Allopurinol tablets are taken by mouth as an individualised daily treatment for gout, uric-acid kidney stones, or a high uric-acid burden during cancer treatment. They lower uric acid production by…
Allopurinol tablets are taken by mouth as an individualised daily treatment for gout, uric-acid kidney stones, or a high uric-acid burden during cancer treatment. They lower uric acid production by blocking xanthine oxidase and help reduce the formation of painful crystals.
Taken by mouth as an individualised daily treatment, Allopurinol tablets lower uric acid production for people with gout, uric-acid kidney stones, or a high uric-acid burden during cancer treatment. They block xanthine oxidase, reducing the urate that can form painful joint crystals or collect in the urinary tract.
The product is Allopurinol in tablet form for oral use. Its active component lowers uric acid production by blocking xanthine oxidase. The amount per tablet is not specified here and treatment is individualised.
Allopurinol is used for chronic hyperuricaemia, meaning persistently raised uric acid where crystal disease or urate complications are present. The main use is prevention of recurrent gout attacks and progressive urate deposition. It can also reduce recurrent uric-acid stone formation in people with high urinary uric acid, known as hyperuricosuria.
In oncology, tumour lysis syndrome can occur when many cancer cells break down rapidly after treatment. Their contents release purines, which are converted into uric acid. Allopurinol may be used preventively in selected treatment plans to reduce this urate load.
| Clinical setting | Treatment goal |
|---|---|
| Gout with raised urate | Reduce crystal formation and future flares |
| Recurrent uric-acid nephrolithiasis | Lower urinary uric acid |
| Tumour lysis syndrome prevention | Limit uric-acid rise from cell breakdown |
The 2020 American College of Rheumatology guideline supports urate-lowering therapy for people with frequent gout flares, tophi, or gout-related radiographic damage, with serum urate used to guide treatment adjustment. [2]
Uric-acid kidney stones form when urine contains excess uric acid, especially when urine is acidic. Allopurinol can reduce uric acid entering the urine, while urine alkalinisation and adequate fluid intake may be used where clinically appropriate. It is not a general treatment for every type of kidney stone.
Kidney function changes dosing.
The HLA-B*58:01 genetic variant is strongly associated with severe allopurinol hypersensitivity in people from populations where this variant is more common. CPIC guidance supports genotype-informed prescribing in relevant higher-risk groups before treatment is started. [3]
Allopurinol is not for you if you have previously had a serious allergic or hypersensitivity reaction to allopurinol. This includes severe rash, blistering reactions, liver inflammation or systemic illness linked to earlier treatment.
Stop taking allopurinol and seek urgent medical assessment for rash with blistering, mouth ulcers, facial swelling, fever, sore throat, swollen glands, yellowing of the skin, or unexplained widespread illness. These may signal a severe cutaneous adverse reaction, including Stevens-Johnson syndrome or toxic epidermal necrolysis.
Many people tolerate allopurinol well when the dose is introduced carefully. Nausea, diarrhoea, abdominal discomfort, drowsiness, headache and mild skin rash can occur. A temporary increase in gout flares is also common when urate levels begin to fall.
The serious limitation is rare but potentially life-threatening hypersensitivity. Risk is higher with reduced kidney function, higher starting doses, thiazide use and HLA-B*58:01 carriage. Fever with rash or symptoms affecting the mouth, eyes, skin or breathing requires urgent assessment.
Allopurinol can sometimes affect liver tests or blood counts. Ongoing treatment may include serum urate, kidney function, liver function and blood-count monitoring, chosen around the person’s clinical situation.
Allopurinol is a xanthine oxidase inhibitor. Xanthine oxidase is an enzyme involved in breaking down purines, natural substances from body cells and food, into uric acid. Blocking this enzyme lowers uric acid in both blood and urine. It prevents rather than relieves pain. Allopurinol is converted partly to oxypurinol, an active metabolite that continues to inhibit xanthine oxidase after the tablet has been absorbed. Lower urate levels gradually dissolve existing monosodium urate deposits and reduce formation of new crystals in joints, tendons and kidneys. The HPRA Summary of Product Characteristics describes allopurinol as long-term urate-lowering treatment rather than treatment for the pain of an active flare. [1]
Purines are converted through several metabolic steps into hypoxanthine and xanthine. Xanthine oxidase normally converts these compounds into uric acid. Allopurinol interrupts this final pathway, so less uric acid enters the bloodstream and less reaches the urine.
