Allopurinol for Gout: Practical Guide
Allopurinol is the drug most people with gout are offered first, and it works by shutting down the enzyme that makes uric acid in the first place. Used properly it does not just reduce attacks — over a few years it can dissolve the crystal deposits already sitting in your joints, which is what actually ends the cycle of flares. The catch is that it has to be dosed to a blood number rather than to a fixed tablet, and the first few months feel worse than the last few.
What allopurinol does inside the body
Uric acid is the end product of purine breakdown. The last two steps of that chain — hypoxanthine to xanthine, xanthine to urate — are both run by one enzyme, xanthine oxidase. Allopurinol blocks it. Less urate is produced, the blood level falls, and once it falls far enough the fluid in your joints becomes undersaturated and existing monosodium urate crystals start to dissolve back into solution.
That last part matters. Painkillers and colchicine deal with the inflammation a crystal causes; allopurinol deals with the crystal. It is why gout can be controlled to zero attacks in most people — though not cured, since the crystals return if the drug stops.
Why the target is a blood number, not a dose
A very common gap in gout care is putting someone on 100 mg or 300 mg, never rechecking the blood test, and assuming the job is done. Guidelines from both the American College of Rheumatology and EULAR are built on treat-to-target: the dose is whatever it takes to get serum urate below 6 mg/dL (360 µmol/L), and below 5 mg/dL (300 µmol/L) if you have visible tophi to dissolve. Held below that threshold, new crystals should not form and the old ones slowly dissolve.
Two people can need very different doses to reach the same number, because kidney function, body weight, other medicines and how much urate you make all differ. A dose that leaves you at 7.2 mg/dL (430 µmol/L) is not protecting you, however long you have been taking it. If you have never seen your own number, that is the thing to ask for — we cover what it means in the uric acid target that actually matters.
Start low and titrate upwards
Typical starting doses used in practice are low — often 100 mg a day, and lower still if kidney function is reduced — then increased in steps every few weeks with a urate test before each step. Starting low reduces the flare storm that comes with a sudden drop in urate, and it makes a hypersensitivity reaction less likely. The licensed range goes considerably higher than 300 mg for people who need it, and stopping short at 300 mg out of habit is a frequent reason treatment underperforms.
What your own steps and endpoint should be is a decision for the person prescribing it, who can see your kidney results and your other medicines. Nothing here is a dose recommendation, and doses should never be adjusted on your own initiative.
The genetic test that should come before the first tablet
A small number of people react to allopurinol with a severe hypersensitivity syndrome, and the risk is strongly associated with carrying the HLA-B*5801 gene variant. That variant is far more common in people of Han Chinese, Thai, Korean and some other Asian ancestries, and is also more frequent in people of African descent, than it is in white European populations. Guidelines therefore recommend testing for HLA-B*5801 before starting allopurinol in those higher-risk groups, and choosing a different urate-lowering drug if the test is positive.
If nobody has raised this with you and it might apply to your background, it is a reasonable thing to ask about before you take the first tablet. The full picture of what to watch for is in our piece on allopurinol side effects.
Why flares are expected early — and why prophylaxis comes with it
Here is the part people are rarely warned about properly. When urate levels fall, crystals at the surface of old deposits begin to shed, and shedding crystals provoke the same inflammatory response as new ones. Flares in the first weeks and months of treatment are common and expected. They are not a sign the drug has failed, and they are not a reason to stop it.
Because of this, prescribers usually co-prescribe a prophylactic anti-inflammatory alongside allopurinol for the first three to six months — most often low-dose colchicine, sometimes an NSAID or low-dose steroid. It is there specifically to cover the bumpy period. The mechanism is explained more fully in why allopurinol causes flares at first.
What the first year actually looks like
| When | What is usually happening | What is being checked |
|---|---|---|
| Week 1 | Low starting dose, prophylaxis started alongside it. No noticeable change in how you feel. | Nothing yet; sometimes baseline kidney and liver bloods if not already done. |
| Month 1 | Urate falling. Flares may appear or feel more frequent. Dose often increased for the first time. | Serum urate; kidney function and liver enzymes in many practices. |
| Month 3 | Further dose steps if the target is not met. Flares typically starting to settle. | Serum urate again; decision on whether prophylaxis continues. |
| Year 1 | Stable maintenance dose, urate held below target, attacks much less frequent or absent. Tophi shrinking slowly. | Urate every 6–12 months, plus kidney function; review of any new medicines that could interact. |
How long you stay on it
For most people with established gout, allopurinol is a long-term and usually lifelong treatment. Stop it and urate returns to its old level within weeks. The absence of attacks after a year is the drug working, not evidence it is no longer needed — and coming off it is a conversation with your prescriber, not a decision to make quietly at home.
Diet still has a place alongside it. Whole-diet change moves serum urate by roughly 0.3–1.3 mg/dL (about 18–78 µmol/L) — real, but rarely enough on its own for established gout. It makes the drug’s job easier rather than replacing it.
The one question worth asking: at your next appointment, ask what your most recent serum urate was and whether it is below 6 mg/dL (360 µmol/L). If nobody has measured it since your dose was set, that single test tells you more about whether your treatment is working than any symptom will.
Frequently Asked Questions
Can I take allopurinol during an attack?
If you are already established on it, current guidance is to keep taking it through a flare rather than interrupting it, because stopping and restarting causes further urate swings. Whether to start it for the first time mid-attack is a judgement call your doctor makes, and practice varies. Either way, the flare itself is treated with anti-inflammatories, not with allopurinol.
How long before allopurinol stops the attacks?
Blood urate falls within a couple of weeks of reaching an effective dose, but dissolving existing deposits takes far longer. Most people see a clear reduction in attacks somewhere between six and twelve months, and large tophi can take several years to disappear. The lower you hold the urate, the faster the dissolving happens.
Does allopurinol damage the kidneys?
It is cleared by the kidneys rather than being toxic to them, which is why doses are adjusted when kidney function is reduced. In people with both gout and chronic kidney disease it is generally used with a cautious start and slower titration. Your kidney results are one of the reasons your prescriber wants periodic blood tests.
What if allopurinol does not get me to target?
The first question is whether the dose was actually pushed high enough, because many people are left on a dose that was never adjusted. If the maximum tolerated dose still falls short, or if you cannot take it, alternatives exist — see allopurinol vs febuxostat for the main one.
What to read next
- Allopurinol side effects: an honest look
- Gout medications compared
- Colchicine for gout: dose and timing
- The uric acid target that actually matters
