By reducing uric acid production, Allopurinol helps prevent future attacks rather than relieving pain during an acute flare. Allopurinol is used as a long-term treatment to reduce the risk of further…
By reducing uric acid production, Allopurinol helps prevent future attacks rather than relieving pain during an acute flare. Allopurinol is used as a long-term treatment to reduce the risk of further uric acid crystal formation.
Allopurinol tablets are taken by mouth, usually after food with water, according to an agreed dosing plan. They lower uric acid in adults with gout, persistent hyperuricaemia, or uric acid kidney stones.
They lower uric acid in adults with gout, persistent hyperuricaemia, or uric acid kidney stones.
Allopurinol is commonly prescribed when a person has:
Asymptomatic hyperuricaemia is not automatically treated. Many people with a raised urate result never develop gout, so treatment decisions depend on the level, kidney health, stone history, and wider clinical picture.
Allopurinol contains the active ingredient allopurinol and belongs to the xanthine oxidase inhibitor class. Xanthine oxidase is an enzyme involved in producing uric acid from purines. Blocking this enzyme lowers the amount of uric acid entering the bloodstream.
The tablets are intended for long-term urate-lowering treatment. Allopurinol is not a painkiller and does not remove uric acid crystals immediately from an inflamed joint.
The active ingredient is allopurinol. The product is supplied as tablets for oral use. Strength selection and the daily amount depend on serum urate results, kidney function, age, other medicines, and the reason for treatment.
Allopurinol reduces uric acid production rather than forcing the kidneys to remove more uric acid. A useful comparison is to think of it as turning down the source of uric acid while the body gradually clears the excess already present.
NICE and European Alliance of Associations for Rheumatology guidance generally use a serum urate target below 360 micromol/L for most people with gout. A lower target below 300 micromol/L may be used for severe tophaceous gout or persistent crystal deposition [1].
The medicine does not act as a rescue treatment. Uric acid already sitting in a joint may continue to trigger symptoms while the blood urate level falls.
Allopurinol is commonly prescribed when a person has:
Asymptomatic hyperuricaemia is not automatically treated. Many people with a raised urate result never develop gout, so treatment decisions depend on the level, kidney health, stone history, and wider clinical picture.
Allopurinol inhibits xanthine oxidase, an enzyme involved in producing uric acid from purines. By blocking this enzyme, it reduces uric acid production and lowers the amount of uric acid entering the bloodstream. The body can then gradually clear excess uric acid and existing crystals.
Allopurinol is taken orally. How much to use and how often depends on the purpose of treatment and is agreed with a doctor or pharmacist.
A typical clinical approach is:
The dose should be individualised. It is not safe to select a dose based only on the number of tablets supplied.
Take the tablet after food with a full glass of water. Taking it at the same time each day can make missed doses less likely and supports steady exposure.
Kidney disease does not automatically rule out Allopurinol. It does mean that treatment usually starts more cautiously, with closer monitoring of renal function and serum urate.
In practice, the starting dose may be reduced for lower estimated glomerular filtration rates. Dose increases are made gradually, balancing the urate result against adverse effects. Underdosing can leave urate above target and allow crystals to persist.
The BNF and NICE guidance support a treat-to-target approach with appropriate adjustment rather than abandoning urate-lowering therapy solely because kidney disease is present [2].
Take a missed dose when remembered unless the next dose is nearly due. Skip it when the next dose is close. Never take two doses together to compensate.
Treatment usually continues after symptoms improve. Crystals dissolve slowly, and stopping when the joints feel better allows urate to rise again. The treatment plan is based on measured serum urate. Consistent dosing supports gradual crystal removal. Follow-up tests help guide adjustments.
Starting Allopurinol can temporarily increase the risk of a gout flare because changing urate levels can disturb existing crystals. A prescribed anti-inflammatory may be used as flare protection during the initial treatment period.
