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Allopurinol is the standard medication for the long-term treatment of gout — and at the same time the one with the most usage errors. Gout affects roughly 1–2% of adults (a German figure, broadly similar across Western countries), and considerably more in older age groups. Anyone who starts it in the middle of an acute attack can even make the attack worse — allopurinol works preventively, not acutely.
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Allopurinol is NOT newly started during an acute gout attack. Severe skin reactions (Stevens-Johnson syndrome) are rare, but life-threatening — take warning signs seriously. Last updated: May 2026.
Allopurinol has for decades been the standard medication for the long-term treatment of gout and one of the best-researched uric acid lowerers of all. Below are the most important key facts for a quick orientation — the individual points are explained in detail in the following chapters.
| Property | Details |
|---|---|
| Active substance | Allopurinol |
| Trade names | Zyloric, numerous generics |
| ATC code | M04AA01 |
| Substance class | Uric acid lowerer (urostatic) / xanthine oxidase inhibitor |
| Mechanism of action | Inhibition of xanthine oxidase → reduced uric acid production |
| Active metabolite | Oxypurinol (long half-life → once-daily intake) |
| Dosage form | Tablets (100 mg, 300 mg) |
| Usual start | 100 mg/day, increase slowly ("start low, go slow") |
| Maintenance dose | individual, often 300 mg/day — by uric acid target value |
| Maximum dose | up to 800–900 mg/day in exceptional cases |
| Uric acid target value | usually < 6 mg/dl, lower still with tophi |
| Prescription status | Yes |
| Most important note | Do NOT newly start during an acute gout attack! |
Allopurinol is the standard medication for the long-term treatment of gout — the most common inflammatory joint disease. It lowers the uric acid level in the blood and thereby prevents gout attacks and consequential damage. It is known under the trade name Zyloric, but there are numerous generics. Allopurinol has been used for decades and is well researched.
The most important thing for understanding allopurinol: it is a preventive long-term medication, not a remedy against acute pain. It does not treat the acute gout attack, but lowers uric acid in the long term so that attacks do not arise in the first place. This distinction is central — and disregarding it is one of the most common mistakes in handling allopurinol.
With correct use, allopurinol can control gout very well, prevent attacks, and even dissolve existing uric acid deposits (gouty tophi). For this to succeed, some particular features must be observed — above all the slow dose increase, the right starting time, and the accompanying attack prophylaxis at the start.
Allopurinol inhibits the enzyme xanthine oxidase. This enzyme is the last step in the formation of uric acid — it converts the precursors hypoxanthine and xanthine into uric acid. Through the inhibition, uric acid production falls, and the uric acid level in the blood drops.
Allopurinol is converted in the body itself into oxypurinol — the actual main active substance, which likewise inhibits xanthine oxidase and has a long duration of action. This explains why the once-daily intake is enough. Through the persistently lower uric acid, no new uric acid crystals can deposit in the joints — and existing deposits gradually dissolve.
Allopurinol is well absorbed and predominantly metabolised into oxypurinol, which is excreted via the kidneys. That is why a dose adjustment is important with restricted kidney function (a separate chapter). The uric-acid-lowering effect sets in within days, but the full effect on the gout (dissolution of deposits, freedom from attacks) takes months.
To understand allopurinol, a look at the disease helps. Gout arises through a permanently raised uric acid level (hyperuricaemia). Uric acid is a breakdown product of purines — building blocks that the body forms itself and that also occur in the diet.
If uric acid is permanently too high, it can no longer remain fully dissolved and forms sharp-edged crystals that deposit above all in joints — classically in the base joint of the big toe. These crystals trigger violent inflammations: the acute gout attack with strong pain, redness, swelling, and warmth. Over years, larger deposits (tophi) and joint damage can form, and the kidneys can also take harm (uric acid stones, kidney damage).
This is where allopurinol comes in: by lowering uric acid permanently below a critical threshold, it prevents crystal formation — and existing crystals slowly dissolve again. This is a causal long-term therapy, in contrast to the pure treatment of the acute attack (with anti-inflammatory remedies).
