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GOUT ARTHRITIS

Blondina Marpaung
Rheumatology Division
Internal MedicineDepartment
Medical Faculty Sumatera Utara University

Hippocrates abad ke-5 :


Podagra
Galen abad ke-3 :
Tophi
Leeuwenhoek 1679 :
Tophi crystal
SYDENHAM 1683
self suffered Gout
- clinical finding

SCHEELE 1776:
Uricacidinurine
-renalstone

WOLLASTON
Uricacidfromthopus

GARROD 1856
HyperuricaemiatestinGout
EMIR FISCHER
Structureofpurine
-Corelationuricacidwithpurine

Inflammation process due to crystal deposition in tissue joint /


deposisi kristal asam urat pada jaringan sendi/sekitar (tophi).

Gout (gutta/drop) exist as evil drop


in to joint

The King of Diseases and The Disease of King

GOUT ARTHRITIS = JICHT = PIRAI = GOUT


METABOLISM DISORDER
DISORDER
:-Arthritis acute violent recurrent parroxysms
- Hyperuricemia
- Deposits Sodium Urate ( Thopi )
- Calculi Uric Acid ( Kidney )
HYPERURICEMIA:1.OverProductionofUricAcid
HYPERURICEMIA
2.ReducedExcretion
3.Combination1&2
NORMAL VALUE:Man
3,5-6,0mg/100cc
VALUE
Women3,0-5,0mg/100cc

NEVER GOUT :

Hippokrates

1.EUNUCHHippokrates

2.BeforeMENOPAUSE

3.BeforeCOITUS

MANwillsufferedgoutifknow
andpassionateawoman
Womanwillsufferedgoutifdoesnt
passionateaman

Gout
Clinical syndromes due to monosodiumurat monohidrat (MSU) crystal deposit
Deposit cristal MSU at the joint will arise
acute inflammation attack
Onset acute : attack on acute artritis
monoartikuler leg joint
Complete remision, remision with high
frequency that occurs more frequently

Painful

arthritis episodic

intermitten,

monoarticular, foot thumb,


ankle and knee joint

Can

develop to oligo or poliartikuler

Tends
Can

to NSAID and steroid abuse

be trigger by stress, ex operation,


blood tranfusion.

Perjalanan Klasik Gout

3 stage : hiperurikemia asimptomatik, gout akut


intermiten dan gout kronik tofaseous

The stage from hiperurikemia asimptomatik to


gout kronik tofaseous is variation from a patient
to another.

Dependent from factor endogen and factor


eksogen.

Artritis Gout Akut

Gout acute attack is so painful.

Mainly occurs at early morning and its peak in


couple of hours.

The patient cant prop up their own weight, more


over touch the blanket also can make the patient
in pain.

The skin color is red and hot, body sudfebril,


leukositosis, LED and CRP elevation.
Diffrential Diagnose: infection

Urid acid level in serum cant be use to diagnose a


Gout, the level can be high, normal or decrease.

Analizing joint liquid with polarize microscope can


diffrentiate gout or infection/pseudogout.

Gout attack phase


1. monosodium urat crystal presipitation (consentration > 9
mg/dl)
- cartilage
- synovium
- para articular tissue (bursa)
- tendon and tendon sheath
* Uric acid sheated with protein stimulates
neutropil with IgG crystal formation.

2. Response leucocytePMN :
Crystal produces chemotaksis factor
PMN response
crystal phagoscytosis by leucocyte.
3. phagoscytosis :
Cristal difagositosis by leukosit
formates phago lisosom
vakuole membrane been surrounded by
kristal join with membrane leukositik lisosom.

4. Kerusakan lisosom
Hidrogen binding with the cristal surface nenbrane
lisosom.
damage the membran lisosom,
and release the enzim and radical oxide in the
sitoplasma.