Allopurinol prevents future crystal formation by lowering urate production. Flare treatments reduce inflammation during an attack. They have different jobs and are often used together during the early months.
| Treatment | Main role and key limitation |
|---|---|
| Allopurinol | Long-term urate lowering; may trigger early flares; requires gradual adjustment |
| Febuxostat | Alternative xanthine oxidase inhibitor when Allopurinol is unsuitable or ineffective; cardiovascular history needs review |
| Colchicine, NSAIDs or corticosteroids | Flare control or prevention; do not remove the long-term urate burden |
Both medicines inhibit xanthine oxidase, but they have different molecular structures and dosing considerations. Allopurinol remains a common first-line option in UK guidance because of extensive clinical experience and long-term use.
Febuxostat may be considered when Allopurinol is not tolerated or does not achieve the urate target. The MHRA has highlighted cardiovascular safety considerations for febuxostat in people with established cardiovascular disease, so the choice requires an individual risk assessment [5].
Allopurinol is the long-term prevention component. Colchicine, an NSAID, or a corticosteroid is used to reduce inflammation during a flare or to provide protection while urate levels change.
Neither approach replaces the other. Treating pain alone leaves the underlying urate burden in place, while taking Allopurinol alone may leave early flares insufficiently controlled.
Stopping when the pain disappears. The correction is to continue the prescribed long-term plan because symptom relief does not mean that crystals have dissolved.
Stopping during every flare. A flare does not necessarily mean treatment has failed. Anti-inflammatory treatment is often added while Allopurinol continues.
Increasing the dose without a blood test. Symptoms do not reliably show whether serum urate has reached its target. Dose changes should follow measured urate and kidney function.
Missing monitoring appointments. Urate, renal function, liver function, and blood counts may be relevant, especially after dose changes or when interacting medicines are used.
Ignoring a rash. Waiting to see whether a rash disappears can delay treatment of a serious reaction. A new rash needs same-day medical assessment.
Allopurinol is unsuitable for anyone who has previously experienced a serious hypersensitivity reaction to allopurinol or a related reaction involving severe skin, liver, kidney, or blood abnormalities.
The most important interaction is with azathioprine or mercaptopurine. Allopurinol can greatly increase exposure to these medicines and cause life-threatening bone marrow suppression. If the combination is clinically necessary, the thiopurine dose is usually reduced to about one quarter with close blood-count monitoring.
Other relevant interactions include:
The BNF and MHRA safety information advise reviewing the full medicine list before starting treatment [4].
NOT for you if: you have had a serious hypersensitivity reaction to Allopurinol or a related severe skin reaction.
Tell the prescriber about any previous rash caused by a medicine. The detail matters: a brief isolated itch is assessed differently from blistering, mouth ulcers, fever, or facial swelling.
Most people tolerate Allopurinol without major difficulty, but a new rash requires prompt attention. A rash can be the first sign of a severe hypersensitivity reaction.
Possible early effects include:
Mild digestive symptoms may settle during the first weeks. Taking the tablet after food can reduce stomach irritation.
A rash should not be dismissed as a minor nuisance. Stop taking Allopurinol and obtain urgent medical advice the same day if a rash develops, especially if it spreads or occurs with fever.
Allopurinol hypersensitivity syndrome, also called AHS, is rare but potentially life-threatening. Severe cutaneous reactions can include Stevens–Johnson syndrome, toxic epidermal necrolysis, and DRESS, meaning drug reaction with eosinophilia and systemic symptoms.
Seek urgent medical help on the same day for:
Stop Allopurinol if a serious rash or hypersensitivity symptom appears unless an urgent clinician specifically directs otherwise. Published clinical series report substantial mortality from severe AHS, sometimes around 20–25%, which explains the strict response to warning signs [3].
HLA-B*58:01 screening may be considered before treatment in people of Han Chinese, Thai, or Korean ancestry because this allele is associated with a higher risk of severe allopurinol hypersensitivity.
