Allopurinol

Allopurinol is a xanthine oxidase inhibitor used to lower raised uric acid levels in adults. It is prescribed for gout, hyperuricaemia, uric-acid kidney stones, and some uric acid deposition disorders. By reducing uric acid production, it helps prevent urate crystals from building up in joints and tissues.

Allopurinol tablets contain allopurinol, a urate-lowering medicine. It is used for long-term management of chronic gout, gouty arthritis, recurrent uric-acid kidney stones, and hyperuricaemia caused by increased uric acid production.

High uric acid does not always cause pain immediately. Problems develop when monosodium urate crystals settle in a joint, often the big toe, ankle, knee, wrist, or elbow. These crystals trigger the intense inflammation recognised as a gout attack.

Allopurinol can also be used where high uric acid is linked with certain enzyme disorders or with treatments that rapidly break down cancer cells. Its role is prevention and control, not rapid pain relief during an acute flare.

• Drug class: xanthine oxidase inhibitor
• Primary purpose: lowering serum uric acid levels
• Main uses: chronic gout, hyperuricaemia, uric-acid stone prevention and selected uric acid deposition disorders
• Form: oral tablets

• Take the prescribed dose of Allopurinol pills by mouth; the exact strength in mg and number of pills are stated on the pack and prescription.
• Take Allopurinol at the prescribed frequency, usually once daily when directed by a clinician.
• Take the pills at the prescribed time of day; the exact timing in relation to meals is stated on the pack or provided by a clinician.
• Use Allopurinol for long-term prevention of raised uric acid and gout, continuing for the duration prescribed by a clinician.
• If a dose is missed, follow the instructions on the pack or from a clinician; do not take two doses together unless specifically instructed.
• Continue treatment as prescribed even when symptoms improve, unless a clinician advises otherwise.

Allopurinol reduces the body’s production of uric acid from purines. Purines are natural substances found in human cells and in foods such as red meat, offal, some seafood, and alcohol.

The enzyme xanthine oxidase completes key steps in converting purines into uric acid. Allopurinol blocks this enzyme. Its active metabolite, oxypurinol, continues the xanthine oxidase inhibition after the tablet has been absorbed.

Lower uric acid means fewer crystals form over time. Existing urate deposits can gradually dissolve when serum urate stays below the treatment target. This is why allopurinol is called urate-lowering therapy rather than an acute gout painkiller.

The World Health Organization includes allopurinol on its Model List of Essential Medicines for conditions where uric acid reduction is clinically indicated ^[1].

Allopurinol is a first-line option for long-term gout prevention. NICE recommends treat-to-target urate-lowering therapy for people with multiple or troublesome flares, tophi, chronic gouty arthritis, chronic kidney disease, or diuretic-related gout ^[2].

Its benefit is cumulative. A lower serum urate level reduces the conditions that allow crystals to form. With sustained treatment, this can reduce attack frequency, support resolution of tophi, and protect joints from progressive urate deposition.

The usual target is below 360 micromol/L, equivalent to 6 mg/dL. People with tophi or severe gout may be managed towards a lower target determined by the prescriber. Blood tests guide dose adjustment and show whether the urate-lowering plan is working.

Allopurinol does not treat the immediate pain, swelling, or redness of an acute gout attack. Colchicine, a non-steroidal anti-inflammatory drug, or a short corticosteroid course may be used for acute symptoms where clinically appropriate.

Allopurinol and febuxostat lower uric acid production. Colchicine has a different role: it controls inflammation during a flare and can prevent early flares when urate-lowering treatment begins.

The American College of Rheumatology recommends allopurinol as preferred first-line urate-lowering therapy, including for many people with chronic kidney disease, with treatment titrated to a serum urate target ^[3].

Febuxostat can be considered when allopurinol is not tolerated or does not achieve the target. It has its own cautions, including cardiovascular considerations in people with established heart disease. Colchicine does not replace allopurinol because it does not lower uric acid.

Several patterns make allopurinol appear less helpful than it really is.

• Taking it only when joint pain starts, rather than as regular preventive treatment.
• Stopping it during every gout flare without assessing the reason for the flare.
• Doubling a missed dose.
• Assuming early flares mean the treatment has failed.
• Ignoring a rash, fever, mouth ulcers, or facial swelling.
• Skipping blood tests used to assess uric acid, kidney function, and dose response.
• Taking azathioprine or mercaptopurine without ensuring the prescriber knows all medicines being used.

Alcohol can contribute to gout flares and raise uric acid, especially beer and spirits. It may also make dehydration more likely after a social event, which is a familiar trigger for attacks.

In clinical practice, doctors focus on the urate result rather than judging success only by whether a person has had a recent flare. Someone can feel well between attacks while urate crystals continue to accumulate.

Doctors also expect treatment to be adjusted. A low starting dose is often chosen to reduce adverse effects and flare risk, then altered step by step after blood monitoring. This approach is more precise than using the same dose for every person.

Another recurring issue is the belief that dietary changes alone can always control established gout. Reducing alcohol intake, avoiding dehydration, losing excess weight gradually, and moderating high-purine foods can help. For recurrent gout with raised urate, lifestyle measures often work alongside urate-lowering treatment rather than replacing it.