5. Cell damaging
enzim lisosom release in the sinovial fluid
imflamation response elevation intensity
tissue damaging

Uric acid :
ThemainEndProductfromMet.Purine.
excreted:-viaKidney
-viaintestinaltract.
NormalG.F.R.+Hyperuricaemia
uricacidexcretionviaurine:Normal
except:
uricacidconcentration>9mg/100ml
inserum
High uric acid concentration
Notalways:GOUT
Renalstone

SERUM URIC ACID :


:
Higherlevel

Longerduration(persistent)

Higherpossibilityhavegout

INCREASED FORMATION OF URIC ACID :


1.SPECIFICENZYMEABNORMALITIES
=HYPOXANTINE-
GUANINPHOSPHORIBOSYL
TRANSFERASEACTIVITY
=PHOSPHORIBOSYLPYROPHOSPHATE
SYMTHETASEACTIVITY
2.TURNOVEROFNUCLEOPROTEIN
=DIET(PURINES)

DECREASED EXCREATION OF URIC ACID


1.ALTERATIONINRENALFUNCTIONAND
CONTRACTIONOFEXTRACELLULAR
FLUIDVOLUME
2.DRUGS(DIEURETICS)
3.LACTICACIDAEMIA
4.STARVATIONANDKETOSIS
5.ESSENSIALHYPERTENTION
6.LEADPOISIONING
7.HYPERCALCAEMIA

Urate crystals from synovial fluid


viewed with compensated
polarised light

Slide8

AllOverTheWorldAndRas
NegroLess
SouthEastAsiaandPasific
Polynesia&Micronesia
Filipines(inU.S.)
Maori(NewZealand)10.2/100(highst)
INDONESIA??
Intakepurine,alcohol
clearanceuricacid
kidneyfunction&hypertension

FILIPINA
NEWZEALAND
POLINESIA
LesserUricacidexcretion
Lowintakepurinefromdiet
Changesdietpattern(highpurine,alcohol)uricacid
serumlevelincrease,alwayshaveGOUT

CLINICAL FEATURES :
MTP-Iacuteandexplosive
fever&malaise
uricacidstone
recurrentafter1-2years
tophi:MTP,olecranon,synovium,bursa,achilles
forearm,helixoftheear
pres.factor:-stress
-trauma
-dehydration
-purine&alcoholintake
-drug

Slide 11

Slide 6

Slide 7

Classicpodagra:acutegoutyarthritisoffirstmetatarsophalangealjoint

Acute gouty olecranon bursa

Deforming gouty arthritis

Gout patient :
Kidney stone is the first sign, before is
gouty arthritis
AS.U.DARAH
5 - 7 mg%
7 - 9 mg%
9 - 11 mg%
11 - 13 mg%
13 mg%

PADA
83
472
498
144
38

BATU (%)
9 = 11%
87 = 18%
123 = 25%
41 = 28%
20 = 53%

AS.U.URINE
300 - 500
500 - 700
700 - 900
900 - 1100
1100

PADA
360
317
154
39
18

BATU (%)
72 = 20%
66 = 21%
53 = 34%
15 = 40%
9 = 50%

Serum Uric Acid


8 mg %
8 - 9 mg %
9 - 10 mg %
10 - 11 mg %
11 mg %

90%
70%
50%
46%
29%

without tophi
without tophi
without tophi
without tophi
without tophi

5 th

70%

without tophi

10 th
15 th
20 th
40 th

50 %
39%
29%
26%

without tophi
without tophi
without tophi
without tophi

RONTGENT :
PUNCHED-OUTAREAPADAPERMUKAANSENDI
BONEEROTION
JOINTDESTRUCTION
SUBCUTANEUSTOPHI
CALCIFICATIONOFTOPHI
ASIMMETRICALPERIARTICULERSWELLING

DIAGNOSIS APPROACH
Suspect Gout :
Monoartritis at young male
Artritis acute at MTP I, talocruralis or knee
Artritis with hiperurisemia

Aspiration and joint fluid analyze

MSU +

Using light
microscope
And polarization

Check serum uric acid


And
Urine uric acid 24 hours

MSU

See the 12 criteria ACR


Do it match 6 from
12 criteria that its have

Gout

Not Gout

Observation and evaluate


others examination

DIAGNOSIS :
Anamnese&clin.Features
Uratecrystalinthejointfluid
Uratecrystalinthetophi
CholchisineResponseDramatically
(oral:1-48h;IV:1-12h)

