Allopurinol is a xanthine oxidase inhibitor widely used to lower uric acid levels and prevent gout attacks, kidney stones, and urate nephropathy. It works by reducing uric acid production, helping dissolve existing crystals and preventing new ones. Clinically proven, cost-effective, and used long-term, Allopurinol is taken daily and requires dose adjustments in kidney disease. It should not treat acute flares; start only when attacks are controlled. Regular lab monitoring is essential to target serum urate <6 mg/dL. This overview covers uses, dosing, safety, interactions, and U.S. prescription rules to help you discuss Allopurinol with your clinician and make informed decisions.
Allopurinol is a first-line urate-lowering therapy used to prevent gout attacks, shrink tophi, and reduce long-term joint damage. By inhibiting xanthine oxidase, it decreases production of uric acid, allowing urate crystals to dissolve gradually and minimizing new crystal formation. It is not a pain reliever and does not treat an acute flare, but it helps stabilize uric acid levels over time to prevent future attacks.
Beyond gout, Allopurinol helps prevent recurrence of uric acid kidney stones in people with hyperuricosuria, especially when dietary measures alone are insufficient. It is also used to manage chronic hyperuricemia related to kidney disease or certain genetic conditions that lead to overproduction of uric acid. In oncology, clinicians sometimes use Allopurinol to reduce uric acid spikes associated with tumor lysis syndrome when starting cytotoxic chemotherapy.
Clinical guidelines typically recommend Allopurinol as the initial xanthine oxidase inhibitor for most patients due to its effectiveness, affordability, and extensive track record. It is suitable for many patients, including those with chronic kidney disease, provided dosing is individualized and monitoring is consistent.
Allopurinol dosing is individualized and should be guided by a clinician. Treatment usually starts low and is titrated to reach a serum urate target below 6 mg/dL (or below 5 mg/dL in severe tophaceous gout). Typical adult starting doses are 100 mg once daily; in chronic kidney disease, clinicians may begin at 50 mg daily. The dose is increased gradually—often every 2 to 5 weeks—until the urate goal is reached, up to a maximum of 800 mg/day in divided doses in the U.S.
Do not initiate Allopurinol during an acute gout flare. If you are already taking it and a flare occurs, do not stop; continue the medication and treat the flare with appropriate anti-inflammatory therapy as directed by your clinician. When starting Allopurinol, many patients are prescribed low-dose colchicine, an NSAID, or low-dose corticosteroids for 3 to 6 months as prophylaxis against flare-ups that can occur during the early phase of urate lowering.
For uric acid kidney stone prevention, Allopurinol is combined with hydration and urine alkalinization strategies. In oncology settings (e.g., tumor lysis syndrome prophylaxis), dosing and timing differ and are determined by the oncology team, often starting 2 to 3 days before chemotherapy and continuing for 10 to 14 days, with careful lab monitoring.
Take Allopurinol after meals with a full glass of water to reduce stomach upset and support kidney excretion of urate. Maintain adequate daily fluid intake unless otherwise advised. Because oxypurinol (the active metabolite) is renally cleared, dosing is adjusted in kidney impairment. Regular checks of serum urate, kidney function, and liver enzymes help ensure safe, effective therapy.
A rare but serious reaction called allopurinol hypersensitivity syndrome (AHS) can involve severe rash, fever, hepatitis, kidney injury, and eosinophilia. The risk is higher in certain genetic backgrounds, particularly carriers of HLA-B*58:01. Screening for HLA-B*58:01 is recommended in specific high-risk groups, notably people of Han Chinese, Thai, or Korean descent, especially if concomitant chronic kidney disease is present. If you develop a rash, stop Allopurinol and seek care immediately.
Tell your clinician about all medications and supplements. Special caution is needed with azathioprine and mercaptopurine, whose doses must be drastically reduced and closely monitored due to potentially severe toxicity when combined with Allopurinol. Additional vigilance is warranted with diuretics and ACE inhibitors (rash risk), warfarin (enhanced anticoagulation), and theophylline (levels may rise).
