Allopurinol — patient guide

This page covers allopurinol — the main urate-lowering tablet for gout in AU. If you have been started on Zyloprim, Progout, or a generic with “allopurinol” on the box, this is your page. Febuxostat (Adenuric) and probenecid (Probalan) are covered briefly below as alternatives.

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Find your medicine

Generic name	Common brand names	Strengths	How often
Allopurinol	Zyloprim, Progout, generics	100 / 300 mg	Once daily (can be split if higher dose causes stomach upset)

Other urate-lowering options patients sometimes ask about

Generic name	Brand	Strengths	When used
Febuxostat	Adenuric	40 / 80 / 120 mg	Alternative xanthine oxidase inhibitor when allopurinol is unsuitable
Probenecid	Probalan	500 mg	Older uricosuric — used uncommonly in AU now; supply has been intermittent

Why not febuxostat by default? Both drugs lower uric acid by blocking the same enzyme. The CARES trial (NEJM 2018) flagged a safety signal. It reported higher cardiovascular and all-cause mortality with febuxostat compared with allopurinol in patients with heart disease. The later FAST trial (Lancet 2020) did not confirm that signal in a broader group. So the AU and international position is simple. Allopurinol is the usual first choice. This is especially true after a prior cardiovascular event. Febuxostat is held in reserve. It is used when allopurinol is not tolerated, when a person is HLA-B*5801 positive without another path, or when urate cannot reach target on tolerated allopurinol doses. Sources: CARES NEJM 2018, FAST Lancet 2020.

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What it treats

Allopurinol is prescribed for more than just acute gout. Your reason may be one or more of:

• Long-term prevention of gout flares — the most common reason. Allopurinol is not a treatment for an acute flare; it prevents future flares by keeping serum urate below the level at which crystals form.
• Shrinking gout tophi — visible or imaged crystal deposits in joints, ear, fingers, or soft tissue. The lower urate target (below 0.30 mmol/L) dissolves these over months to years.
• Prevention of tumour lysis syndrome during chemotherapy for certain cancers (specialist setting).
• Hyperuricaemia of malignancy — high uric acid driven by some blood cancers.
• Recurrent uric acid kidney stones in selected cases — usually with urinary alkalinisation and hydration.

The drug does not numb a flare. If you are mid-flare, the treatment is a separate set of options (NSAID, colchicine, or short-course steroid). Allopurinol is the long game.

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The basics

1. Take it at the same time every day. Once daily is standard. With or without food. A glass of water helps.
2. Do not stop on your own if a flare hits. A flare in the first 3-6 months is expected and is not a sign the tablet has failed.
3. Tell every prescriber if you also take azathioprine, 6-mercaptopurine, warfarin, or theophylline. These interact significantly with allopurinol.
4. Watch the skin in the first 2 months. Any new rash, blistering, mouth or eye ulcers, fever, or feeling generally unwell — stop the tablet and seek urgent assessment the same day.

Everything else — initiation strategy, the blood tests, the integrative angle — is below.

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HLA-B*5801 testing before starting

This is the most important pre-start step for some patients and is missed often.

Who needs the test. People of Han Chinese, Thai, Korean, Indonesian, Filipino, or Indigenous Australian ancestry. In these populations roughly 10-15% of people carry the HLA-B*5801 gene, compared with about 1-2% in people of Caucasian ancestry (Hung et al. PNAS 2005).

Why it matters. Carriers of HLA-B*5801 have approximately an 80-fold higher risk of severe cutaneous adverse reactions (SJS, TEN, DRESS) on allopurinol. These reactions are rare in absolute terms, but when they happen they carry a real mortality risk.

What happens if the test is positive. The usual alternative is febuxostat (Adenuric), which does not share the same HLA association.

Funding pathway. HLA-B*5801 is not universally Medicare-funded in AU. Some pathology providers offer it as a private test. Your GP will discuss the cost and the pathway. If a positive result will change the plan, the test is worth doing before starting.

For patients without an at-risk ancestry, routine HLA-B*5801 testing is not current AU standard practice — the much lower carriage rate means the test changes management in too few people to justify the cost as a default.

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Starting allopurinol — what to expect

Start low. 50-100 mg once daily is the standard starting dose, regardless of how high the serum urate is. A higher start does not lower urate faster — it raises the risk of a hypersensitivity reaction without speeding the win (Stamp et al. Arthritis Rheum 2012).

Titrate slowly. Step up by roughly 100 mg per month, with a serum urate check before each step, until you reach the target.

The target.

