Allopurinol 100 mg and 300 mg Tablets: Prescription Xanthine Oxidase Inhibitor for Chronic Gout Prevention and Uric Acid Reduction

Information last reviewed: May 2026 — for educational purposes only.

Allopurinol (Zyloprim) is a prescription xanthine oxidase (XO) inhibitor — the cornerstone urate-lowering therapy (ULT) for chronic gout prevention. Xanthine oxidase is the enzyme responsible for the final steps of purine metabolism, converting hypoxanthine to xanthine and xanthine to uric acid. Allopurinol blocks XO, reducing the production of uric acid and consequently lowering serum urate levels. When serum uric acid is maintained chronically below the solubility threshold (6 mg/dL), monosodium urate crystals that have deposited in joints slowly dissolve, tophi gradually shrink, and gout attack frequency decreases substantially over months to years.

Allopurinol is indicated for hyperuricaemia with gout (recurrent gout attacks, tophaceous gout, gout with renal complications), uric acid kidney stones, and as urate-lowering prophylaxis in patients undergoing chemotherapy for haematological malignancies (tumour lysis syndrome prevention). It is a long-term medication — once started for gout prevention, it should be continued indefinitely. Many patients experience an initial increase in gout flares when starting allopurinol (due to urate crystal mobilisation as serum urate falls), which is why it should be started 2–4 weeks after an acute attack resolves, with colchicine or NSAID prophylaxis cover for the first 3–6 months.

What Is Allopurinol?

Allopurinol itself acts as a competitive inhibitor of xanthine oxidase. Its metabolite oxypurinol (alloxanthine) is an even more potent non-competitive XO inhibitor and has a much longer half-life (~18–30 hours) — responsible for most of the sustained uric acid-lowering effect. Because oxypurinol is renally excreted, dose adjustment is mandatory in patients with renal impairment: standard starting dose for CKD patients is 50–100 mg/day (not 300 mg as for normal renal function). Dose titration is based on serum uric acid measurements every 2–4 weeks until target urate (<6 mg/dL) is achieved.

Prescription Status

Allopurinol is prescription-only in the United States. It requires physician oversight for proper dosing, monitoring of renal function, and awareness of critical drug interactions. Regular serum uric acid and renal function monitoring are standard of care during dose titration.

Strengths and Available Forms

• 100 mg tablets — starting dose (100 mg once daily with food or after meals to reduce GI upset); dosing initiated low to reduce risk of hypersensitivity reactions and mobilisation flares
• 300 mg tablets — most common maintenance dose; many patients achieve serum uric acid <6 mg/dL on 300 mg/day; dose can be titrated up to 600–800 mg/day if needed (if renally tolerated)
• Allopurinol 500 mg/vial injection — hospital-only IV formulation for patients unable to take oral medications who require urate lowering (e.g., tumour lysis in critical care)

Standard dosing: Start 100 mg/day with food. Increase by 100 mg every 2–4 weeks based on serum uric acid. Target serum uric acid <6 mg/dL (or <5 mg/dL in severe tophaceous gout). Maximum dose 800 mg/day. Reduce dose proportionally for CKD (GFR-based dosing). Maintain adequate hydration (≥2 L/day) to prevent xanthine kidney stone formation.

Price of Allopurinol

Generic allopurinol 100 mg and 300 mg tablets are available at very low cost at US pharmacies — among the most affordable prescription chronic medications available. It is on the $4 generic list at major pharmacy chains. Brand-name Zyloprim is more expensive but rarely necessary. Insurance coverage is universal.

Frequently Asked Questions

Critical drug interaction: allopurinol and azathioprine or mercaptopurine

This is one of the most dangerous drug interactions in medicine. Azathioprine (Imuran) and mercaptopurine are immunosuppressants metabolised by — xanthine oxidase. When allopurinol inhibits XO, it dramatically increases the plasma levels of azathioprine and mercaptopurine (typically by 3–4 fold), causing potentially fatal bone marrow suppression (agranulocytosis, aplastic anaemia). If allopurinol must be co-prescribed with azathioprine (e.g., in a transplant patient who develops gout), the azathioprine dose must be reduced by 75% and haematological monitoring must be intensive. Many physicians avoid the combination entirely, using febuxostat (a different XO inhibitor not affecting azathioprine metabolism) instead.

Why does starting allopurinol sometimes cause more gout attacks initially?

When serum uric acid rapidly drops after starting allopurinol, urate crystals in joint spaces and tissues mobilise (partially dissolve and shift), triggering local inflammatory reactions — producing what appears to be a gout flare. This is a well-recognised predictable phenomenon, not an adverse drug reaction or treatment failure. It is prevented or reduced by starting at a low dose (100 mg/day) and increasing gradually, and by prescribing prophylactic colchicine (0.6 mg once or twice daily) or a low-dose NSAID for the first 3–6 months of allopurinol therapy. Patients should be advised in advance that early flares do not mean the medication is not working and not to stop allopurinol during an acute gout attack.

What is allopurinol hypersensitivity syndrome?

Allopurinol hypersensitivity syndrome (AHS) is a rare but potentially life-threatening reaction characterised by severe cutaneous adverse reactions (SCAR) — including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) — combined with systemic involvement (hepatitis, nephritis, eosinophilia). AHS is strongly associated with HLA-B*58:01 genotype, common in patients of Han Chinese, Korean, and Thai descent — genetic testing before starting allopurinol is recommended for these populations by several national guidelines. In other populations, AHS risk is low but not zero. Starting allopurinol at low doses and increasing gradually, and stopping immediately at the first sign of a skin rash, are the key safety measures. Any skin rash on allopurinol should be assumed to be a hypersensitivity reaction until proven otherwise.

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