Allopurinol

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Allopurinol on Prescriptsy

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What is Allopurinol?

Allopurinol is a prescription medicine used for the long-term prevention of gout attacks and the management of hyperuricaemia (elevated uric acid levels in the blood).

It belongs to a class of drugs known as xanthine oxidase inhibitors.

By blocking the enzyme responsible for producing uric acid, allopurinol reduces blood uric acid concentrations and prevents the deposition of monosodium urate crystals in joints, soft tissues, and the urinary tract.

Gout is the most common inflammatory arthritis in the United Kingdom, affecting approximately 2.5% of adults.

It occurs when uric acid levels rise above the saturation point (approximately 360 micromol/L), leading to crystal formation and deposition.

The resulting acute attacks cause intense joint pain, swelling, redness and warmth, most commonly in the first metatarsophalangeal joint (the base of the big toe).

Without urate-lowering therapy, gout tends to become more frequent and may progress to chronic tophaceous gout with permanent joint damage.

Active ingredient and pharmacology

Allopurinol is a structural analogue of hypoxanthine, a naturally occurring purine base.

It acts as a competitive inhibitor of xanthine oxidase, the enzyme that catalyses the oxidation of hypoxanthine to xanthine and xanthine to uric acid.

By blocking this pathway, allopurinol reduces the production of uric acid and simultaneously increases the levels of hypoxanthine and xanthine, which are more soluble and more readily excreted by the kidneys.

Allopurinol's principal active metabolite, oxipurinol (alloxanthine), also inhibits xanthine oxidase and has a much longer half-life (approximately 15 to 28 hours compared with 1 to 2 hours for allopurinol itself).

It is oxipurinol that is primarily responsible for the sustained urate-lowering effect of the drug.

Licensed indications

• Gout, prevention of acute gouty arthritis, tophi, joint destruction, and uric acid nephrolithiasis in patients with a confirmed diagnosis of gout.
• Hyperuricaemia, management of elevated uric acid levels associated with conditions such as haematological malignancies (tumour lysis syndrome prophylaxis), Lesch-Nyhan syndrome, and enzyme disorders of purine metabolism.
• Renal calculi, prevention of recurrent uric acid and calcium oxalate kidney stones.

When should Allopurinol be started?

Current BSR (British Society for Rheumatology) and NICE guidelines recommend discussing urate-lowering therapy with all patients after a confirmed diagnosis of gout.

The traditional advice to wait until a patient has had two or more acute attacks before starting allopurinol has been revised.

Early initiation of urate-lowering therapy is now considered appropriate, particularly for patients with tophi, renal impairment, uric acid kidney stones, or frequent attacks (two or more per year).

In my clinical practice, I find that the key to successful allopurinol therapy is patient education.

Many patients are surprised to learn that allopurinol is a long-term, often lifelong treatment rather than something taken only during an acute attack.

Starting allopurinol during an acute flare was historically avoided, but recent evidence suggests that initiating treatment during a mild attack, with appropriate anti-inflammatory cover, does not prolong the flare and may improve long-term adherence.

How Allopurinol is used in practice

Starting treatment

The BSR guideline recommends a "start low, go slow" approach to allopurinol dosing.

Treatment typically begins at 100 mg once daily (or 50 mg in patients with renal impairment), with dose increases of 100 mg every four weeks until the target serum uric acid level is achieved.

The target for most patients is a serum uric acid level below 300 micromol/L (0.30 mmol/L), which is well below the saturation point and allows existing crystal deposits to dissolve over time.

Flare prophylaxis during initiation

Starting allopurinol can paradoxically trigger acute gout attacks in the first few months as urate crystal deposits begin to dissolve and release microcrystals into the joint space.

To prevent this, prescribers typically co-prescribe a low-dose anti-inflammatory agent such as colchicine 500 micrograms once or twice daily, or a low-dose NSAID, for the first six months of treatment.

This prophylactic cover significantly reduces the frequency and severity of initiation flares.

Monitoring

Regular blood tests are essential during dose titration.

Serum uric acid should be measured every four to six weeks until the target is reached, then every six to twelve months thereafter.

Renal function and liver function tests should also be monitored, particularly in patients with pre-existing kidney disease.

Allopurinol vs. Febuxostat

Febuxostat (Adenuric) is an alternative xanthine oxidase inhibitor available in the UK.

It is generally reserved for patients who cannot tolerate allopurinol or in whom allopurinol fails to achieve the target uric acid level at maximum tolerated doses.

Febuxostat is more selective for xanthine oxidase and does not require the same degree of dose adjustment in mild to moderate renal impairment.

However, it is significantly more expensive than allopurinol, which is available as an inexpensive generic, and cardiovascular safety data require ongoing monitoring.

Lifestyle factors in gout management

While allopurinol is the cornerstone of pharmacological gout management, lifestyle modifications play a supporting role. I advise my patients on the following:

• Hydration: drink plenty of water throughout the day. Adequate hydration promotes renal uric acid excretion.
• Diet: reduce intake of purine-rich foods such as organ meats, game, sardines, and anchovies. Limit alcohol, particularly beer and spirits. Moderate wine consumption appears to carry lower risk.
• Weight management: obesity is a significant risk factor for gout. Gradual weight loss through sustainable dietary changes can reduce uric acid levels.
• Fructose: high intake of fructose-sweetened drinks is associated with increased uric acid levels and gout risk.
• Dairy: low-fat dairy products may have a protective effect and can be encouraged.

