Aetiology of Gout and Hyperuricaemia
1-Increased production of uric acid
2-Decreased renal excretion of uric acid
• Renal failure • Lead poisoning • Alcohol • Drugs-diuretics, low-dose aspirin, pyrazinamide,
cyclosporin, levodopa • Lactic acidosis • Hyperparathyroidism • Myxoedema • Down's syndrome
• Unidentified inherited defects
• The full natural history of gout comprises four stages:
1. Asymptomatic hyperuricaemia.
2. Acute gouty arthritis.
3. Intercritical period.
4. Chronic tophaceous gout (tophi and chronic gouty arthritis).
• The onset may be insidious or explosively sudden.
• The metatarsophalangeal joint of the great toe is the site of the first attack of acute gouty arthritis (podagra) in 70% of patients.
• Other joints that can get affected include tarsal joints, ankles, knees and wrists. Central joints such as hips, shoulders and spine are seldom affected, possibly because higher temperatures in these joints are not conducive to crystallisation.
• The affected joint is hot, red and swollen with shiny overlying skin and dilated veins. The joint is excruciatingly painful and tender. These joint manifestations may be associated with anorexia, nausea, fever, leucocytosis and raised ESR.
• The joint manifestations may last only a day or two, or up to several weeks, but characteristically subside spontaneously.
• Gout can also cause bursitis and tenosynovitis.
• This is followed by an asymptomatic phase (intercritical period) that is diagnostically important.
• In chronic tophaceous gouty arthritis, crystal deposits appear in cartilage, synovial membranes, tendons and soft tissues. The classic location of a tophus is the helix and antihelix of the ear.
• Nephropathy is seen in 90% of subjects with gouty arthritis. Two types of parenchymal renal damage have been described:
• Urate nephropathy results from deposition of urate crystals in the interstitial tissue, leading to alburninuria, isosthenuria or renal failure.
• Obstructive uropathy (nephrolithiasis) results from the fonnation of uric acid crystals in the collecting tubules, renal pelvis or ureter with blockage of urine flow. The formation of urate calculi is favoured by hyperuricosuria, purine overproduction, excessive purine ingestion, uricosuric drugs and acidic urine.
• Gout may be associated with increased incidence of hypertension and cardiovascular disorders.
• On the other hand, hypertension is also a risk factor for development of gout.
Cardinal features of gout
• Increase in serum uric acid concentration (>7.0 mg/dL in males and >6.0 mg/dL in females)
• Recurrent attacks of a characteristic acute arthritis, in which crystals of monosodium urate monohydrate are demonstrable in leucocytes of synovial fluid
• Aggregated deposits of monosodium urate monohydrate (tophi) in and around the joints
• Renal disease involving interstitial tissue and blood vessels
• Uric acid nephrolithiasis
• Serum uric acid levels are elevated. However, during an acute attack serum uric acid may be normal in 50% cases.
• Synovial fluid examination done by compensated polarised microscopy can demonstrate urate crystals. They are seen as slender, needle-shaped and negatively birefringent structures.
• Plain radiographs are helpful to differentiate chronic tophaceous gout from RA.
• Erosions in gout are characteristically punched out with overhanging sclerotic margins and are situated away from joint margins, sometimes outside the joint capsule.
• RA causes marginal erosions, always within the limits of the joint capsule. Periarticular osteopenia is absent and joint space is preserved in gout.
• Avoidance of alcohol.
• Avoidance of meat and seafood. However, consumption of oatmeal and purine-rich vegetables (for example, peas, beans, lentils, spinach, mushrooms and cauliflower) does not produce increased risk of gout.
• Controlled weight reduction in obese patients.
TREATMENT AT DR. SOHAN LAL CLINIC
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