantitative bacteriology of dentoaveolar

Lewis M A O, MacFarlane TW, McGowan D A, MacDonald D G, (1988). Assessment of the Pathogenicity

Schuen N J, Panzer J D, Atkinson W H, (1974). A comparison of clindamycin and penicillin in the

von Konow L, Nord C E, (1983). Ordnidazole compared to phenoxymethylpenicillin in the treatment of

Williams B L, McCann G F, Schoenknecht F D, (1983). Bacteriology of dental abscess of endodontic

Received for Publication: 07/11/2007

Zagga AD1 and Saidu SA2

Normal anatomy of the sella turcica.

Large sella without local bone destruction

Large sella with local bone destruction or erosion

Erosion of undersurface of anterior clinoid processes and chiasmatic sulcus

Erosion of upper surface of anterior clinoid processes

Localized erosion of floor

Erosion of dorsum and posterior clinoid processes

Local bony sclerosis and change in texture

Changes in sella in increased intracranial pressure

Erosion of top of dorsum sellae:

Changes in anterior clinoid processes:

Erosion of lamina dura

Erosion of top and back of dorsum sellae

Erosion of planum sphenoidale:

Changes in sella in childhood.

Changes in sella with relief of raised intracranial pressure.

Received for Publication: 07/11/2007

POST PRANDIAL BLOOD PRESSURE CHANGES IN PATIENTS WITH CHRONIC RENAL

Onyemekeihia UR1, Esume CO 2, Bamgboye LE,3 Anyanwu BE4

KEYWORDS: Postprandial, blood pressure, changes, patients, chronic renal failure,

TABLE 1: MEAN BP AT VARIOUS TIMES DURING HD

TIME(HR) TEST(MMHG) CONTROL(MMHG)

recognized in 1977 by Seyer-Hanseen in a patient with Parkinson’s disease (Seyer-Hanseen 1977).

TABLE 2: BP WITH RESPECT TO SEX AT VARIOUS TIMES

0 hr 1 hr 2 hrs 3hrs 4hrs

females 173 23 172 29 186 29 184 30 188 28

AIMS AND OBJECTIVES

MATERIALS AND METHOD

There was no isolated Systolic Blood Pressure Postprandial hypotension.

Hypotension though a complication of hemodialysis may be worsened by eating during or before

to splanchnic sequestration or decreased vascular resistance due to splanchnic vasorelaxation (Barakat et

Seyer-Hansen K. (1977): Postprandial hypotension. Br Med. J. 2:1262

Received for Publication: 28/12/2007

AN EPIDEMIOLOGICAL STUDY OF ADDICTION AND PSYCHOSOCIAL BEHAVIOUR AND RISK

Khalid U Khayyam1, Sazina Muzammil2, Mohd Yunus1, Zulfia Khan1

Method: A prospective study in an urban health training center of

Conclusion: The addiction of alcohol, pan and abnormal psychosocial behaviour

KEY WORDS: Obesity, Addiction, Psychosocial behaviours, Urban population,

Table 1: Distribution of Obesity According to Addiction

Alcohol Tobacco Smoking Pan-Masala Pan Drug None

MATERIAL AND METHODS

Psycho- social behaviour:

Table 2: Distribution of Obesity According to Psycho- Social Behaviour

P 0.1 0.001 0.5 N.S. 0.01 N.S. 0.001