Allopurinol may be used in chronic kidney disease with cautious titration, but dehydration and sudden changes in renal function increase adverse event risk. Patients with liver disease may require lab monitoring to detect hepatotoxicity. In pregnancy and breastfeeding, risk–benefit should be individualized with a clinician; if treatment is needed, close monitoring is standard. Avoid excessive alcohol, which can raise uric acid and undermine therapy.
Allopurinol is contraindicated in patients with prior serious hypersensitivity to allopurinol or oxypurinol, including Stevens–Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), drug reaction with eosinophilia and systemic symptoms (DRESS), or AHS. Do not rechallenge after such reactions. Immediate discontinuation and emergency evaluation are required if severe cutaneous adverse reactions develop.
Concomitant pegloticase is generally contraindicated; xanthine oxidase inhibitors can mask rising urate levels that would otherwise alert clinicians to increased risk of infusion reactions with pegloticase. Use of Allopurinol with azathioprine or mercaptopurine is not absolutely contraindicated, but it requires expert management with substantial dose reduction and close monitoring due to life-threatening myelosuppression risk.
Common side effects include mild rash, itching, gastrointestinal discomfort (nausea, diarrhea, abdominal pain), headache, and drowsiness. These are often transient, but any new rash warrants urgent attention, as it can occasionally progress to more serious reactions. Lab abnormalities may include transient liver enzyme elevations or mild changes in blood counts.
Serious adverse reactions are uncommon but can be life-threatening. AHS, SJS/TEN, hepatitis, cholestatic jaundice, eosinophilia, vasculitis, interstitial nephritis, and severe bone marrow suppression have been reported. Risk factors include certain HLA genotypes, renal impairment, high starting doses, and diuretic use. Early recognition and drug discontinuation are critical. Seek immediate medical evaluation for fever, facial swelling, mucosal sores, dark urine, jaundice, widespread blistering, or peeling skin.
Gout flares may increase temporarily after starting Allopurinol due to mobilization of tissue urate. This is not an allergy and is mitigated by anti-inflammatory prophylaxis and slow dose titration. Staying on Allopurinol during flares, unless a serious adverse reaction occurs, supports long-term control.
Allopurinol inhibits xanthine oxidase, a key pathway for metabolizing azathioprine and 6-mercaptopurine. When combined, the dose of azathioprine/6-MP usually must be reduced to approximately 25–33% of the typical dose, with intensive monitoring for bone marrow suppression and infection. This combination should be managed only by clinicians experienced with these agents.
Warfarin’s anticoagulant effect may be enhanced, necessitating closer INR monitoring and possible dose adjustment. Theophylline levels can increase, particularly at higher Allopurinol doses. Concomitant use with ampicillin or amoxicillin is associated with a higher rate of rash. Cyclophosphamide and other myelosuppressive agents may increase hematologic toxicity; careful blood count monitoring is advised.
Didanosine levels rise significantly with Allopurinol, increasing the risk of toxicity; avoid coadministration. Cyclosporine concentrations may also increase. Aluminum hydroxide antacids can reduce Allopurinol absorption if taken simultaneously—separate administration times. Thiazide diuretics and ACE inhibitors can raise the risk of hypersensitivity reactions. Do not use Allopurinol concurrently with pegloticase; stop urate-lowering therapy before pegloticase initiation to avoid masking rising uric acid, which is used to detect nonresponse and reduce infusion reaction risk.
If you miss a dose, take it as soon as you remember unless it is close to the time of your next dose. If it is nearly time for the next dose, skip the missed dose and resume your regular schedule. Do not double up to “catch up.” Setting reminders can help maintain consistent urate control.
Symptoms of Allopurinol overdose may include nausea, vomiting, diarrhea, dizziness, and rash; severe cases can involve kidney dysfunction or hepatitis. Seek emergency medical attention. Management is supportive, with aggressive hydration and correction of electrolyte abnormalities. Oxypurinol is dialyzable, so hemodialysis may be considered in select severe overdoses or significant renal impairment.
