Gout

Gout develops when chronic hyperuricaemia allows monosodium urate (MSU) crystals to deposit in joints and peri-articular tissues. The crystals are engulfed by immune cells, activating the NLRP3 inflammasome and producing a powerful inflammatory response. That response brings neutrophils into the joint, which explains the abrupt onset of severe pain, warmth, erythema, swelling, and marked tenderness. A flare is the visible consequence of crystal-driven inflammation; it is not the same as the underlying urate burden. Crystals may remain after the pain settles, so untreated hyperuricaemia can produce repeated attacks, tophi, reduced range of motion, and progressive joint destruction. The first metatarsophalangeal joint is the classic site, a pattern called podagra. Knees, ankles, and other peripheral joints can also be affected. Chronic kidney disease increases risk because urate excretion falls. Other contributors include thiazide or loop diuretics, cyclosporine after transplant, obesity and metabolic syndrome, alcohol—particularly beer and spirits—purine-rich foods, and fructose-sweetened beverages. Postmenopausal loss of oestrogen’s uricosuric effect also increases risk. Hyperuricaemia alone does not establish gout. The clinical pattern and, when needed, crystal analysis determine whether the patient has gout or...