Drugs for Gout
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Direct answer
Treat the attack first, lower urate second — the two agendas of gout therapy must never be swapped. An acute flare responds to a full anti-inflammatory dose of an NSAID (indomethacin or naproxen), low-dose colchicine (1 mg at onset, then 500 µg after one hour, then 500 µg every 8–12 hours — the modern regimen that ended the old "dose until diarrhoea" teaching), or oral prednisolone 30–40 mg when renal disease forbids the others. Urate-lowering therapy — allopurinol 100 mg daily as the first-line start, titrated monthly toward a serum urate below 6 mg/dL — is indicated for recurrent attacks, tophi, radiographic damage or urolithiasis, and is continued lifelong. Urate targets do not treat pain; anti-inflammatories cover the first months of urate lowering while crystal mobilisation can provoke flares.
What you must remember
- Acute flare triad: NSAID (naproxen 500 mg twice daily with a proton pump inhibitor), colchicine 1 mg then 500 µg an hour later, or prednisolone 30–40 mg for about five days; ice and rest the joint.
- Colchicine inhibits microtubule-mediated neutrophil migration; toxicity is gastrointestinal (diarrhoea precedes toxicity as the classic warning); dose-reduce in renal impairment and with strong CYP3A4/P-gp inhibitors — the fatal combination is clarithromycin plus colchicine in renal failure.
- Allopurinol: xanthine oxidase inhibitor, first-line including most chronic kidney disease; start 100 mg daily (even lower in severe renal impairment) and titrate — starting high triggers flares and the allopurinol hypersensitivity syndrome (SJS/TEN, especially with renal dysfunction).
- *HLA-B5801** screening is recommended before allopurinol in Han Chinese, Thai and Korean populations; Indian data also report the association, so a family history of severe allopurinol reactions should steer therapy to febuxostat.
- Febuxostat 40–80 mg is the alternative xanthine oxidase inhibitor; the CARES trial reported more cardiovascular deaths, so it is second-line with cardiovascular caution.
- Uricosurics (probenecid) suit under-excretors with preserved renal function and no stones; losartan has a mild uricosuric effect — a neat trick for the gouty hypertensive.
- Never start or abruptly stop urate-lowering therapy as sole management of an acute flare — anti-inflammatory cover is required; aspirin at low dose paradoxically raises urate.
- Asymptomatic hyperuricaemia is not treated with drugs in routine practice; Indian labs report it constantly and over-treatment is a genuine outpatient error.
A typical exam case, worked through
A 46-year-old businessman wakes with an exquisitely painful, red, swollen first metatarsophalangeal joint after a beer-and-meat dinner. Serum uric acid drawn that morning is actually normal or low — acute inflammation is uricosuric — so the diagnosis rests on clinical pattern, and aspiration showing negatively birefringent needle crystals settles doubt. He gets naproxen 500 mg twice daily with food; within 48 hours he walks. Three flares in a year qualify him for urate-lowering therapy: once the current flare has fully settled, start allopurinol 100 mg daily with colchicine 500 µg twice daily as flare prophylaxis for the first three to six months, and titrate allopurinol monthly by 100 mg toward urate under 6 mg/dL — under 5 mg/dL if tophi are present.
Six weeks later he returns with a milder flare despite therapy — this is expected crystal mobilisation, not drug failure; keep allopurinol going, treat with colchicine, and continue titration. If he later develops stage 4 chronic kidney disease with a documented severe rash history, switch to febuxostat 40 mg, counsel on cardiovascular risk, and recheck urate. The full pathway — attack first, cover the induction, titrate to target, treat for life — is exactly the sequence NBE options try to scramble.
Where students slip
Two mix-ups dominate. The first is analgesia versus urate control: a stem describing an acute first metatarsophalangeal flare asks for the immediate drug, and the correct answer is an NSAID or colchicine, never allopurinol — candidates who mechanically link "gout = allopurinol" lose the mark. The second is timing: modern guidance permits starting allopurinol during a settling flare with anti-inflammatory cover, but the principle that urate-lowering alone does not treat pain still frames every question. Finally, remember that thiazides and low-dose aspirin raise urate while losartan lowers it — a hypertension-stem crossover that appears when a gouty patient needs a diuretic; the swap is losartan, or amlodipine, and fenofibrate (uricosuric) is the lipid choice in the same patient.
Frequently asked questions
What is the current first-line drug for acute gout flare?
A full-dose NSAID such as naproxen, low-dose colchicine (1 mg then 500 µg after an hour), or oral prednisolone 30–40 mg; choice follows renal function and comorbidity.
When is urate-lowering therapy started?
After recurrent flares, tophi, joint damage or uric acid stones; allopurinol 100 mg daily is first-line, titrated monthly toward serum urate below 6 mg/dL with anti-inflammatory cover.
Why is febuxostat reserved as second line?
Following the CARES trial signal of higher cardiovascular and all-cause mortality compared with allopurinol, febuxostat is used when allopurinol fails or causes hypersensitivity.
Which gene test is linked to allopurinol hypersensitivity?
HLA-B*5801, strongly associated with severe cutaneous reactions in East and South-East Asian ancestry; screening is recommended in those groups.
Do diuretics matter in gout?
Thiazides and loop diuretics raise serum urate and provoke flares; losartan lowers urate and is the preferred antihypertensive in a gouty patient.