Allopurinol
Is It Right for You?
A complete guide to Allopurinol — what it treats, how it works, dosages, side effects, and when a clinician may prescribe it following an online consultation.
What Is Allopurinol?
Allopurinol is a xanthine oxidase inhibitor used in the long-term management of gout, hyperuricaemia (elevated uric acid levels), and uric acid kidney stones. It is the most widely prescribed urate-lowering therapy in the UK and is included on the World Health Organization's List of Essential Medicines. By reducing the production of uric acid, allopurinol prevents the formation and deposition of monosodium urate crystals in joints, soft tissues, and the kidneys — the underlying cause of gout, tophi, and uric acid nephrolithiasis.
Allopurinol does not relieve acute gout attacks — it is a preventative, long-term medication. It must be started carefully, as initiating allopurinol during or immediately after an acute gout attack can paradoxically precipitate a further attack by mobilising urate crystals from tissue deposits. Treatment is typically lifelong, as stopping allopurinol allows uric acid to rise again.
Available as 100 mg and 300 mg tablets, allopurinol is suitable for adults and, in specialist settings, for children with specific metabolic conditions.
Allopurinol is a prescription-only medication in the UK. A licensed clinician must assess your serum uric acid levels, renal function, and medical history before it can be prescribed — which can now be done quickly and conveniently through a telehealth consultation.
What Conditions Is Allopurinol Used For?
Allopurinol is prescribed for:
long-term prevention of recurrent gout attacks in patients with established gout or hyperuricaemia requiring treatment.
elevated serum uric acid associated with metabolic conditions, diuretic use, renal impairment, or high purine diet.
prevention of recurrent uric acid kidney stones.
prevention of hyperuricaemia in patients undergoing chemotherapy or radiotherapy for haematological malignancies.
a rare genetic disorder causing severe hyperuricaemia; allopurinol is used in specialist management.
Allopurinol must not be started during an acute gout attack, as it can prolong and worsen the attack. Acute attacks are treated with NSAIDs, colchicine, or corticosteroids. Allopurinol should be started only when the acute attack has fully resolved — typically 2 to 4 weeks after resolution. Once started, attacks may initially increase in frequency before improving; prophylactic colchicine or an NSAID is often co-prescribed for the first 3 to 6 months of allopurinol therapy.
How Does Allopurinol Work?
Allopurinol is a structural analogue of hypoxanthine — a purine base that is a natural substrate for the enzyme xanthine oxidase. Xanthine oxidase catalyses the sequential oxidation of hypoxanthine to xanthine and then xanthine to uric acid — the final steps in purine catabolism in humans. Uric acid, the end product, has limited solubility in biological fluids; when serum concentrations exceed the saturation point (approximately 360–420 µmol/L), urate crystallises and deposits in joints and soft tissues, causing the inflammatory arthritis of gout.
Allopurinol competitively inhibits xanthine oxidase. Its active metabolite, oxipurinol, is an even more potent and long-acting inhibitor that binds tightly to and irreversibly inactivates xanthine oxidase. The result is a dramatic reduction in uric acid production, with corresponding increases in the more soluble precursors hypoxanthine and xanthine, which are readily excreted by the kidneys.
By maintaining serum urate below the saturation threshold (target typically < 360 µmol/L, or < 300 µmol/L in patients with tophi), allopurinol allows existing crystal deposits to gradually dissolve over months to years, preventing future gout attacks and resolving tophi.
Dosages & Administration
The correct dose depends on the type and severity of infection, age, weight, and kidney function. Always follow your clinician's instructions. The table below is for general reference only.
Administration Tips
Take allopurinol after food — taking it with or after meals reduces the risk of gastrointestinal side effects.
Take once daily, ideally at the same time each day. For doses above 300 mg, the dose may be divided.
Drink plenty of fluids — maintaining good hydration (at least 2 litres of fluid per day) helps flush uric acid through the kidneys and reduces the risk of xanthine kidney stones.
Do not start allopurinol during an acute gout attack — wait until the attack has fully resolved.
Continue allopurinol during acute attacks — if you are already established on allopurinol and have a gout attack, do not stop allopurinol. Stopping causes urate levels to fluctuate, which can perpetuate attacks. Treat the acute attack separately.
Allow 3 to 6 months before judging the full preventative benefit — the frequency of attacks typically reduces over this period as crystal deposits dissolve.
Side Effects of Allopurinol
Allopurinol is generally well tolerated with long-term use. Most patients experience no side effects. Serious reactions are rare but can be severe.
- Rash (maculopapular — the most common side effect requiring assessment)
- Nausea or gastrointestinal discomfort
- Acute gout attacks (particularly in the first months of treatment)
- Headache
- Drowsiness
- Allopurinol hypersensitivity syndrome (AHS) — a severe, potentially fatal systemic hypersensitivity reaction including exfoliative dermatitis, fever, hepatitis, renal failure, and vasculitis; most commonly occurs in the first 2 months of treatment; risk is significantly higher in patients carrying the HLA-B*58:01 genetic allele (more common in Han Chinese, Thai, and Korean populations)
- Stevens-Johnson Syndrome / Toxic Epidermal Necrolysis — severe blistering mucocutaneous reactions; can occur as part of AHS
- Hepatotoxicity — elevated liver enzymes, hepatitis, hepatic failure (rare)
- Blood dyscrasias — thrombocytopenia, agranulocytosis (rare)
- Renal failure — particularly in patients with pre-existing renal impairment
Any rash developing during allopurinol treatment — even mild — should prompt immediate contact with your clinician. Allopurinol hypersensitivity syndrome is a severe, potentially fatal systemic reaction that typically begins with a rash. Stop allopurinol and seek same-day medical review if any rash develops. If the rash is associated with fever, blistering, mouth sores, or mucosal involvement, call 999 immediately.
