Gout

Gout is the most common inflammatory arthritis in men. It is caused by chronic hyperuricaemia (urate >360 μmol/L), leading to crystal deposition when the physiological saturation point is exceeded. Risk factors include male sex, obesity, high-purine diet (e.g., red meat, seafood), alcohol (especially beer), and medications such as thiazide diuretics and low-dose aspirin. An acute attack is characterised by rapid onset (often overnight) of severe pain, redness, and swelling. Between attacks, patients are typically asymptomatic, but chronic gout can lead to 'tophi' (white urate deposits under the skin) and joint destruction. Management is split into acute symptom control and chronic prevention through Urate Lowering Therapy (ULT). NICE (NG219) now recommends a 'treat-to-target' approach for all patients after the first or second attack, aiming for a serum urate level <360 μmol/L (or <300 μmol/L in severe/tophaceous gout).

Uric acid is the end-product of purine metabolism, excreted primarily by the kidneys. Hyperuricaemia arises from either overproduction (e.g., cell turnover in malignancy, Lesch-Nyhan syndrome) or, more commonly, under-excretion (e.g., CKD, diuretics). When urate concentrations exceed solubility in synovial fluid, monosodium urate (MSU) crystals precipitate. These crystals are phagocytosed by macrophages, which triggers the NLRP3 inflammasome pathway. This results in the release of pro-inflammatory cytokines, particularly Interleukin-1β (IL-1β), leading to the recruitment of neutrophils and the classic intense inflammatory response of an acute flare.

An acute flare presents with the 'cardinal signs of inflammation': Dolor (pain), Calor (heat), Rubor (redness), and Tumor (swelling). The pain is often so severe that patients cannot tolerate the weight of a bedsheet. While the 1st MTP is most common, the midfoot, ankles, and knees are also frequently involved. Chronic gout results in polyarticular involvement and tophi, typically found on the ear helix, olecranon bursa, or Achilles tendon. Complications include 'punched-out' bone erosions on X-ray and urate urolithiasis (kidney stones). Gout is also a strong marker for metabolic syndrome and cardiovascular disease.

- Bedside: Joint aspiration (Gold Standard) showing needle-shaped, negatively birefringent MSU crystals.
- Bloods: Serum uric acid (wait 2-4 weeks after a flare for accurate baseline); Renal function (affects drug dosing); CRP/WBC (elevated during flare).
- Imaging: X-rays in early gout are normal or show soft tissue swelling; chronic gout shows 'punched-out' erosions with sclerotic margins and overhanging edges.

Acute Flare: First-line is either an NSAID (e.g., Naproxen, Diclofenac) or Colchicine (500mcg 2-4 times daily). Oral steroids are an alternative if others are contraindicated. Do not stop or start Allopurinol during an acute flare. Chronic Management (ULT): Offer Allopurinol to all patients with a firm diagnosis. Start at 100mg OD (lower in CKD) and titrate up every 4 weeks until urate <360 μmol/L. Co-prescribe Colchicine (500mcg BD) for the first 3-6 months of ULT to prevent titration-induced flares. Febuxostat is second-line for those intolerant to Allopurinol. Lifestyle: Weight loss, reduced alcohol and purine intake.