• Below 0.36 mmol/L for most patients with gout.
• Below 0.30 mmol/L if there are tophi — the lower target dissolves crystal deposits faster.

Typical maintenance dose is 300-600 mg/day, sometimes higher in resistant cases. Many patients sit on 300 mg long-term once the target is reached.

Renal impairment. Start lower (50 mg/day if eGFR is below 60; 50 mg every other day if eGFR is below 30) and titrate more slowly. Modern AU and international practice is to keep titrating cautiously until urate is at target — the older habit of capping the dose at a low level in renal impairment under-treated gout and is no longer recommended.

Flare cover for at least 3 months. Colchicine 0.5 mg twice daily (or an NSAID where colchicine is unsuitable) is taken alongside allopurinol initiation to dampen the expected flare risk in the high-flare window. Some specialists extend cover to 6 months in tophaceous disease.

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Why flares often WORSEN at first

This catches almost everyone off guard.

When allopurinol lowers serum urate, the long-standing crystal deposits inside the joints begin to dissolve. The dissolving process itself is recognised by the immune system in the same way a brand-new flare is recognised, and a flare can be triggered. Roughly the first 3-6 months on allopurinol is the high-flare window.

This is expected. It is not a sign the tablet is failing. The opposite — it means urate is dropping and crystals are mobilising.

The standard response is:

• Keep taking allopurinol through the flare. Stopping and restarting actually raises the risk of another flare.
• Treat the flare in the usual way (NSAID, colchicine, or a short course of oral steroid, per your GP’s plan).
• Continue the colchicine 0.5 mg twice daily flare cover for the full 3-6 month window.

Once the crystal burden is gone — months to a year or two — flare frequency drops sharply.

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Red-flag rash — same day, not next week

Severe cutaneous adverse reactions to allopurinol (SJS, TEN, DRESS) are rare but carry a real mortality risk. Onset is typically 2-8 weeks after starting.

Stop the tablet and seek urgent same-day assessment if you develop ANY of these in the first 2 months:

• A new rash, particularly spreading or blistering
• Mouth, eye, or genital ulcers
• Peeling skin
• Fever
• Sore throat with the rash
• Feeling generally unwell out of proportion to a minor virus

These can also appear later than 2 months — the same rule applies if any new rash develops at any time on allopurinol. The rash + fever + mucosal-surface combination is the pattern that matters most.

If you are unsure — stop the tablet and call your GP the same day. The cost of stopping for a day or two is nothing; the cost of missing a severe reaction is substantial.

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Tap any section below to expand the detail.

How does it work?

Allopurinol blocks an enzyme called xanthine oxidase. Xanthine oxidase is what your body uses to produce uric acid from the breakdown of purines (the building blocks of DNA, found in your own cells and in some foods). Blocking the enzyme drops serum urate.

Crystals of uric acid only form above a certain saturation point in joint fluid. Below that point (roughly 0.36-0.40 mmol/L), existing crystals slowly dissolve and new crystals do not form. That is why the goal is a target serum urate number, not a percentage reduction from baseline.

Allopurinol does not numb a current flare. The dissolving and the not-forming take months. The flare-prevention benefit is downstream of getting and keeping urate at target, sustained over time.

Febuxostat (Adenuric) works on the same enzyme by a slightly different mechanism. Probenecid (Probalan) works differently — it acts at the kidney tubules to increase uric acid excretion rather than reducing production.

Side effects in detail

Common (usually mild)

• Acute gout flare in the first 3-6 months. Expected, not a side effect in the usual sense. Continue allopurinol; treat the flare; continue colchicine cover.
• Mild rash. Watch carefully. Any rash that spreads, blisters, comes with fever, or involves mouth or eye surfaces is NOT mild — stop and seek urgent assessment.
• Nausea, diarrhoea, stomach upset. Usually settles. Taking with food can help. Splitting a higher dose into morning and evening can help.
• Headache, drowsiness, dizziness. Usually mild and settles.
• Mild rise in liver enzymes on blood tests in the first few months. Common and usually settles; rarely progresses.

Uncommon

• Metallic taste or reduced taste.
• Hair loss (uncommon, usually reverses on stopping).
• Joint aches separate from gout.