Store Allopurinol tablets at room temperature (ideally 20–25°C/68–77°F) in a tightly closed container, protected from moisture and excessive heat. Keep out of reach of children and pets. Do not use tablets that are discolored, chipped, or past their expiration date. Dispose of unused medication through take-back programs when available.
In the United States, Allopurinol is a prescription-only medication. It is not legal or safe to obtain Allopurinol without a valid prescription from a licensed clinician who has evaluated your health, medications, and goals for urate control. Responsible access typically occurs through in-person clinics, integrated health systems, or legitimate telehealth services that provide proper evaluation, diagnosis, and follow-up with lab monitoring.
Be cautious of websites offering to sell prescription drugs without a prescription; many are unregulated, may dispense counterfeit or substandard products, and can put your health at risk. Look for pharmacies accredited by the National Association of Boards of Pharmacy (NABP), such as those bearing the .pharmacy domain or listed on NABP’s Safe Pharmacy site. Insurance plans, discount programs, and manufacturer or nonprofit assistance can help make therapy affordable when prescribed appropriately.
Some health systems and telemedicine platforms streamline evaluation and prescription for gout management, but a clinician’s involvement is still required. We cannot assist in obtaining Allopurinol without a prescription, and any claims suggesting a workaround should be treated with skepticism. The safest, legal path is to consult a licensed provider who can confirm the diagnosis, order baseline labs, initiate a personalized dosing plan, and monitor your response over time.
Allopurinol is a xanthine oxidase inhibitor that lowers uric acid production. By blocking the enzyme that converts purines into uric acid, it helps prevent gout flares, tophi, some kidney stones, and uric acid spikes from tumor lysis syndrome.
It’s prescribed for recurrent gout, tophaceous gout, uric acid overproduction, uric acid or calcium oxalate kidney stones linked to high uric acid, and prevention of tumor lysis–related hyperuricemia. It’s not for asymptomatic hyperuricemia except in special cases.
Typical starting dose is 100 mg daily (50 mg if advanced chronic kidney disease), titrated every 2–5 weeks to reach serum urate under 6 mg/dL (under 5 mg/dL if tophi). Max dose can be up to 800 mg/day in divided doses if needed and tolerated.
Uric acid starts dropping within days, but clinical benefits build over weeks to months. Flares can paradoxically increase early on, so anti-inflammatory prophylaxis is recommended for at least 3–6 months when starting therapy.
Yes, guidelines allow starting allopurinol during an acute flare as long as flares are treated and prophylaxis (colchicine, NSAID, or low-dose steroid) is used. If you’re already on allopurinol, do not stop it during a flare.
Nausea, diarrhea, mild rash, drowsiness, and liver enzyme elevations can occur. Rarely, severe reactions like allopurinol hypersensitivity syndrome (AHS), Stevens-Johnson syndrome, or toxic epidermal necrolysis may develop and require immediate discontinuation.
AHS is a life-threatening drug reaction with fever, widespread rash, organ involvement (liver, kidney), and eosinophilia. Risks increase with the HLA-B*58:01 allele, chronic kidney disease, higher starting doses, and diuretic use.
Testing is recommended for high-risk groups, including many Han Chinese, Korean (especially with CKD), Thai, and often African American patients. A positive test means allopurinol should generally be avoided.
It raises levels of azathioprine and 6-mercaptopurine (reduce these to 25–33% or avoid), increases didanosine exposure, can potentiate warfarin, and may raise theophylline and cyclosporine levels. Thiazide diuretics and ampicillin/amoxicillin increase rash risk.
Yes, with careful dose selection and titration to target urate. Starting low and going slow reduces adverse effects. Achieving the urate goal is more important than arbitrary dose caps, provided monitoring is in place.