This mechanism differs from anti-inflammatory gout treatments. Colchicine, ibuprofen and prednisone reduce inflammation during a flare; they do not lower urate production. Allopurinol addresses the cause that drives recurrent crystal formation, though the benefit builds gradually.
Several avoidable patterns make allopurinol seem less helpful than it is:
| Approach | Main role | Limitation |
|---|---|---|
| Allopurinol: xanthine oxidase inhibition | Reduces uric acid production | Can trigger early gout flares |
| Febuxostat: xanthine oxidase inhibition | Alternative urate-lowering approach | Cardiovascular history needs consideration |
| Uricosuric treatment | Increases urinary uric acid excretion | May be unsuitable with some kidney stones or renal impairment |
In clinical practice, doctors usually frame allopurinol as prevention, not rescue treatment. It does not work like a painkiller during a midnight gout attack. The target is fewer attacks, less crystal deposition and a lower long-term urate burden.
Prescribers also stress consistency. Serum urate can rise again after treatment stops, even when joints feel settled, because symptom control does not always mean the underlying crystal burden has disappeared. The 2020 American College of Rheumatology guideline uses a treat-to-target approach, adjusting urate-lowering treatment against serial serum urate results rather than leaving the dose unchanged indefinitely. [4]
Allopurinol can cause drowsiness, dizziness or reduced alertness in some people, especially when treatment is new or the amount has changed. The HPRA product information advises caution with driving and machinery until personal response is known. The practical approach in 2026 is simple: the HPRA product information advises against driving or using hazardous equipment if you feel dizzy, sleepy or unable to concentrate normally.
The expected benefit depends on sustained urate reduction rather than immediate pain relief. The 2020 American College of Rheumatology guideline recommends checking serum urate and adjusting treatment to a clinical target when needed. Continued flares, missed doses, impaired kidney function, alcohol intake, dehydration and interacting medicines can all affect results, so the treatment plan should be reviewed rather than self-adjusting the daily amount.
Allopurinol begins reducing uric acid after treatment starts, yet symptoms may take longer to improve because existing crystals dissolve gradually. EULAR guidance published in 2016 explains why flares may occur during the early phase of urate lowering. Reduced flare frequency is usually judged across ongoing follow-up and serum urate results, not by the first few days of tablets.
A prior severe reaction to allopurinol rules out restarting it without specialist assessment. The HPRA product information (2024) classifies severe skin reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis, as serious safety concerns for allopurinol treatment. A history of blistering rash, mucosal sores, facial swelling or fever with a previous course should be clearly recorded in medical records.
Allopurinol does not usually require dose tapering for withdrawal symptoms, because it is not dependence-forming. Stopping it can allow uric acid to rise again, which may lead to renewed crystal formation and later gout flares. The 2020 ACR guideline supports continued urate-lowering therapy for many people with established gout, with decisions based on disease history and urate control.
Allopurinol may be used in children for selected specialist indications, including certain disorders with excessive uric acid production and tumour lysis prevention. It is not routine treatment for ordinary childhood aches or joint pain. The WHO Model Formulary for Children (2010) describes paediatric use as condition-specific and requiring weight- and renal-function-based prescribing.
Keep tablets in a dry place, protected from excessive heat and out of reach of children. Bathrooms, cars and window ledges can expose medicines to moisture or temperature swings. During travel, carrying tablets with a current medicine list helps maintain continuity of treatment if medical care is needed; the HPRA product information (2024) advises keeping prescribed medicines stored securely.
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Based on 4 reviews
I had fewer ankle attacks after staying on it consistently. The first flare after starting it was frustrating, but I had been warned that urate treatment can stir things up before it settles.
Several months 15 Oct 2026The tablets themselves were easy to fit into my routine. I missed doses when working shifts, and my urate result did not improve as much as expected until I started taking it after the same meal each day.
Four months 23 Oct 2026My gout in the big toe became more active early on, so I thought the tablets were causing harm. The treatment plan included anti-inflammatory cover, and I continued rather than stopping on my own.
Two months 7 Oct 2026I developed an itchy rash and stopped taking it straight away. It turned out not to be severe, but the review was needed because I knew rash can be a warning sign with allopurinol.
Six weeks 2 Nov 2026