Rare but serious — stop and seek urgent same-day assessment

• Severe cutaneous adverse reactions (SJS, TEN, DRESS). See the red-flag rash section above. Onset typically 2-8 weeks after starting.
• Allopurinol hypersensitivity syndrome — overlaps with DRESS. Rash, fever, hepatitis, kidney inflammation, and a raised eosinophil count on a full blood test. Stop and seek urgent assessment.
• Bone marrow suppression. Unexplained bruising, bleeding, frequent or severe infections, mouth ulcers — urgent full blood count.
• Severe liver injury (rare). Yellowing of the eyes or skin, dark urine, persistent vomiting — urgent assessment.
• Peripheral neuropathy (rare). New persistent tingling, numbness, or burning in the feet or hands — review with your GP.

Drug interactions — the ones that matter

Tell every prescriber and pharmacist about allopurinol before any new medicine is started. The big ones:

• Azathioprine (Imuran) and 6-mercaptopurine (Puri-Nethol). This is the most dangerous interaction. Allopurinol blocks the enzyme that clears these drugs, causing severe accumulation and bone marrow toxicity. The standard response is to reduce the azathioprine or 6-MP dose by roughly 75% under specialist supervision, OR switch to an alternative urate-lowering agent. NEVER combine without that adjustment.
• Warfarin. Allopurinol can raise the INR. Check INR within 1-2 weeks of starting allopurinol or after a dose change.
• Theophylline (a less commonly used asthma and COPD medicine). Allopurinol reduces theophylline clearance and can raise blood levels into the toxic range. Specialist supervision if both are needed.
• Ciclosporin (transplant medicine). Possible raised ciclosporin levels — monitoring needed.
• Cyclophosphamide (some cancer chemotherapy). Possible increased bone marrow toxicity — specialist supervision.
• Ampicillin / amoxicillin antibiotics. Small increased risk of rash when combined with allopurinol. Not a reason to avoid these antibiotics when they are needed — just be aware.
• ACE inhibitors and thiazide diuretics together with allopurinol — possible increased risk of hypersensitivity reactions in some reports, particularly in renal impairment. Not an absolute contraindication.

Colchicine is INTENTIONALLY co-prescribed during initiation — 0.5 mg twice daily for at least 3 months as flare cover. Colchicine dose is reduced in renal impairment.

Food. No specific food restrictions for the medicine itself. Dietary changes that lower serum urate (less alcohol, less fructose-sweetened drinks, less organ meats) help alongside the tablet but do not replace it.

Alcohol. Light to moderate intake is okay from a medicine-safety perspective. Heavy drinking — particularly beer and spirits — raises serum urate and triggers flares; cutting back helps gout control regardless of allopurinol.

Monitoring — blood tests and timing

• Before starting: serum urate (baseline), kidney function (eGFR + creatinine), liver enzymes (LFTs), full blood count. HLA-B*5801 testing if you are of Han Chinese, Thai, Korean, Indonesian, Filipino, or Indigenous Australian ancestry.
• 2-4 weeks after starting: LFTs and full blood count (early hepatotoxicity or marrow effect detection). Serum urate.
• Before each dose step-up (roughly monthly during titration): serum urate, kidney function. Repeat LFTs if the previous result was abnormal.
• Once on a stable maintenance dose: serum urate every 6 months until consistently at target; then annually with kidney function and LFTs unless something changes.
• Anytime you start a new medicine (including over-the-counter and supplements), get gastro, or feel persistently unwell — message us or your GP.

The goal of monitoring is two things: confirming serum urate is at target (below 0.36 mmol/L for most, below 0.30 mmol/L if tophi), and catching the rare but serious side effects (severe rash, hepatotoxicity, marrow suppression) early.

Pregnancy and breastfeeding

Pregnancy. Limited human safety data. Allopurinol is not started routinely during pregnancy and is generally avoided unless the gout burden is severe and uncontrolled. Decisions are made case-by-case with rheumatology and obstetric input.

• Planning a pregnancy: tell your GP before trying. The conversation is about whether to continue, hold, or swap.
• Already on allopurinol and just found out you are pregnant: contact your GP as soon as possible. Do not stop suddenly without that conversation — abruptly stopping can trigger a flare. The plan is individualised.

Breastfeeding. Limited safety data. Allopurinol and its metabolite oxipurinol do pass into breast milk. Case-by-case decision with your GP and (if available) a specialist obstetric pharmacist.

Sick day rules and missed doses

Missed dose. Take it as soon as you remember on the same day. If it is closer to your next dose, skip the missed one. Do not double up.

Vomiting or severe diarrhoea. A short pause is reasonable while you cannot keep tablets down. Restart once you are eating, drinking, and feeling better — usually 24-48 hours. If you are on a thiazide or loop diuretic as well, the bigger concern in dehydration is kidney function — message your GP.