This is one of the most common and most consequential mistakes in handling allopurinol. The reason: every rapid change of the uric acid level — whether up or down — can "set crystals in motion" and trigger or intensify an attack. If you lower uric acid in the middle of the acute attack, you are thus pouring oil on the fire.
An at first confusing but important phenomenon: in the first weeks to months of allopurinol therapy, there can paradoxically be increased gout attacks — although uric acid is falling and the medication is actually working.
The reason: when uric acid falls, existing crystal deposits are mobilised and partly dissolved — this remodelling process can trigger inflammations and thus attacks. This is not a sign that the therapy is not working — on the contrary, it shows that the crystals are coming into motion. But it is frustrating for patients and a common reason to break off the therapy prematurely.
To avoid this initial cluster of attacks, an accompanying anti-inflammatory remedy for prevention is often given at the start of allopurinol therapy — mostly low-dose colchicine or an NSAID, over the first months. This attack prophylaxis is an important standard and makes the start of therapy considerably more pleasant.
The dosage of allopurinol follows the principle "start low, go slow" and is oriented towards a uric acid target value — not towards a fixed standard dose.
| Situation | Dose | Note |
|---|---|---|
| Gradual start | 100 mg/day | Lower still with a restricted kidney |
| Dose increase | Increase by 100 mg | Every 2–4 weeks, by uric acid value |
| Maintenance dose (usual) | 300 mg/day | Individual, often more or less |
| Maximum dose | up to 800–900 mg/day | Only in special cases, mostly considerably less needed |
| Uric acid target value | < 6 mg/dl | Lower still with tophi (< 5 mg/dl) |
| Restricted kidney function | Adjustment to eGFR | Low start, closer monitoring |
Important to understand: allopurinol is mostly a long-term therapy over years or for life. If it is stopped, uric acid rises again, and the gout returns.
Allopurinol has several areas of use, which all hang together with an excessive uric acid production:
| Indication | Details |
|---|---|
| Gout (chronic hyperuricaemia) | The main indication — long-term therapy for attack prevention and dissolution of deposits |
| Repeated gout attacks | When attacks occur more frequently or tophi/joint damage are present |
| Uric acid stones of the kidney | For prevention with uric-acid-related kidney stones |
| Tumour lysis syndrome | Prevention in cancer therapy, when much uric acid arises in the breakdown of many cells |
| Rare enzyme defects | Certain congenital disorders of purine metabolism |
Not every raised uric acid without complaints has to be treated — the indication for a long-term therapy is set by the doctor on the basis of attacks, uric acid height, deposits, and accompanying diseases. More under gout.
Allopurinol is well tolerated overall. Most side effects are mild and occur above all in the dose-increase phase:
| Side effect | Description |
|---|---|
| Skin rash | The most common side effect — mostly harmless, but ALWAYS take it seriously (see the next chapter) |
| Increased gout attacks at the start | A paradoxical initial phenomenon — crystals are mobilised |
| Gastrointestinal complaints | Nausea, diarrhoea |
| Headaches | Mostly mild and temporary |
| Raised liver values | Mostly mild — are checked over the course |
| Fatigue | In individual cases |
With every skin rash on allopurinol it should be clarified medically whether it is a harmless or a beginning severe reaction — for allopurinol is among the medications with a rare but serious risk of skin reactions.
An important safety topic. In rare cases allopurinol can trigger severe hypersensitivity reactions — among them the allopurinol hypersensitivity syndrome (also DRESS syndrome) and very rare but life-threatening skin reactions such as Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN).
These reactions occur mostly in the first weeks to months of the therapy. Warning signs at which one must act immediately:
A certain genetic marker (HLA-B*5801) raises the risk considerably — it is more common in some population groups (above all certain Asian ethnicities), which is why a genetic test before the start of therapy is partly recommended there. A restricted kidney function and a too-rapid start of therapy also raise the risk — a further reason for the slow dose increase. Overall, these severe reactions are rare, but the education about warning signs is important.
