Prevents gout attacks rather than treating them. The dose must be titrated to a target, and usually never is.
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Allopurinol is a xanthine oxidase inhibitor. It reduces how much uric acid the body produces, lowering the level in the blood so that crystals stop forming in the joints — and existing deposits gradually dissolve.
It is preventive treatment. It does nothing for an attack that is already happening, which is one of the two most misunderstood things about it.
It is usually started after two or more attacks in a year, or sooner where there are tophi, joint damage, kidney stones or kidney impairment.
Once daily, after food, with plenty of fluid.
The dose is titrated against a blood test, not fixed. This is the single most important point on this page. Treatment starts low — typically 100mg — and is increased every few weeks, checking the urate level each time, until it is below 360 µmol/L, or below 300 where there are tophi.
Being "on allopurinol" at a starting dose that was never increased is the commonest reason it appears not to work. Many people take 100mg for years, continue having attacks, and conclude the drug is useless. It was simply never titrated.
Never stop it during an attack. Changing the urate level in either direction can prolong an attack. Continue as normal and treat the attack separately.
Generally well tolerated. Nausea, diarrhoea and headache are the common complaints.
Rash is the one to take seriously. Stop allopurinol and contact a doctor if you develop a rash. Most are mild, but allopurinol hypersensitivity syndrome — a severe reaction involving rash, fever, and liver or kidney involvement — is rare and can be life-threatening.
Risk of that reaction is substantially higher in people carrying the HLA-B*5801 gene variant, which is considerably more common in people of Han Chinese, Thai and Korean heritage. Testing before starting is recommended in those groups.
Starting allopurinol commonly triggers an attack. This is expected, not a sign it is wrong, and it happens because urate is being mobilised out of the joints. It is why cover with colchicine or an NSAID is usually prescribed for the first few months — and why people who are not warned stop the drug at exactly the wrong moment.
Dose adjustment is needed in kidney impairment, and caution applies in liver disease.
Febuxostat is the usual alternative where allopurinol cannot be used.
Azathioprine and mercaptopurine — a serious interaction. Allopurinol blocks their breakdown and can cause dangerous toxicity. The combination is generally avoided, and where unavoidable requires drastic dose reduction and specialist supervision.
Other interactions: warfarin, ciclosporin, and amoxicillin (which increases rash likelihood).
Monitoring: urate level every few weeks during titration, then periodically once at target. Kidney and liver function before starting and during treatment.
One trap worth knowing: uric acid is often normal or even low during an acute attack, so a normal level then does not exclude gout. Retest a few weeks after it settles.
Yes, and gout is a condition where remote care works well — it is managed on blood results and history.
What that involves: confirming the diagnosis, checking urate at the right time, kidney and liver function, and — crucially — titrating the dose to target rather than starting it and walking away. That means repeat bloods every few weeks initially, which is exactly the follow-up that tends not to happen.
We also review the contributors, which is frequently skipped: diuretics raise urate and can often be switched; beer and fructose matter considerably more than the red meat most people focus on; and gout travels with cardiovascular and metabolic risk that is worth assessing while you are here.
Where we will send you elsewhere: a hot, swollen joint with fever and feeling unwell needs A&E, not us. Septic arthritis has to be excluded in person and it is time-critical.
This page is information, not an offer to supply.
Allopurinol is very cheap. On a private prescription the drug cost plus dispensing fee is usually less than the England NHS prescription charge of around £10, and NHS prescriptions are free in Wales.
Gout is one of the few conditions where treating to a measured target genuinely works — urate below 360 micromol/L, or lower where there are tophi.
That means repeat urate levels while the dose is being titrated, alongside kidney and liver function. Budget for those rather than for the tablets.
Most people left on a starting dose of allopurinol for years are not being treated — they are being prescribed to. The dose has to go up until the target is reached, and that is the single commonest failure in gout care.
Allopurinol is long-term treatment, usually lifelong. Stopping it means urate rises again over weeks and attacks return — often worse than before.
Do not stop allopurinol during an acute attack of gout. Any sudden change in urate level — up or down — can trigger or prolong an attack, and stopping mid-flare makes things worse rather than better.
Equally, if an attack happens while you are already established on it, keep taking it and treat the flare alongside.
Starting allopurinol commonly provokes flares in the first few months, as urate crystals in the joints begin to dissolve. This is expected, it is not the drug failing, and it is the point at which most people abandon treatment.
Cover with colchicine or an anti-inflammatory for the first six months — that is standard practice and is frequently omitted, which is precisely why people stop.
Any rash on allopurinol should stop the drug and prompt medical advice the same day.
Most rashes are mild, but a rare severe hypersensitivity reaction does occur, and it is more likely with a high starting dose, reduced kidney function, and in people of Han Chinese, Thai or Korean background.
Starting low and increasing slowly reduces that risk substantially.
Because falling urate mobilises the crystals already in the joint. Flares in the first few months are expected.
The answer is preventive cover with colchicine or an anti-inflammatory for around six months, not stopping the allopurinol.
No. If you are already established on it, keep taking it and treat the flare separately.
Stopping mid-attack prolongs it.
A urate level below 360 micromol/L, or below 300 where there are tophi or frequent attacks.
This is a treat-to-target condition, and being left on the starting dose without rechecking is the commonest reason gout carries on.
Usually, yes. It controls urate rather than curing the tendency to produce it.
Stopping means the level rises and the attacks return, often within months.
Rarely. Diet has a much smaller effect on urate than most people expect.
Cutting beer, spirits and sugary drinks helps more than avoiding red meat — but neither substitutes for reaching the target.
Stop the tablets and seek advice the same day.
Most rashes are minor, but the rare severe reaction is serious, and it is not something to watch and wait on.
Tell your prescriber if you take azathioprine or mercaptopurine — that combination can be dangerous.
Warfarin and amoxicillin also interact, the latter by making a rash more likely.
Kidney function determines the safe dose, and gout itself is more common when kidney function is reduced.
Slower titration is used where the kidneys are impaired, not a lower ceiling by default.
No. It is substantially genetic — how efficiently your kidneys excrete urate is largely inherited.
Diet and alcohol modify it; they rarely cause it, and the old caricature of gout as a rich man's indulgence has done real harm to how seriously it is taken.
Clinically reviewed by Dr Mohammad Zubair Khan, GMC 7563469
Last reviewed
August 24, 2026
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