Hospital admission or surgery. Tell the admitting team you are on allopurinol. It is usually continued through surgery unless there is a specific reason to hold it. The interactions list above matters most during an admission — new antibiotics, new pain medicines, and new anticoagulants all need cross-checking.

Stopping allopurinol

Do not stop without talking to your GP first.

If side effects are the issue, the conversation is usually about swapping (to febuxostat) rather than stopping urate-lowering therapy altogether — leaving gout untreated lets crystals re-form and flares return.

If a severe rash appears in the first 2 months, stop immediately and seek urgent same-day assessment. Do not restart without specialist input.

If you have been flare-free for years, on a stable dose, with no tophi, normal kidney function, and a significant lifestyle change (major weight loss, alcohol reduction) — a slow trial off allopurinol with monitoring is possible but not standard. The conversation is with your GP. Most people with established gout stay on urate-lowering therapy long-term because gout is a deposition disease — stop the tablet, urate climbs, crystals re-form.

Before planned surgery, allopurinol is usually continued — confirm with your anaesthetist.

Cost

Allopurinol is on the PBS. From 1 January 2026, the PBS co-payment is:

• General patient: up to $25.00 per script
• Concession card holder: up to $7.70 per script

Allopurinol is one of the cheaper long-term medicines on the PBS. Generic versions cost the same as branded ones at PBS pricing and work the same. Your actual charge may be lower if the medicine is under-co-payment. Confirm with your pharmacist — they can show you the exact price.

Febuxostat (Adenuric) PBS status is more restricted — typically authority criteria apply (e.g. intolerance to allopurinol or HLA-B*5801 positive). Your GP or rheumatologist will work the authority pathway if febuxostat is the choice.

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The integrative view

Most patients want to do everything they reasonably can in addition to taking the tablet. This is the longer version of that conversation, with the caveat that frames everything: diet alone does not fix established gout. The strongest dietary intervention reduces serum urate by around 10% at best — enough to cut flare frequency, not enough on its own to dissolve tophi or to keep serum urate consistently below the target in someone with established disease.

Two principles. First: allopurinol works and it is well-evidenced. Lifestyle measures also work. Combined, they work better than either alone. Second: dietary triggers are a flare-frequency lever, not a cure. Once the tablet is at target dose, the dietary lever is icing — useful, not load-bearing.

Strong evidence — these reliably move serum urate or flare frequency

• Reducing alcohol. Beer and spirits raise serum urate more than wine. Cutting to within Australian guidelines (no more than 10 standard drinks per week, no more than 4 in any single day) reduces flare frequency in cohort and intervention studies. The largest single dietary lever for most patients.
• Reducing fructose-sweetened drinks. Soft drinks, cordials, and fruit juices sweetened with high-fructose corn syrup raise serum urate consistently in observational and intervention data. Glucose-sweetened drinks raise urate less. Switching to water or unsweetened drinks is a real win.
• Reducing high-purine animal foods. Organ meats (liver, kidney, brain), anchovies, sardines, mussels, and yeast extracts are the highest-purine foods. Cutting them back reduces serum urate by roughly 5-10%. Note that purine restriction is a smaller lever than alcohol and fructose for most patients.
• Gradual weight loss if overweight. A modest reduction (5-10% body weight, sustained) lowers serum urate by a small but real amount. The key word is gradual. Avoid crash diets and prolonged fasting — they raise serum urate transiently and can trigger flares.

Moderate evidence — likely helpful

• Cherries — 2 servings per day. Zhang et al. Arthritis Rheum 2012 reported roughly a 50% reduction in flare risk associated with cherry intake over the prior 2 days. Observational only — effect sizes commonly shrink in randomised trials. Reasonable adjunct.
• Vitamin C at doses around 500 mg per day has been studied as a dietary adjunct — small RCT and meta-analytic data (Juraschek et al. Arthritis Care Res 2011) show a modest serum urate reduction of roughly 0.02-0.05 mmol/L. Useful as a supplement adjunct, not a replacement for allopurinol. Discuss starting any supplement with your GP first.
• Low-fat dairy. Protective in epidemiological cohorts. 1-2 serves per day is a reasonable target if tolerated.
• Coffee. Moderate intake (2-4 cups per day) is associated with lower serum urate and lower gout incidence. Not a reason to start drinking coffee; not a reason to stop either.
• Hydration. Aim for urine output above 2 L per day, particularly if you have a history of uric acid kidney stones. Water is the right vehicle.

