Gout

A chronic disease caused by deposition of monosodium urate crystals in joints, soft tissues and kidneys. Gout occurs when serum uric acid is sufficiently elevated (usually >0.42mmol/L), though acute gout can occur with a normal serum uric acid, and asymptomatic hyperuricaemia is itself a risk factor for developing gout. Incidence increases with age; rare before menopause in women, rare in children.

Risk factors

• Purine-rich foods (meat, seafood), alcohol (beer, spirits), fructose- sweetened drinks — though the evidence for meat specifically triggering attacks in established gout is weak, and avoiding seafood should be weighed against its cardiovascular benefits
• High cell-turnover states (haematological malignancy, severe psoriasis)
• Drugs reducing renal urate excretion: thiazide/loop diuretics, ciclosporin
• Comorbidities: hypertension, CKD, dyslipidaemia, T2DM, obesity (high endogenous insulin also inhibits renal urate excretion)
• Catabolic states (sepsis) or dehydration
• Any rapid rise or fall in serum urate can precipitate/prolong an acute attack — including starting/increasing urate-lowering therapy (ULT) or other dietary changes

Clinical features

Acute gout:

• Usually monoarticular — classically the first MTP joint (“podagra”) or elsewhere in the foot; very painful, red, swollen; may mimic septic arthritis; may present with fever, malaise, leucocytosis and raised inflammatory markers
• Untreated, an attack typically subsides over days to 1–2 weeks
• In women, the first attack may be polyarticular (hands) and with tophi
• Without ULT, most patients have a second attack within 2 years
• Ischaemic heart disease, hypertension and CKD are independent risk factors for recurrence
• Young-onset or atypical presentations warrant caution — don’t assume gout explains all oligoarthritis without confirming the diagnosis (registry: ajgp-gout-oligoarthritis-case-2021; verified 2026-07-23)

Chronic gout:

• Untreated recurrent attacks may fail to resolve fully, progressing to chronic destructive arthritis
• May be oligo/polyarticular with symmetrical small-joint involvement mimicking RA or psoriatic arthritis (urate can also be elevated in psoriasis from increased cell turnover, further confusing the picture)
• Tophi typically at the elbows (olecranon bursae), knees (prepatellar bursae) and peripheral joints — untreated, tophaceous gout is destructive and disabling

Diagnosis

• Definitive diagnosis requires monosodium urate crystals under polarised microscopy in synovial/bursal fluid or a tophus — worth confirming, since gout requires lifelong ULT
• Serum urate should be measured in all suspected cases, but a normal result does not exclude an acute attack
• Colchicine response supports a crystal arthritis diagnosis but does not distinguish gout from CPPD (pseudogout) — it doesn’t replace aspiration
• Plain X-ray may show joint damage; check renal function (both a risk factor for, and a consequence of, gout — affects treatment choice/dosing)
• Ultrasound and dual-energy CT scan may help if the diagnosis is uncertain and aspiration isn’t feasible/available.

Management

General principles

Rapid symptom relief for acute attacks; lifelong ULT; flare prophylaxis when starting/increasing ULT; address modifiable risk factors and comorbidities (especially cardiovascular risk).

• Switch or reduce a contributing diuretic if clinically feasible
• Losartan and fenofibrate have modest uricosuric effects — may be preferable choices for hypertension/dyslipidaemia respectively if otherwise appropriate
• Low-dose aspirin modestly inhibits urate excretion, but given gout’s strong cardiovascular comorbidity it should usually be continued, adjusting ULT as needed
• Patient education (nature of disease, need for lifelong ULT adherence, lifestyle advice) — Arthritis Australia has patient information on Gout” and “Gout and diet”. “There is strong evidence lifestyle factors increase gout risk, but only weak evidence that correcting them improves outcomes once established
• Adherence and long-term engagement remain the biggest barrier to good gout outcomes in practice — patients are often under-treated to target or mistakenly stop ULT during a flare (registry: ajgp-chronic-gout-barriers-2018; verified 2026-07-23)

Acute attack

• Any NSAID may be used; indomethacin is traditional (short-acting, easily titrated) but not mandatory
• Systemic corticosteroids (oral or IM) are as effective as NSAIDs with fewer acute adverse effects: prednis(ol)one 15–30mg daily until symptoms abate (typically 3–5 days)
• Colchicine reduces pain/inflammation but has a high GI side-effect burden: 1mg initially, then 500microg 1 hour later (total 1.5mg as a single-day course); further low-dose regimens (e.g. 500microg 8–12 hourly) may be considered if symptoms persist, but total dose should not exceed 6mg over 4 days — reduce dose in renal impairment
• Paracetamol as an analgesic adjunct only, not monotherapy
• Local corticosteroid injection is appropriate for 1–2 affected joints/bursae once infection is excluded
• Continue ULT during an acute attack if already established — do not stop it

Long-term: urate-lowering therapy

Lifelong ULT is recommended for all patients with confirmed gout, titrated using a treat-to-target approach. Target serum urate:

• <0.36mmol/L (6mg/dL) for non-tophaceous gout
• <0.30mmol/L (5mg/dL) for tophaceous gout

Allopurinol (first-line, xanthine oxidase inhibitor): start 50mg daily for 4 weeks, then increase by 50mg every 2–4 weeks (or 100mg every 4 weeks) to target, up to 900mg/day maximum. Reduces azathioprine/mercaptopurine metabolism — avoid combination or reduce their dose. Allopurinol hypersensitivity syndrome is rare but potentially fatal (rash, fever, hepatitis, eosinophilia, worsening renal function). Probenecid (weak uricosuric) may be added if target not reached on monotherapy.

Febuxostat (second-line, xanthine oxidase inhibitor) or probenecid: febuxostat 40mg daily, increasing by 40mg every 2–4 weeks to a maximum of 120mg/day. Not recommended with pre-existing major cardiovascular disease; use cautiously in hepatic/moderate-severe renal impairment; same azathioprine/mercaptopurine interaction as allopurinol.

Flare prophylaxis (when starting/increasing ULT)

• Colchicine has the strongest evidence: 500microg once or twice daily (reduce in renal impairment)
• NSAIDs if colchicine contraindicated/ineffective
• Oral corticosteroids under specialist advice only (prednis(ol)one 5mg daily) — long-term adverse effects
• Combination colchicine + NSAID or prednis(ol)one for multiple recurrent attacks despite prophylaxis; avoid concurrent NSAID + corticosteroid (increased GI toxicity, no added benefit)
• Continue prophylaxis for at least 6 months (longer with tophi), generally until attack-free and target urate achieved