Gout

Gout is a form of inflammatory arthritis characterised by episodic attacks of acute joint inflammation triggered by the deposition of monosodium urate (MSU) crystals. These crystals form in joints, tendons, and surrounding tissues when blood uric acid levels (hyperuricaemia) exceed the saturation threshold — typically above 360 µmol/L (6 mg/dL).

Gout is the most common inflammatory arthritis in men and its prevalence is rising worldwide, driven by increasing rates of obesity, hypertension, renal disease, and diuretic use. It is more common in men (who develop it 3–4 times more frequently than women) and typically begins between ages 30 and 50. After menopause, women's rates approach those of men.

**How uric acid accumulates:**

Uric acid is the end product of purine metabolism. The body produces uric acid when it breaks down purines — compounds found naturally in all cells and in certain foods. Uric acid normally dissolves in the blood and is excreted by the kidneys. Hyperuricaemia results from either overproduction of uric acid, underexcretion by the kidneys, or both.

**Triggers and risk factors:** - Diet rich in purines: red meat, organ meats, shellfish, oily fish - Sweetened beverages and foods (fructose promotes uric acid synthesis) - Alcohol, especially beer (high in purines) and spirits - Obesity and metabolic syndrome - Hypertension, chronic kidney disease, and heart disease - Medications: thiazide diuretics, low-dose aspirin, ciclosporin, pyrazinamide - Family history (genetic predisposition to hyperuricaemia) - Dehydration, trauma, surgery, or sudden illness (triggers acute attacks in the setting of existing hyperuricaemia)

**Clinical stages:**

1. *Asymptomatic hyperuricaemia:* elevated uric acid without symptoms; treatment is not routinely indicated but risk factors should be addressed 2. *Acute gout flare:* sudden onset of severe monoarticular pain, swelling, warmth, and redness — classically in the first MTP joint (podagra), but any joint can be affected (ankle, knee, wrist, elbow, fingers). Pain peaks within 12 hours and typically resolves spontaneously in 7–14 days without treatment 3. *Intercritical gout:* asymptomatic intervals between attacks; MSU crystals persist in the joint 4. *Chronic tophaceous gout:* repeated attacks without adequate urate-lowering therapy lead to tophus formation (palpable deposits of MSU crystals under the skin at fingers, ears, elbows, and tendons), persistent joint inflammation, and erosive joint damage

**Complications:** kidney stones (uric acid nephrolithiasis), chronic kidney disease, and cardiovascular disease (gout is associated with an increased risk of myocardial infarction and stroke).

**Treatment:**

*Acute attacks:* NSAIDs (indomethacin, naproxen), colchicine, or corticosteroids (oral or intra-articular injection). Begin as early as possible — ideally within the first few hours.

*Long-term urate-lowering therapy (ULT):* allopurinol or febuxostat, targeting a serum urate below 360 µmol/L (below 300 µmol/L in tophaceous gout). Initiated after the acute flare has fully resolved.

*Lifestyle:* low-purine diet, adequate hydration, weight loss, alcohol reduction, medication review.