Allopurinol works best with lifestyle support: hydrate well, limit beer and spirits, reduce purine-rich meats and shellfish, and cut back on high-fructose corn syrup. Weight loss and managing blood pressure, lipids, and diabetes lower gout risk.
Yes, continue allopurinol to maintain urate control unless your clinician advises otherwise. Stopping abruptly can trigger flares.
Check every 2–5 weeks during dose titration until the target is reached, then every 6–12 months (or sooner if flares, kidney function changes, or medication adjustments occur). Periodically monitor kidney and liver function and CBC.
Yes. It lowers urinary uric acid to help prevent uric acid and some calcium oxalate stones in hyperuricosuria, and it’s used to prevent hyperuricemia in tumor lysis syndrome when rasburicase isn’t indicated.
Data are limited. Use in pregnancy is generally reserved for compelling indications after risk–benefit discussion. Allopurinol and its metabolite appear in breast milk; if used, infants should be monitored, and alternatives may be preferred when feasible.
Take the missed dose when remembered unless it’s close to the next one; don’t double up. Do not stop abruptly without medical advice—sudden discontinuation can raise uric acid and precipitate gout flares.
Both are xanthine oxidase inhibitors. Febuxostat can be slightly more potent at standard doses, but with proper titration, many patients achieve target urate on allopurinol. Choice depends on comorbidities, tolerance, cost, and access.
The CARES trial signaled higher cardiovascular and all-cause mortality with febuxostat in high-risk patients, leading to a U.S. boxed warning. The FAST trial did not confirm increased CV risk versus allopurinol in a lower-risk group. Clinicians individualize decisions based on cardiovascular history.
Both can be used in CKD with appropriate dosing. Febuxostat’s hepatic clearance can be convenient in advanced CKD, but allopurinol is also effective when started low and titrated. Drug choice hinges on overall risks, interactions, and cost.
Severe cutaneous reactions are strongly linked to allopurinol, especially in HLA-B*58:01 carriers. Febuxostat can cause rash but has a lower association with life-threatening skin reactions. Genetic testing doesn’t predict febuxostat reactions.
Both dangerously interact with azathioprine and 6-mercaptopurine, requiring major dose reductions or avoidance. Allopurinol has more noted interactions with theophylline and didanosine; febuxostat can raise levels of these too, but profiles differ slightly. Always review the full interaction list.
Generic allopurinol is typically far less expensive and widely covered. Febuxostat is often costlier and may need prior authorization.
Most guidelines recommend allopurinol as first-line urate-lowering therapy for gout, including in CKD, due to long-term experience, cost, and effectiveness. Febuxostat is a common second-line option when allopurinol is not tolerated or insufficient.
No. Combining xanthine oxidase inhibitors offers no benefit and can increase adverse effects. If target urate isn’t reached on a maximally tolerated XOI, clinicians may add a uricosuric (e.g., probenecid where appropriate) or consider pegloticase for refractory disease.
Consider switching for persistent urate above goal despite maximally tolerated dosing, significant side effects, or HLA-B*58:01 positivity precluding safe allopurinol use. The transition is typically done by tapering one while initiating the other under medical supervision.
Oxypurinol is the active metabolite of allopurinol and a xanthine oxidase inhibitor itself, but a standalone oxypurinol product isn’t widely available. Some centers use allopurinol desensitization protocols after mild rashes; severe reactions are a contraindication.
Topiroxostat is a xanthine oxidase inhibitor available in some countries (e.g., Japan). Data suggest urate-lowering efficacy comparable to other XOIs, but global experience and availability are limited. Allopurinol remains the more established option.
For non-severe, non–mucosal rashes, desensitization under specialist supervision can be considered if allopurinol is strongly preferred. Any severe cutaneous reaction (SJS/TEN/AHS) mandates permanent avoidance; switching to febuxostat or another class is appropriate.
Many patients tolerate both, but febuxostat may cause fewer rashes and requires no HLA-B*58:01 screening. However, cost, cardiovascular warnings, and individual response matter. Allopurinol’s long track record and affordability keep it the default choice.