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Allopurinol for Gout: How It Works, Dosing & UK Prescription Guide
A clinically reviewed UK guide to allopurinol — the first-line urate-lowering therapy for gout prevention. How it works, correct dosing, why attacks can worsen initially, target serum urate levels, and how to get it in the UK.
This guide covers long-term gout prevention with allopurinol. For treating an acute gout attack: Naproxen for acute gout → · Colchicine for gout →
First-line
NICE first-line urate-lowering therapy for gout prevention
100mg
Starting dose — titrated upward every 4 weeks
<360
Target serum urate in µmol/L (<300 in tophaceous gout)
Lifelong
Treatment is long-term — stopping causes rapid recurrence
What Is Allopurinol and Why Is It Used?
Allopurinol is a xanthine oxidase inhibitor — a prescription medicine that lowers the level of uric acid in the blood by blocking its production. It is the first-line urate-lowering therapy (ULT) for gout in UK clinical practice, recommended by NICE for all patients who have had two or more gout attacks, developed tophi, have chronic kidney disease, or are taking diuretics that raise uric acid levels.
Allopurinol does not treat an acute gout attack — it prevents future attacks by reducing the serum urate concentration below the level at which monosodium urate crystals form and deposit in joints. When maintained consistently, it can achieve complete remission from gout attacks and, over years, dissolve existing joint deposits.
How Allopurinol Works: Xanthine Oxidase Inhibition
Uric acid is the end product of purine metabolism. Purines are broken down through a series of steps to xanthine, and then converted to uric acid by the enzyme xanthine oxidase. Allopurinol and its active metabolite oxypurinol are structural analogues of xanthine that competitively and irreversibly inhibit xanthine oxidase — blocking this final conversion step.
The result is accumulation of xanthine and hypoxanthine (which are more soluble than uric acid and more easily excreted) and a dose-dependent reduction in serum urate. With adequate dosing, allopurinol can reduce serum urate to below the saturation threshold, at which point monosodium urate crystals gradually dissolve from existing joint and soft tissue deposits.
Who Should Be Offered Allopurinol?
NICE guidance recommends offering urate-lowering therapy with allopurinol to patients with:
- Two or more gout attacks within 12 months — the most common indication
- Tophi — visible or palpable urate deposits in soft tissue or joints
- Chronic kidney disease (CKD) — gout in CKD requires dose adjustment of allopurinol; dose per eGFR
- Urolithiasis (kidney stones) from uric acid
- Diuretic use that cannot be stopped — thiazide and loop diuretics raise serum urate significantly
Allopurinol should not be started during an acute gout attack. It should be initiated 2–4 weeks after the attack has fully resolved. Starting during an attack can prolong or worsen inflammation.
Starting Dose and Titration
| Step | Dose | Timing |
|---|---|---|
| Start | 100mg once daily | 2–4 weeks after the acute attack has fully resolved |
| Titrate up | Increase by 100mg every 4 weeks | Based on serum urate response; check urate every 4 weeks during titration |
| Usual maintenance | 200–300mg once daily | For most patients with normal renal function |
| Maximum | Up to 900mg daily | In patients with normal renal function who need higher doses to reach urate target |
| CKD adjustment | Start at 50mg; titrate cautiously | Allopurinol and oxypurinol accumulate in renal impairment; dosing per eGFR |
Why Attacks Can Worsen When Starting Allopurinol
Many patients experience more frequent or more severe gout attacks in the first 3–6 months of allopurinol treatment. This is not a sign that the medicine is causing harm — it is a well-understood and expected consequence of falling serum urate levels.
As uric acid levels drop, existing monosodium urate crystal deposits in joints begin to dissolve and shed crystal fragments into the synovial fluid. These crystals trigger the same acute inflammatory response as a fresh deposit. The process is called crystal mobilisation and is actually evidence that the treatment is working.
To reduce the risk of mobilisation attacks, NICE recommends co-prescribing a prophylactic anti-inflammatory — typically low-dose colchicine (500 micrograms twice daily) or a low-dose NSAID — for the first 6 months of allopurinol therapy. This does not mean stopping allopurinol when an attack occurs; stopping and restarting causes repeated crystal shedding and prolongs the process.