A gout flare after starting Allopurinol does not prove that the medicine is unsuitable. The flare can occur because urate crystals are shifting as the blood urate level changes.
Do not stop Allopurinol automatically during a flare. The prescriber may add or continue flare protection while the urate-lowering treatment continues.
From a clinical perspective, Allopurinol is intended for consistent long-term use to reduce uric acid and help prevent future crystal formation. It does not provide immediate relief during an acute flare, so patients should follow the agreed treatment plan and seek medical advice if symptoms worsen, treatment is difficult to tolerate, or further attacks occur.
Older adults can use Allopurinol, but treatment usually starts cautiously because kidney function, dehydration, and interacting medicines become more common with age. NICE guidance updated in 2025 supports dose adjustment to renal function and serum urate rather than excluding older patients by age alone. The BNF recommends reviewing the full medicine list before titration.
Allopurinol and febuxostat both reduce uric acid production by inhibiting xanthine oxidase, but febuxostat is generally reserved for selected patients who cannot use or do not respond adequately to Allopurinol. MHRA cardiovascular safety advice from 2023 supports careful assessment in people with established heart disease. Neither medicine treats the pain of an acute flare directly.
Stopping Allopurinol usually allows serum urate to rise again, which can promote renewed crystal formation and future flares. NICE CKS guidance reviewed in 2025 does not require routine tapering, but an agreed stopping plan is important when treatment is being changed. Do not stop suddenly after a rash without urgent clinical advice, because severe reactions require a different safety response.
Take the missed tablet when remembered unless the next dose is nearly due, then omit it and return to the usual schedule. NHS medicines guidance from 2024 advises against doubling a dose after a missed tablet. Contact a pharmacist if missed doses become frequent. A single missed dose is usually less important than repeated missed doses over several days.
A previous serious hypersensitivity reaction to Allopurinol rules out routine re-exposure. MHRA safety guidance from 2023 treats blistering rash, mucosal ulcers, fever, facial swelling, or organ involvement as urgent warning signs. Kidney disease alone does not automatically rule out treatment, although it requires cautious dosing and monitoring.
Allopurinol is generally avoided during pregnancy, especially in the first trimester, unless specialist assessment finds a clear clinical need. UKTIS information reviewed in 2025 describes limited pregnancy data, so the prescriber should reassess treatment rather than the patient stopping independently. Breastfeeding also requires an individual review of maternal benefit and infant exposure.
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Alcohol can contribute to higher urate, with beer and spirits posing more concern than occasional modest intake. Diet changes can help, but diet alone rarely normalises urate when recurrent gout is established. Evidence for cherry extract supplements remains limited and does not replace urate-lowering therapy.
Patients may report that the tablets are easy to take but feel frustrated by an early flare. The first weeks can be confusing because the medicine may be working on urate levels while flares still occur.
Some notice no immediate change, which is expected because urate crystals dissolve gradually rather than overnight. Others describe mild nausea that improved after taking the tablet after food. A smaller group reports headaches, loose stools, or a rash; the rash group needs urgent assessment rather than routine observation.
Based on 3 reviews
Reading, took a low starting dose for several weeks and continued flare protection. He reported two attacks during the first months, then fewer symptoms after the urate result improved. The gradual start felt slow, but he found the daily routine manageable.
Reading Several weeks 26 Oct 2026Milton Keynes, had been taking Allopurinol for several months when he missed monitoring blood tests. He felt well and assumed the treatment was finished, but a later flare showed that his urate remained above target. Dose adjustment and renewed monitoring gave him a clearer plan.
Milton Keynes Several months 30 Sept 2026Leicester, developed a widespread itchy rash shortly after starting treatment. He stopped the tablets and sought same-day medical advice. The experience was unsettling, but he was glad the warning had been treated as urgent rather than waiting for it to settle.
Leicester Shortly after starting treatment 13 Oct 2026