PRESENCEF 6 OF THE FOLLOWING 12 :


1.Morethanoneattack

2.Max.inflam.Developedwithin1day
3.Attackofmonarticulararthritis
4.Jointredness
5.MTP-Ijointpaintfullorswollen
6.UnilateralattackinvolvingMTP-I

7.Unilateralattackinv.Tarsaljoint
8.Suspectedtophus
9.Hyperuricemia
10.Asimetricswellingwithinajoint
11.Subcorticalcystwithouterosion
12.Neg.microorganismcultureofjointfluid

DIFFERENTIAL DIAGNOSIS :
Pseudogout
RheumatoidArthritis
RheumatoidVariant
Osteoarthritis
Sarcoidarthritis
PsoriaticArthritis
InfectiousArthritis
Cellulitis
AcuteBursitis
AcuteRheumaticFever

Hiperurikemia

Its not the only conditin to diagnose Gout.

The Risk from gout rise with the stage and the
longer of hiperurikemia

Hiperurikemia can be cause by a lot of condition,


genetic or acquired, metabolic or renal.

Hiperurikemia asimptomatic cant make the things


worst before it turn to Gout.

PENGOBATAN GOUT
Prevent

acute attack: cold compress, NSAID,


kolkisin, (artrosentesis)
Change the life style
Cure the disease thats occur
Avoid the risk factors, ex drugs
Defend the normourikemia
Proflaksis to avoid the acute attack

Immediatecontrolofacuteattack
PreventRecurrent
PreventComplications
1.=Colchisine:0,6mg/h,max.7mg/d(oral)

2mginSaline20cc,max.4mg(i.v)

=NSAID

2.URICOSURIC:Probenecide,Sulfinpyrazon

3.URICOSTATIC:Allupurinol(Zyloric)

Beware of Over diagnose and over


treated
Simptommuskuloskletalandhyperuricemia
butNon-Goutnoneededdrugloweringuricacid

Pengobatan artritis gout akut

Colchicine, NSAIDs dan kortikosteroid, cold application,


arthrocentesis can be use to prevent the acute attac

Terapy to make the serum uric acid decreace, therefore is


best not to be done in acute phase, it will slow down the
healing process.

The drug choosing is depend on efication, attack condition


and the patient condition.

Colchicine
Prevent
Block

fagositosis uric cristal by neutrofil

the realease of chemotactic factors

Decrease

the mobility and adhesi leucosyt


polimorfonuklear

Prevent

phosphorilation of tyrosin and forming


leukotrin B4

Inhibits upregulated neutrophil-endothelial adhesion

Increases cAMP

Inhibits crystal-induced tyroisne kinase activation

Selectively inhibits mediator release (e.g. decreases


IL-1 and chemotactic cytokine release, but not IL-1 ra
antagonist)

Inhibits crystal-induced PLA2 activity, and PLAP and


LTB4 release

Colchicine Oral
Efective dose is closer to the side effect in traktus
gastrointestinal
Primary dose 1 mg, continue with 0.5 mg after 2
hour until it feel discomfort at abdomen / diare or
total dose 8 mg.
The pain loss in 18 hours & diare 24 hour.
75- 80% pasien inflamation decrease in 48
hours
Caution to patient with liver and kidney problem
and to old person.

Acute Gout prophylaxis therapy

Acute Gout attack can be prevent with small


dose of colchicine or OAINS.
Profilaksis therapy must be given before
lowering hiperurikemia level been done.
Profilaksis with colchicine, proven to prevent
the recurrent attack, whether in normal level of
uric acid or not.
The period of the therapy is at least one year
after serum uric acid concentration is back to
normal.
May be added NSAID if colchicine is proven
ineffective.

WHEN TO TREAT
HYPERURICEMIA?
If

the cause is uncorrected, for example


obesity, hypertension, hypercholesterolemia.
Two or three true gout attack per year.
Gout with tophy.
Gall bladder stone > 800 mg/day.
Tumor lysis (acute uric acid nefropathy risk).