Serum Urate Targets
- <360 µmol/L — standard target for most patients; below the saturation threshold for monosodium urate crystal formation
- <300 µmol/L — target for patients with tophi; the lower target accelerates crystal dissolution from tophaceous deposits
Serum urate should be checked every 4 weeks during dose titration, and at least annually once stable. Maintaining urate below target long-term leads to gradual dissolution of crystal deposits and complete remission from attacks in most patients.
Side Effects
- Increased gout attacks initially — expected; see crystal mobilisation above; do not stop allopurinol
- Rash — mild rash in around 2% of patients; stop and seek advice; rarely progresses to severe hypersensitivity reactions (Stevens-Johnson syndrome, DRESS). Risk is significantly higher in patients carrying the HLA-B*5801 allele, which is more prevalent in Han Chinese, Korean, and Thai populations; genetic screening is recommended in these groups before starting
- Gastrointestinal effects — nausea, diarrhoea; take with food to reduce
- Liver function changes — rare; LFTs monitored if clinically indicated
Stop allopurinol and seek medical advice immediately if you develop a skin rash, mouth ulcers, fever, or blistering. These may indicate a severe hypersensitivity reaction requiring urgent assessment.
Drug Interactions
| Drug | Interaction |
|---|---|
| Azathioprine / mercaptopurine | Most important interaction: allopurinol inhibits their metabolism, causing marked toxicity; dose of azathioprine must be reduced to 25% if combination unavoidable; specialist supervision required |
| Warfarin | Allopurinol may enhance anticoagulant effect; INR monitoring required |
| ACE inhibitors (particularly captopril) | Increased risk of hypersensitivity reactions; monitor |
| Thiazide diuretics | Increase allopurinol toxicity risk, particularly in renal impairment; review diuretic where possible |
Getting Allopurinol in the UK
Allopurinol is prescription-only. It can be prescribed by a GP or, following assessment, by a GPhC-registered pharmacist independent prescriber at an online pharmacy. Because allopurinol requires serum urate monitoring and dose titration, ongoing GP review is an important part of management.
Prescription Gout Treatment at Access Doctor
Prescription naproxen for acute gout attacks and allopurinol for prevention are available following online consultation. GPhC-registered pharmacist independent prescribers. GPhC pharmacy #9011198.
View Gout Treatments →Frequently Asked Questions
What is allopurinol used for?
Allopurinol is used to prevent recurrent gout attacks by lowering serum uric acid levels. It is the first-line urate-lowering therapy recommended by NICE and is taken long-term to keep serum urate below the threshold at which crystals form in joints.
When should I start allopurinol?
Allopurinol should be started 2–4 weeks after a gout attack has fully resolved — never during an acute attack. Starting dose is 100mg once daily, titrated upward every 4 weeks based on serum urate response.
Why does gout get worse when I start allopurinol?
This is an expected and common effect. As uric acid levels fall, existing crystal deposits dissolve and shed crystal fragments into the joint, triggering inflammatory attacks (crystal mobilisation). This is evidence the treatment is working. NICE recommends taking prophylactic low-dose colchicine or NSAID for the first 6 months of allopurinol to reduce this risk. Do not stop allopurinol when attacks occur.
What is the target uric acid level on allopurinol?
The standard target is serum urate below 360 µmol/L. For patients with tophi, the target is below 300 µmol/L to accelerate dissolution of crystal deposits. Serum urate should be checked every 4 weeks during dose titration.
How long do I need to take allopurinol?
Allopurinol is a lifelong treatment. Stopping causes serum urate to rise again and attacks to return. Most patients who maintain target serum urate levels become completely free of gout attacks over time.
References
- NICE CKS. Gout. Updated 2023.
- BNF. Allopurinol. bnf.nice.org.uk
- NHS. Allopurinol. nhs.uk/medicines/allopurinol
Medical disclaimer: This article is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before starting or changing any treatment. In a medical emergency, call 999.