Gout flares result from uric acid crystal deposition in joints — triggering intense inflammation. Flares are often precipitated by dietary purine intake (red meat, shellfish, organ meats), alcohol (particularly beer), dehydration, certain medications (diuretics, low-dose aspirin), illness, or surgery. The first metatarsophalangeal joint (big toe) is classically affected.

Treatment initiated within the first 24 hours of a flare produces significantly faster resolution. NSAIDs, colchicine, or oral corticosteroids — started early — are all effective. Waiting to start treatment allows the inflammatory response to amplify and prolongs the flare duration and severity substantially.

Urate-lowering therapy (allopurinol, febuxostat) should not be started or adjusted during an acute flare — changes in uric acid levels can prolong or trigger new flares. It is initiated 2–4 weeks after the flare fully resolves, with anti-inflammatory prophylaxis co-prescribed for the first 3–6 months to prevent flare mobilization.

Diet modification can modestly reduce uric acid levels — limiting red meat, shellfish, organ meats, fructose-sweetened beverages, and alcohol (especially beer) helps. However, dietary changes alone rarely normalize uric acid to target levels in people with recurrent gout. Medication is usually required for sustained prevention.

NSAIDs carry GI and renal risks — take with food and limit duration. Colchicine commonly causes diarrhea and GI upset, particularly at higher doses; the low-dose regimen is better tolerated. Corticosteroids cause short-course side effects including blood sugar elevation. Allopurinol may cause rash — rarely, the serious DRESS syndrome; HLA-B*5801 testing reduces this risk in high-prevalence populations. Gout Flare (Gout Attack) visit What to expect from a Gout Flare (Gout Attack) visit