URICOSURIC AGENT
PROBENECID
SUPHINPIRAZONE
-Renaltubularreabsorptioninhibition.
-Increasingurinaryoutput
SALICILATEDOSISTINGGI

URISCOSTATIC AGENT
ALLOPURINOL
-COMPETITIVELYINHIBIT
XANTINEOXIDASEENZYME.
-PURINEBIOSYNTHESISSUPPRESSION
SERUMANDURINEURICACIDDECREASING
CONCENTRATION
USUALDOSE300-400mgSINGLEDOSE
(INITIALDOSE100mgGRADUALLY
INCREASINGDOSE)

Rapidlydecreasinguricacidserum,causing

goutattackbythebeginning/firstweekmay
appear,indicationfor:
-COLCHISINE3x05,
-PHENYLBUTAZON3x100,
-INDOMETHACINE3x25,
-NSAID

Uricosuric agent
Increase uric secretion. Indicated for low uric
clearance patient.
Dangerous if high urine uric acid concentration.
Contraindicated for low urine stream ( <1
ml/minute), kidney stone history or inadequate
renal function ( CCT < 50 ml/m)
Probenesid 1 g - 2 g /day, effect(-) if CCT < 50
ml/m
Sulfinpirazon 50 100 mg 2x/day, gradually
increase by 200 - 400 mg 2X/day. Ineffective if
renal impairment exist.

Xanthine-oxidase inhibitor
(Alopurinol)
Preventing late stage of uric acid synthesis.
Indicated for high uric acid production
Main side effect alopurinol : hypersensitivity
Capable of lowering uric acid serum in
overproduction and under excretion or both
Given dose is adjusted by creatinine swap
value.

GOUT AND DIET


Purine

in diet :
NOT NECESSARILLY CAUSING concentration
serum uric acid of more than 1.0 mg/dl.
ADEQUATE Purine consumption (compared to
constant low purine diet) indicated to those
who usually consume high purine diet.
Low purine diet consumption in HIGH
QUANTITY produce INCREASING PURINE
LOAD than high purine consumption in small
quantity.

BAHAN MAKANAN YANG BOLEH DAN TIDAK BOLEH


DIBERIKAN

INGREDIENTSUNPROHIBITED
PROHIBITED
FOOD

FOOD
carbo
hydrate

all-

animal
protein

meat/chicken,
tuna,
tenggiri,bawal,
bandeng50g/h
egg,milk

sardine.clamshell,heart,
liver,gut,spleen,lung
brain,meatextractdaging/kaldu
duck,bird

protein

beans,
emping25g,
tofu,tempeand
oncom50gsehari

fat

limitedamountof
oil


INGREDIENTSUNPROHIBITED
FOOD
vegetable

allvegetablesexcept
asparagus,beans,spinach,
cauliflower
mushroommax50gperday

PROHIBITED
FOOD
-

fruit allfruitisavailable

drinks

tea,coffee,soda

alcohol

spices

allspicesisavailable

yeast

PREVENTION ATTACK
I. avoidance

a.farwalking

b.tightshoes
c.longperiodofdriving
d.repetitive/heavyhandwork
e.physicalandmentallyfatigue
f.emotionalstress
g.excessivepurine
h.alcoholdrinking
i.longtermofdiureticuse
j.longtermofaspirinuse

II.Weightlosingdietandlowpurineintake

(highpurineingut,sardine,clamshell, duck,
yeast,cauliflower,etc)
III.DailyAllopurinol
IV.Lifetime/longtermAllopurinolin:

-morethan5attacksayear
-tophyexistence
-renalstoneexistence
-urate-nephropathyexistence
V.NSAIDorColchicineavailability

When The pasient need to


be consult

Do not ignore septic joint

Fever before and during monoarthritis


indicating septic arthritis
Persistent Monoarthritis (and fever) despite the
given NSAID or colchisine, indicating septic
arthritis.
If there hesitation, septic arthritis therapy given
Gout and septic arthritis may occur together!

Signs of impaired renal function.


Acute gout attack occurs very often and pain is
unmanageable pain
If etiology is uncorrected
Multiple tophies and large tophy that tends to
damage the joint or secondary infection

THANK YOU