Comorbidities and gout

Gout frequently coexists with cardiovascular disease, chronic kidney disease, hypertension, type 2 diabetes, and metabolic syndrome. When prescribing allopurinol, I always review the patient's full medication list.

Certain antihypertensives (particularly losartan, which has a mild uricosuric effect) may be preferred in patients with both hypertension and gout.

Thiazide diuretics, conversely, can raise uric acid levels and may need to be reconsidered.

Obtaining Allopurinol in the United Kingdom

Allopurinol is a prescription-only medicine. It is widely available as a generic medicine and is one of the least expensive treatments on the NHS.

The standard NHS prescription charge is £9.90 per item in England, with prescriptions free of charge in Scotland, Wales, and Northern Ireland.

Your GP can prescribe allopurinol following a clinical assessment and blood test confirming hyperuricaemia.

Online prescriber services accredited by the CQC and GPhC may also be able to provide prescriptions for established patients.

Clinical evidence

Allopurinol has been in clinical use since the 1960s and has an extensive evidence base.

Landmark studies have demonstrated that maintaining serum uric acid below 360 micromol/L significantly reduces the frequency of acute attacks, and levels below 300 micromol/L promote dissolution of existing tophi.

The BSR 2017 guideline for the management of gout provides a comprehensive summary of the evidence supporting treat-to-target urate-lowering therapy.

Long-term adherence to allopurinol is associated with a reduced risk of gout flares, regression of tophi, preservation of joint function, and potentially a reduction in cardiovascular events, although the cardiovascular data remain an active area of research.

Patient adherence and the challenge of preventive treatment

Allopurinol adherence is notoriously poor.

Studies suggest that as many as 50% of patients prescribed allopurinol discontinue it within the first year, often because they feel well between attacks and see no immediate benefit from a daily tablet.

The problem is compounded when early mobilisation flares occur, which patients may interpret as the medicine making them worse rather than better.

In my practice, I invest significant time in patient education before starting allopurinol.

I explain that gout is a chronic condition caused by years of urate crystal accumulation, and that allopurinol works by gradually dissolving those crystals over months to years.

I use the analogy of draining a swimming pool: you cannot drain it in a day, and the water level may splash around as it drops, but persisting with the treatment will eventually empty the pool and eliminate the attacks entirely.

Patients who understand this concept are far more likely to persist through the initial flare period and achieve long-term remission.

Gout and cardiovascular risk

Emerging evidence links hyperuricaemia and gout to an increased risk of cardiovascular disease, including heart failure, coronary artery disease, and stroke.

The precise nature of the relationship, whether uric acid is a direct causative factor, an innocent bystander, or a marker of shared metabolic risk factors, remains under investigation.

Several large observational studies have suggested that allopurinol treatment may reduce cardiovascular events in gout patients, though randomised controlled trial data remain limited.

The ALL-HEART trial investigated whether allopurinol reduces cardiovascular events in patients with ischaemic heart disease without gout; the primary results did not demonstrate a benefit in that population, but the question remains open for gout patients with high urate burdens.

Storage

• Store allopurinol tablets below 25 degrees Celsius in a dry place.
• Keep in the original packaging to protect from light and moisture.
• Do not use after the expiry date on the packaging.
• Keep out of the sight and reach of children.

Frequently asked questions

Why did I get a gout attack after starting allopurinol?

This is a well-recognised phenomenon known as a mobilisation flare.

As allopurinol lowers uric acid levels, existing urate crystal deposits begin to dissolve, releasing small crystals that trigger inflammation.

This is actually a sign that the treatment is working.

Flare prophylaxis with colchicine or an NSAID can help manage these episodes, and they typically diminish within three to six months as the crystal burden reduces.

Do I need to take allopurinol forever?

In most cases, allopurinol is a long-term or lifelong treatment. If you stop taking it, uric acid levels will rise again and gout attacks are likely to return.

The benefits of continuous treatment include prevention of attacks, dissolution of tophi, and protection of kidney function.

I always explain to my patients that allopurinol is like a blood pressure medicine, it works while you take it and stops working when you stop.

Can I drink alcohol while taking allopurinol?

Moderate alcohol consumption is generally acceptable, but bear in mind that alcohol (especially beer and spirits) raises uric acid levels and can trigger gout attacks regardless of allopurinol use.

I advise patients to stay within the UK Chief Medical Officers' guidelines of no more than 14 units per week, spread across the week with several alcohol-free days.

Can allopurinol affect my kidneys?

Allopurinol is generally protective of kidney function in gout patients by reducing uric acid levels and preventing urate nephropathy.

However, the dose must be adjusted in patients with existing renal impairment, as oxipurinol is primarily excreted by the kidneys.

Your GP will monitor your kidney function with regular blood tests.

Sources

• EMC, Electronic Medicines Compendium (SmPC)
• BNF, British National Formulary
• BSR, British Society for Rheumatology (Gout guideline 2017)
• NICE CKS, Gout
• NHS, Gout