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Adi Asraf b Yusof
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` Gout is defined as a peripheral arthritis resulting
from the deposition of sodium urate crystals in one
or more joints.
` Uric acid or urate (its salt) is the end product ofpurine metabolism
` Ethnic groups in Malaysia and China have higher
mean urate levels than most Caucasian
populations.
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` Typical sequence involves progression through: asymptomatic hyperuricemia
acute gouty arthritis
x Acute, self limiting, monoarticular
x Lower limbs more commonly affected
interval or intercritical gout
chronic or tophaceous gout
x Polyarticular, formation of tophi
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` Tophi chalky deposits of MSU crystal
Subcutaneous & painless
Firm, nodular & fusiform swelling Common sites include, digits of hands and feet
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Feature Typical Gout Elderly onset
Age of onset Peak in mid 40s Over 65 yrs
Sex distribution Men > women Men = women,
If over 80 yrs old
men < women
Presentation Monoarticular
Lower extremity
(podagra mostly)
Polyarticular
Upper extremity
Tophi After yrs of attack May occur early
Associated feature Obesity
Hyperlipidemia
HPT
Heavy drinker
Renal insufficiecy
Diuretic use
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` Clinical diagnosis Fulfill 2 out of 4 criteria
x History of at least 2 attacks of painful joint swelling with
complete resolution within 2 weeks
x Clear history/observation ofpodagra
x Presence of tophus
x Rapid response to colchicine within 48 hrs after tx started
` Definitive diagnosis Synovial fluid analysis (monosodium urate, MSU crystal
seen in synovial fluid)
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` a painful condition of the big toe caused by gout
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` Baseline investigation Full blood count (FBC)
Renal profile
RBS
Lipid profile
Urinalysis
` Further investigation 24-hour urinary excretion
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` Useful if renal calculus prove to be urate in nature
` Indicated if uricosuric agent used
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` Joint aspiration Definitive
Based on synovial fluid char + crystal identification
(MSU)
` Skeletal X-ray Usually normal in acute gouty arthritis
Chronic tophaceous gout: soft tissue abnormalities +
erosive bone lesion
` Renal imaging
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Acute gouty arthritis Chronic tophaceous gout
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` Aim to: Achieve IBW
Prevent acute attacks of gout
serum urate level
` Weight reduction gradual (0.5-1 kg/week)` Restrict alcohol intake - renal excretion of purine
` Reduce purine-rich food intake (i.e. red meat,seafood)
` Consume low fat dairy product` Maintain adequate fluid intake (2-3L)
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Asymptomatic Hyperuricaemia
` Serum urate conc abnormally high (male: >7.0 mg/dL,female: 6.0 mg/dL)
` But with no signs/symptoms of urate deposition
` Investigate the contributing factors` If drug-induced (i.e. thiazide diuretics), discontinued or
changed if clinically appropriate.
` Generally, no pharmacologic treatment required
unless Persistent severe hyperuricaemia
Persistent elevated urinary excretion of urate
Tumour lysis syndrome
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` group of metabolic complications that can occur after
treatment of cancer, usually lymphomas and leukemia,
and sometimes even without treatment. These
complications are caused by the break-down products
of dying cancer cells and include hyperkalemia,
hyperphosphatemia, hyperuricemia and
hyperuricosuria, hypocalcemia, and consequent acute
uric acid nephropathy and acute renal failure.
` Treatment targeted at specific metabolic syndrome
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` Acute Gouty arthritis` NSAIDs
Any NSAIDs other than aspirin Rapidly effective in inflammation and pain, particularly ifgiven right
away after acute attack. C/I in pt with hx of peptic ulcer disease, hypertension, renal impaired &
cardiac failure` COX2 inhibitor
For those at risk ofpeptic ulcer disease or intolerant to NSAIDs Better safety profile in terms ofgastric bleeding C/I in pt with active peptic ulcer disease, HPT, renal impaired and cardiac
failure.
` Colchicine Alternative drug for those C/I with both NSAIDs and COX2 inhibitor However, most prominent side effect is profuse diarrhea thus limit it
usefulness particularly in elderly pt.
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` Acute Gouty arthritis
` Glucocorticoids In elderly people and those C/I with either NSAIDs & COX2
inhibitor, glucocorticoids may be preferred.
Only forshort term treatment, thus side effects are rare
Several RoA are available; intrarticular, intramuscular and also
oral.
`
Allopurinol* Not to be started unless the acute attack had resolved
If pt on long term allopurinol, DO NOT STOP the treatment
during acute attack
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` Chronic Gouty arthritis Aim to reduce sUA level < 6.0mg/dL
Started afteracute attack well controlled (1-2 wks)
NSAIDs, colchicine DO NOT urate level
Hypouricaemic drugs NO analgesic + anti-
inflammatory effect
Lifelong treatment
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` Allopurinol Xanthine oxidase inhibitor -> hypouricaemic drugs
Superior than probenecid
Adjust in renal impaired pt
In normal pt start at 100-150mg OD, increase by 100-
150mg every 4 weeks -> 300mg OD
Max dose: 800mg daily
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` Probenecid Alternative to allopurinol
C/I in pt with UA overproduction + overexcretion, urate
nephropathy
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` Urate nephropathy urine output
x Maintain water intake of 3L/day or more
x In ESRF, limit fluid intake
urine pH
x Target urine pH: 6.5 7
x Potassium citrate
urate excretion
x By dietary purine intakex Allopurinol
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` Urate nephrolothiasis Radioluscent in nature
Ultrasound imaging preffered
Extracorpeal shockwave lithotripsy & percutaneous
nephrolithotomy can be used to treat intrarenal stones (5-
15mm) and complex staghorn stones
Pure urate stones readily chemolysed by potassium
citrate or sodium bicarbonate.
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25
Purine nucleotides
Hypoxanthine
Xanthine
Uric acid
Xanthine
oxidase
Alimentary
excretion
Urinary
excretion
Tissue deposition
in excess
Urate crystal microtophi
Phagocytosis
with acute
inflammation
and arthritis
Uricosurics
Colchicine NSAIDs
Allopurinol
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` Last resort
` Considered in Advanced tophi deposition -> major joint destruction
Loss of joint movement + severe pain Tophi collection -> pressure symptom
Tophaceous ulcer
Cosmetic (i.e. ear lobe tophi)
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` CPG: Management ofGout (Oct 2008)
` MICROMEDEX(R) Healthcare Series Vol. 146
` Lexi-Comp Drug Information Version 1.4.1
` http://www.gout.com/professional/gout_information/prevalence_and_incidence.aspx
` MOH Drug Formulary 2009
` http://www.merriam-webster.com
` http://www.buzzle.com/articles/purine-rich-foods.html
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