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A disorder of purine metabolism characterized by hyperuricaemia, deposition of mono sodium urate monohydrate crystals in joints and per-articular tissues and recurrent attacks of acute synovitis. Late change include cartilage degeneration, renal dysfunction & uric acid urolithiasis

  1. Epidemiology
    1. Hyperuricaemia serum urate concentration higher than (7mg/dl) for men & 6mg/dl L for women
    2. About 5% of men & <1% of women have hyperuriacemia the majority suffer no pathological consequences and they remain asymptomatic throughout life.
    3. Although the risk of developing clinical features of gout increases with increasing levels of serum uric acid, only a fraction of those with hyper uricaemia develop symptoms
    4. Any factor that causes either an abrupt increase or decrease in the serum urate levels may provoke an acute attack, the best correlations being factors that cause an abrupt fall.
    5. Serum uric acid levels can be normal or low at the time of acute attack, Since lowering of uric acid with hypouricemic therapy or other medications limits the value of serum uric acid determination for diagnosis of gout.
    6. Despite these limitations, serum uric acid is almost always elevated at some timeQ and can be used to follow the cource of hypouricemic therapy
  2. Pathology
    Tophi (=porous stone) are nodular deposits of monosodium urate monohyd rate crystals, with an associated foreign body reaction. It is deposited in minute clumps in connective tissue eg.
    1. Articular cartilage (mc. in small joints of hands & feet)
    2. Tendon (not muscle)
    3. Bursae eg, olecranon bursa
    4. Periarticular tissue
    5. Synovium & joints
    6. Pinnae (cartilage) of ear
    7. Ligaments
    8. Articular ends of bone
    9. Subcutaneous tissue
    10. Kidney
    11. Tophi may ulcerate through skin or destroy cartilage & periarticular bone
  3. Clinical Feature
    1. Sterotype patient is obese, hypertensive male and fond of alcohol
    2. Acute attack is sudden onset of severe joint pain that lasts for a week or two, usually comes out of blue but may be precipitated by minor trauma, illness, unaccustomed exercise or alcohol, steroid withdrawal, hypouricemic therapy, MI, stroke
    3. The commonest sites are metatarsophalangeal joint of big toe > ankle & finger joints and olecranon bursae.
    4. The skin is red, shiny, swollen, hot and extremely tender suggesting a cellulitis or septic arthritis.
    5. Characteristic negatively birefringent urate crystals in the synovial fluid examined by polarizing microscopy is diagnostic. During acute gouty attack strongly birefringent needle and rod shaped mono sodium urate (MSU) crystals with negative elongation are largely intracellular.
    6. During acute attack x- rays show only soft tissue swelling. Chronic gout may result in joint space narrowing & secondary OA Tophi appear as characteristic punched out cysts or deep erosions with over hanging bony edges(Martel’s or G’ sign). These well-defined erosions are larger & slightly further from joint margin than typical RA erosions.
  4. Treatment
    1. Mainstay of treatment during acute attack is administration of antinflammatory drug such as colchicine, NSAIDs (except aspirin) or glucocorticoids
    2. NSAID’s & colchicine may be toxic in elderly particulary in renal insufficiency & g.i. disorders. So glucocorticoids may be prefered.
    3. Uricosuric drugs (probenecid or sulfin pyrazone) can be used if renal function is normal. Allopurinol, a xanthjne oxidase inhibitor is usually preferred.
    4. These drugs should never be started in acute attack, and they should always be covered by an anti-inflammatory preperations or colchicine; otherwise they may actually precipitate an acute attack.
    5. In chronic tophaceous gout and in all patients with renal complications, allopurinol is drug of choice.

Recent Advances: Losartan, fenofibrate and amlodipine have some mild uricosuric effects.


Recent Advances: New Drugs (Ref. Hari 18th ed., Pg-2838)

  1. Febusostat = Xanthine oxidase inhibitor drug (LQ 2012)
  2. Benzbromarone It is new uricosuric drug
  3. Rasburicase: It converts purine to allantois which is a water soluble compound. (LQ 2012)

Basic Biochemistry: Purine pathway. Allopurinol blocks the conversion of xanthine to uric acid. The urate oxidase rasburicase catalyses the oxidation of uric acid to allantoin, a highly water-soluble metabolite readily excerted by the kidney.

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