Drug Interactions
Always disclose all medications and supplements to your clinician or pharmacist before starting allopurinol.
Allopurinol dramatically increases the blood levels and toxicity of azathioprine and 6-mercaptopurine by inhibiting their metabolism via xanthine oxidase. This combination can cause life-threatening bone marrow suppression. If both drugs are required, the azathioprine or 6-mercaptopurine dose must be reduced by approximately 75%, and blood counts monitored closely. This interaction must be flagged to all prescribers.
Allopurinol inhibits theophylline metabolism, raising theophylline levels and increasing the risk of toxicity (seizures, arrhythmias). Theophylline levels should be monitored closely.
Allopurinol may inhibit warfarin metabolism, increasing anticoagulant effect. INR should be monitored.
Concurrent use significantly increases the incidence of skin rash; avoid this combination where possible.
Allopurinol increases didanosine plasma levels, raising the risk of toxicity. Concurrent use should be avoided.
Important Warnings
AHS is a rare but potentially fatal idiosyncratic reaction associated with allopurinol. Risk factors include renal impairment, concurrent thiazide diuretic use, and — critically — carrying the HLA-B*58:01 genetic allele, which is much more prevalent in Han Chinese, Thai, Korean, and other Asian populations. Genetic screening before starting allopurinol is recommended in these ethnic groups. Any rash, fever, or systemic symptoms in the first 2 months of treatment must be treated as a potential AHS until proven otherwise.
Starting allopurinol during an active gout attack can mobilise urate deposits and significantly worsen or prolong the attack. Always wait until the acute episode has completely resolved — usually 2 to 4 weeks — before initiating or resuming allopurinol.
Allopurinol and its active metabolite oxipurinol are renally excreted. In patients with renal impairment, drug accumulation increases the risk of AHS and other serious reactions. Dose reduction is mandatory based on eGFR. Regular monitoring of renal function during treatment is recommended.
The interaction between allopurinol and azathioprine/6-mercaptopurine is one of the most dangerous in clinical practice. Ensure all prescribers are aware if you take both. Bone marrow suppression from this combination can be fatal.
There are limited safety data on allopurinol use in human pregnancy. It should generally be avoided unless the benefits clearly outweigh the risks. Allopurinol passes into breast milk; breastfeeding is generally not recommended during treatment.
Speak to a Clinician About Treatment
Getting advice no longer means sitting in a waiting room. Through The GP Service, you can consult with a licensed clinician in minutes — from home, on your lunch break, or wherever works for you. If treatment is clinically appropriate, your clinician can issue a prescription during the consultation. A consultation does not guarantee a prescription.
The treatment you need, when you need it.
Allopurinol FAQs
This is a very common and expected phenomenon in the first 3 to 6 months of allopurinol therapy. As allopurinol lowers serum urate levels, existing crystal deposits in joints begin to dissolve and mobilise, triggering inflammatory responses. This does not mean allopurinol is not working — it is a sign that the body is clearing the accumulated crystals. Your clinician may co-prescribe colchicine or a low-dose NSAID as prophylaxis during this initial period. Do not stop allopurinol — doing so causes urate levels to fluctuate, which can perpetuate attacks.
The target serum uric acid level on allopurinol is generally below 360 µmol/L (6 mg/dL). In patients with tophi, recurrent attacks, or advanced gout, a lower target of below 300 µmol/L (5 mg/dL) is often recommended to accelerate crystal dissolution. Your clinician will check your uric acid level via a blood test — typically 4 to 6 weeks after starting or adjusting the dose — and titrate the allopurinol dose until the target is achieved.
For most patients with gout, allopurinol is a lifelong treatment. Stopping allopurinol allows serum uric acid to rise again, crystal deposits to reform, and gout attacks to recur. However, some patients with very mild hyperuricaemia who achieve sustained lifestyle changes (dietary modification, weight reduction, reduced alcohol) may be able to reduce or discontinue allopurinol under medical supervision. Discuss with your clinician.
Alcohol — particularly beer and spirits — raises uric acid levels and is a significant trigger for gout attacks. While there is no direct pharmacological interaction between alcohol and allopurinol, heavy or regular alcohol consumption significantly undermines the effectiveness of urate-lowering therapy. Limiting alcohol intake is an important part of gout management.
Stop allopurinol immediately and contact your clinician the same day. Any rash in a patient taking allopurinol should be assessed urgently to exclude allopurinol hypersensitivity syndrome, which can be life-threatening. If the rash is accompanied by fever, blistering, mucosal involvement, or systemic illness, call 999.