Limited or emerging evidence

• Fish oil (EPA/DHA). Anti-inflammatory adjunct. Does not lower serum urate but may reduce flare-related symptoms.
• Tart cherry juice extract in supplement form — smaller dataset than whole cherries.
• Curcumin, quercetin — anti-inflammatory adjuncts with limited gout-specific data.

What to avoid

• Crash diets and prolonged fasting. Transient rise in serum urate and a real flare trigger.
• High-dose niacin (nicotinic acid, vitamin B3) supplements. Raises serum urate. Dietary intake of niacin from food is fine.
• Fructose-sweetened drinks. Worth a second mention — soft drinks and many fruit-juice drinks are the most-overlooked dietary trigger in gout.
• High-protein crash regimens. The combination of crash weight loss and high purine load is the worst-of-both-worlds for serum urate.

About thiazide and loop diuretics

Thiazide diuretics (hydrochlorothiazide, indapamide, chlortalidone) and loop diuretics (furosemide) raise serum urate. If you are on one of these for blood pressure and now have gout, the conversation with your GP is whether the blood-pressure indication still warrants the diuretic, or whether a swap to an alternative class would suit better. Losartan, an angiotensin receptor blocker, has a mild urate-lowering effect built in and is often a sensible swap for blood pressure control in someone with gout. Do not stop the diuretic on your own — that is a planned swap with your GP, not a unilateral move.

What the research says about CKD and heart failure

A common question is whether allopurinol slows kidney disease progression or helps with heart failure. The honest summary:

• Slowing CKD progression — small early RCTs (e.g. Goicoechea et al. 2010) suggested a benefit. Larger trials (CKD-FIX NEJM 2020, PERL NEJM 2020) did not confirm a meaningful effect. Off-label in AU. Not a stand-alone reason to start allopurinol.
• Heart failure — mechanistic interest in xanthine-oxidase inhibition reducing oxidative stress. The EXACT-HF trial did not show symptomatic benefit. Off-label and not a routine recommendation.

If your treating team has discussed these uses, it is in a specific context — talk through the rationale with them.

Earning a lower dose, or even coming off

For most patients with established gout, urate-lowering therapy is long-term. Allopurinol does not change the underlying biology — it suppresses uric acid production while you take it. Stop, and serum urate climbs back to where it was. For people with tophi, recurrent flares, or chronic kidney disease, lifelong therapy is the standard.

For a smaller group — single-episode gout, no tophi, normal kidney function, and a major lifestyle change (significant weight loss, alcohol reduction, removal of an offending diuretic) — a slow trial off allopurinol with monitoring is sometimes possible. This is a conversation with your GP, not a default.

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Track these between now and your next visit

• Any new rash — where, when, whether you have fever, mouth or eye involvement.
• Flares — date, joint, severity, what helped. Particularly important in the first 6 months.
• Blood test reminder — get the next set on time. Serum urate at target is the whole point.
• Any new medicine or supplement — including over-the-counter pain relief, new antibiotics, any “bone health” or “joint health” supplements.
• Anything you have stopped — including alcohol changes, diuretic dose changes, weight changes.

Bring the list to your review appointment.

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This is general information, not personal medical advice. Every patient is different. Decisions about your medicines — which one, what dose, when to stop, what to combine with — are made with the doctor who prescribed them. If anything on this page appears to contradict advice from your treating doctor, follow your doctor; they have context about your situation that this page cannot.

Reading this page does not establish a doctor-patient relationship with Dr Hoebing Lo. If you are not a current patient, please discuss your medicines with your own GP, specialist, or pharmacist.

About the integrative content. The lifestyle, dietary, and complementary recommendations on this page summarise current published research. Effect sizes are approximations from clinical studies — your individual response will vary, and real-world results are commonly smaller than trial results because day-to-day life differs from study conditions. Supplements and herbal products are not interchangeable with prescribed medication and can interact with it. Talk to your doctor and pharmacist before starting any new supplement, herbal product, or significant change in diet.

Currency. This page reflects clinical practice as of the last-reviewed date. Medicine evolves; specific details may date between reviews. Pricing shown is indicative; confirm with your pharmacist.

No commercial relationships. Dr Hoebing Lo has no financial or commercial relationship with the manufacturer of any medicine, brand, or supplement mentioned on this page.

Emergencies. If you have sudden swelling of face, lips, tongue, or throat; difficulty breathing; a new spreading or blistering rash with fever or mouth/eye involvement; severe dizziness or fainting; or unexplained severe bruising or bleeding, call 000 or go to your nearest emergency department. Do not wait, and do not message us first.