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I first started having attacks of gout when I was 31. My doctor failed to diagnose me in the right way, so in a couple of month I addressed a rheumatologist, who prescribed me with Allopurinol. The worst thing is that I've heard people who take these pills can no longer deal without them. But having to choose between gout and pills till the end of the life, I chose Allopurinol

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For the calculation of SMD, MD is divided by the standard deviation, resulting in a unit-less measure of treatment effect.

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The FDA reported on a few cases of reversible clinical hepatotoxicity in people taking allopurinol, and in some people, asymptomatic rises in serum alkaline phosphatase or transaminase have been observed.

Amoxicillin: Allopurinol may enhance the potential for allergic or hypersensitivity reactions to Amoxicillin.

RCT including 57 participants presenting within seven days of onset of an acute attack of crystal-confirmed gout and who met the ARA criteria and compared allopurinol 300 mg daily versus placebo for 10 days.

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No participants were receiving regular hypouricaemic treatment, though many had undergone sporadic treatment in the past.

Duration of treatment was 12 months and outcomes were assessed at two weeks, four weeks and then monthly for 12 months in total) and follow-up extended for another month to assess AEs (13 months in total).

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Allopurinol 300 mg daily probably does not reduce the incidence of acute gout attacks when compared with placebo over 30 days, and allopurinol 100 to 600 mg daily may not reduce acute gout attacks compared with benzbromarone 100 to 200 mg daily or febuxostat 80 mg daily over 16 to 24 weeks.

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When we considered studies sufficiently homogenous in terms of the study population and interventions delivered, we pooled outcome data in a meta-analysis using a random-effects model, irrespective of the I 2 results ().

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There was no between-group differences in the number of tophi, with the exception of a mean percentage reduction in the number of tophi occurring in participants on febuxostat 120 mg daily (-1.

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Early clinical studies and incidence rates from early clinical experience with Allopurinol suggested that these adverse reactions were found to occur at a rate of greater than 1%.

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Prophylaxis with naproxen (250 mg twice daily) or colchicine (0.

The FDA reported the incidence of adverse reactions was less than 1%, and that the most common adverse reaction to allopurinol is skin rash, recommending treatment be discontinued immediately if a rash develops.

One trial that included 37 participants, judged to be at high risk of bias, compared allopurinol (100-150 mg daily initially, titrated to 100, 200 or 300 mg daily according to creatinine clearance) with benzbromarone (100 mg daily titrated with increments of 50 mg daily to 200 mg daily) ().

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While the trial was published in November 2012, after the ACR guidelines were published, it does support ACR recommendations although it may be underpowered (as it is a small trial with 57 participants) and was of short duration.

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An analysis of current usage suggests that the incidence of acute gouty attacks has diminished to less than 1%.

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We included 11 trials (4531 participants) that compared allopurinol (various doses) with placebo (two trials); febuxostat (four trials); benzbromarone (two trials); colchicine (one trial); probenecid (one trial); continuous versus intermittent allopurinol (one trial) and different doses of allopurinol (one trial).

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Both reviews reported similar safety data.

For continuous outcomes, we would have calculated the absolute risk difference as the MD between intervention and control groups in the original measurement units (divided by the scale), expressed as a percentage; we would have calculated the relative difference as the absolute change (or MD) divided by the baseline mean of the control group from a representative trial; however, we did not need to do this.

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ACR: American College of Rheumatology; AE: adverse event; ALT: alanine aminotransferase; APEX: Allopurinol and Placebo-Controlled, Efficacy Study of Febuxostat; ARA: American Rheumatism Association; AST: aspartate aminotransferase; BMI: body mass index; CCT: controlled clinical trial; CI: confidence interval; eCLcr: estimated creatinine clearance; FACT: Febuxostat versus Allopurinol Controlled Trial; FOCUS: Febuxostat Open-label Clinical trial of Urate-lowering efficacy and Safety; ITT: intention to treat; MSU: monosodium urate; NSAID: non-steroidal anti-inflammatory drug; OMERACT: Outcome Measures in Rheumatology; RCT: randomised controlled trial; RR: risk ratio; SAE: serious adverse event; SD: standard deviation; sUA: serum uric acid.

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Two review authors (RS and AK) independently reviewed the results of the search to identify trials that fulfilled our inclusion criteria.

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We searched abstracts from the two major international rheumatology scientific meetings - the ACR and the European League Against Rheumatism (EULAR) - or the years 2011 and 2012, and the reference lists of included articles for additional trials.

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For studies judged as clinically similar, we assessed statistical heterogeneity using the I 2 statistic ().

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Allopurinol is one of the most effective and frequently used urate-lowering drugs for gout.

Past experience suggested that the most frequent event following the initiation of Allopurinol treatment was an increase in acute attacks of gout (average 6% in early studies).

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The mobilization of urates from tissue deposits which cause fluctuations in the serum uric acid levels may be a possible explanation for these episodes.

British Society for Rheumatology and British Health Professionals in Rheumatology guideline for the management of gout.

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There were increased numbers of external malformations in fetuses at both doses of Allopurinol on gestation day 10 and increased numbers of skeletal malformations in fetuses at both doses on gestation day 13.

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Safety as assessed by the number of study participant withdrawal due to AEs or SAEs were not reported, but AEs were reported.

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Asymptomatic hyperuricemia is not an indication for treatment with Allopurinol (see section).

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No data for joint pain, function, quality of life, participant global assessment of treatment success, tophus regression or safety were provided.

None of these trials included an assessment of pain, function or participant global assessment of treatment success.

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While we recognised that was at high risk of bias, a sensitivity analysis excluding this trial did not alter our results for acute gout attack frequency, proportion of participants achieving target serum urate and total AEs.

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These tables provide key information concerning the quality of evidence, the magnitude of effect of the interventions examined and the sum of available data on our seven main outcomes (participant-reported reduction in acute gout attack frequency, proportion of participants achieving a target serum urate level, joint pain reduction, function, tophus regression, number of study participant withdrawals due to AEs and SAEs), as recommended by The Cochrane Collaboration ().

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The second trial with 57 participants, judged to be at low risk of bias, compared the initiation of allopurinol 300 mg during an acute attack of gout versus placebo for 10 days followed by allopurinol 300 mg daily ().

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