A xanthine oxidase inhibitor used as first-line urate-lowering therapy for the chronic management of gout and hyperuricemia. Allopurinol reduces serum uric acid levels by inhibiting the enzyme that converts hypoxanthine and xanthine to uric acid, preventing the formation and deposition of monosodium urate crystals in joints and tissues.
HLA-B*5801 positive patients (strongly associated with severe cutaneous adverse reactions, screen in high-risk populations)
The bottom line
Evidence rating strong. Most-documented uses: reduction of serum uric acid levels, prevention of recurrent gout flares, prevention and dissolution of uric acid kidney stones. 10 sources indexed (2016–2025), with 4 interaction records on file.
The science
How it works, mechanistically.
Core mechanism
Inhibits xanthine oxidase, the enzyme responsible for the conversion of hypoxanthine to xanthine and xanthine to uric acid. By blocking this final step in purine catabolism, allopurinol and its active metabolite oxypurinol reduce serum uric acid production. This lowers the total body urate pool and prevents new crystal deposition.
Class
Xanthine Oxidase Inhibitor (Gout)
Absorption
Water-soluble; take with food
Dosing
Dosing & protocol.
Common range
Start 100 mg daily, titrate by 100 mg every 2–4 weeks to target serum uric acid <6 mg/dL; typical range 200–600 mg daily (max 800 mg/day) (as prescribed by your physician)
Recommended form
Tablet
Take after meals to reduce GI side effects; maintain adequate fluid intake to prevent xanthine stone formation2,7
The interaction between allopurinol and iron is primarily theoretical. In animal studies, allopurinol increased hepatic iron storage by inhibiting the ferritin-xanthine oxidase system responsible for iron mobilization from the liver. However, controlled human studies found no measurable effect of allopurinol on iron absorption, storage, or red cell incorporation. A reversible rise in serum iron with decreased iron-binding capacity was observed at high doses (500-600 mg/day) but normalized at standard doses (300 mg/day).
Recommendation: Standard iron supplementation is generally safe with allopurinol at typical doses (100-300 mg/day). If taking high-dose allopurinol (>300 mg/day), periodic monitoring of serum iron and ferritin may be prudent. No timing separation is typically needed. Inform your prescriber about concurrent iron supplementation.
Allopurinol promotes oxidative stress that can deplete plasma ascorbate levels. Vitamin C supplementation may help offset this depletion and provide additional modest uricosuric effects. However, a clinical trial found that vitamin C 500 mg/day had no clinically significant urate-lowering effect in established gout patients, whether used alone or with allopurinol. The primary benefit of vitamin C with allopurinol may be antioxidant support rather than uric acid lowering.
Recommendation: Vitamin C supplementation (500-1000 mg/day) is safe with allopurinol and may help replenish ascorbate depleted by allopurinol-related oxidative stress. Do not rely on vitamin C as a substitute for allopurinol in treating gout. No dose adjustment or timing separation is needed.
Alcohol can trigger gout attacks and raise the urate burden that allopurinol is meant to control. Beer and spirits are the clearest concerns, and even short-term alcohol intake can increase recurrent flare risk. This is not solved by spacing doses because the issue is alcohol's effect on urate production, renal urate handling, and gout inflammation.
Recommendation: Limit or avoid alcohol while using allopurinol, especially during dose titration or if flares are still occurring. If you drink, keep intake low, hydrate well, and track whether attacks follow drinking. Tell your prescriber if flares continue despite allopurinol because the urate-lowering plan may need adjustment.
High-dose Vitamin B3 products that contain niacin or nicotinic acid can raise uric acid and have been associated with drug-induced gout. This can work against allopurinol's goal of keeping serum urate below target. The concern is mainly with lipid-dose niacin or high-dose supplements, not small dietary amounts.
Recommendation: Avoid starting high-dose Vitamin B3 while gout is active or serum urate is above target unless your clinician specifically recommends it. If niacin is necessary, check serum urate after starting or changing the dose and watch for new flares. Do not stop allopurinol during a flare unless your prescriber tells you to.
Chen J, Zhang Y, Wang Y et al.. Comparative efficacy and safety of febuxostat and allopurinol in chronic kidney disease stage 3-5 patients with asymptomatic hyperuricemia: a network meta-analysis. Renal failure. 2025
Alem MM. Allopurinol and endothelial function: A systematic review with meta-analysis of randomized controlled trials. Cardiovascular therapeutics. 2018
Chen AT, Malmstrom T, Nasrallah HA. Allopurinol augmentation in acute mania: A meta-analysis of placebo-controlled trials. Journal of affective disorders. 2018
Deng G, Qiu Z, Li D et al.. Effects of Allopurinol on Arterial Stiffness: A Meta-Analysis of Randomized Controlled Trials. Medical science monitor : international medical journal of experimental and clinical research. 2016
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