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Rheumatology Advance Access originally published online on April 21, 2006
Rheumatology 2006 45(11):1422-1431; doi:10.1093/rheumatology/kel071
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Effectiveness of interventions for the treatment of acute and prevention of recurrent gout—a systematic review

S. Sutaria, R. Katbamna and M. Underwood

Barts and The London, Queen Mary, University of London, Institute of Health Sciences, London, UK.

Correspondence to: Shailen Sutaria, Barts and The London, Queen Mary, University of London, Institute of Health Sciences, London, UK. E-mail: shailen000{at}yahoo.co.uk


   Abstract
Top
 Abstract
Introduction
 Method
 Treatment of acute gout
 Prevention of recurrent gout
 Discussion
 Acknowledgements
 References
 
Objective. To determine the evidence for the effectiveness of treatments for acute gout and the prevention of recurrent gout.

Method. Seven electronic databases were searched for randomized controlled trials of treatments for gout from their inception to the end of 2004. No language restrictions were applied. All randomized controlled trials of treatments routinely available for the treatment of gout were included. Trials of the prevention of recurrence were included only if patients who had had gout and had at least 6 months of follow-up were studied.

Results. We found 13 randomized controlled trials of treatment for acute gout, two of which were placebo controlled. Colchicine was found to be effective in one study; however, the entire colchicine group developed toxicity. The only robust conclusion from studies of non-steroidal anti-inflammatory drugs is that pain relief from indometacin and etoricoxib are equivalent. We found one randomized controlled trial, reported only as a conference abstract, of recurrent gout prevention.

Conclusion. The shortage of robust data to inform the management of a common problem such as gout is surprising. All of the drugs used to treat gout can have serious side effects. The incidence of gout is highest in the elderly population. It is in this group, who are at a high risk of serious adverse events, that we are using drugs of known toxicity. The balance of risks and benefits for the drug treatment of gout needs to be reassessed.

KEY WORDS: Gout, Treatment, Systematic review


   Introduction
Top
 Abstract
 Introduction
Method
 Treatment of acute gout
 Prevention of recurrent gout
 Discussion
 Acknowledgements
 References
 
Gout is a common problem affecting 1% of adult males in developed countries [1]. Recurrent attacks of gout are common. It is the commonest cause of inflammatory joint disease in men aged over 40 yrs; increasing obesity and an ageing population mean that it is becoming more frequent [2, 3]. Gout is essentially a disorder of urate metabolism [4]; however, diet and alcohol intake can affect its incidence [5, 6]. Deposition of urate crystals in hyperuricaemic individuals results in acute gout, characterized by agonizing pain and inflammation of rapid onset, most frequently affecting the first metatarsophalangeal joint, resulting in short-term disability [4]. Aims of the treatment are to relieve the pain and inflammation of the acute attack, and reduce the incidence of recurrent attacks. Internationally, there are considerable variations in management of acute and recurrent gout [7]. The commonest approaches to the treatment of acute gout are non-steroidal anti-inflammatory drugs (NSAIDs) and colchicine. The side effects of these drugs, particularly in the frail, elderly population, who have the highest incidence of acute gout, can be serious. The commonest approach to the prevention of recurrent gout is to use allopurinol, a xanthine oxidase inhibitor. Allopurinol can have serious side effects such as allopurinol hypersensitivity syndrome [8, 9]. We present a systematic review of the randomized controlled trial evidence for the treatment and prevention of recurrent, acute gout.


   Method
Top
 Abstract
 Introduction
 Method
Treatment of acute gout
 Prevention of recurrent gout
 Discussion
 Acknowledgements
 References
 
Identification of randomized controlled trials
We sought to identify all randomized controlled trials of currently available drug treatments, lifestyle and other interventions for the treatment of acute gout and the prevention of recurrent gout. Two of us (S.S. and R.K.), working independently, researched the following electronic databases: Medline, PubMed, Cochrane Controlled Trials Register, ISI Web of Science, Embase, and AMED, from inception to the end of 2004 for all randomized controlled trials of gout treatment using the following search strategy: ‘(gout* or uric* or urate* or hyperuric* or podagra) AND (random* or control* or clinical trial* or placebo* or intervention* or allocat* or blind*)’. No language or date restrictions were used. Citation tracking from identified trials and reviews identified additional randomized controlled trials. We combined the reference lists using Reference Manager (Version 10.1). Still working independently, the two researchers screened titles and abstracts to identify articles for retrieval; they also independently screened retrieved articles for inclusion. One of us (M.U.) mediated disagreements. We excluded non-randomized studies and studies in which one or more intervention is not routinely available for treating gout. These studies are briefly summarized.

Trials of acute gout treatments
We included all randomized controlled trials that included subjects with acute gout (however defined) and compared an active intervention with no treatment, placebo or another active intervention. Our primary outcomes of interest were pain at 24 and 48 h or the nearest equivalent. Our secondary outcomes were any other patient-centred outcomes reported by the authors. Additionally, we extracted any reported adverse event data.

Trials of prevention of recurrent gout
We included all randomized controlled trials of prevention of recurrent gout in subjects with at least one previous attack of acute gout (however defined) who had at least 6 months of treatment and follow-up. Our primary outcome of interest was incidence of recurrent gout and our secondary outcome was difference in serum urate between the intervention and control groups. Additionally, we extracted any reported adverse event data.

Quality assessment
Study quality was assessed using the Jadad criteria [10]. Each included study was rated on a 0–5 scale (0 = low quality, 5 = high quality).

Results
Initial searches identified 9854 references. We identified 13 studies of treatment for acute gout and one study of the prevention of recurrent gout that met our entry criteria (Table 1). Excluded studies are summarized in Table 2. A flow diagram of studies is provided in Fig. 1.


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  		TABLE 1. Randomized controlled trials of available gout treatments

 

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  		TABLE 2. Excluded studies

 

Figure 1
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  		FIG. 1. Studies identified.

 

   Treatment of acute gout
Top
 Abstract
 Introduction
 Method
 Treatment of acute gout
Prevention of recurrent gout
 Discussion
 Acknowledgements
 References
 
Methodological quality
Most of the research was of poor quality. Only 4/13 included studies were of high quality, a Jadad score of 4/5 or 5/5 [11–14]. The median number of participants per study was 34 (range 10–189). Only two studies had sample size calculations [12, 14]. Typically, the quality of reporting was poor with insufficient detail to understand the analyses. There was no consistent approach to reporting of results.

NSAIDs
We found one placebo-controlled trial of reasonable quality that compared tenoxicam 30 mg/day with placebo (n = 30). The knee was affected in 14 cases and the great toe in only two cases. After 24 h, 67% of tenoxicam group had ≥50% reduction in pain compared with 26% of placebo group (P<0.05) [11]. However, at the end of the treatment (4 days), there was no significant difference between the groups.

We found nine studies comparing two NSAIDs [12–20]. Two, both of high quality, were equivalence studies comparing etoricoxib and indometacin [12, 14]. Both studies pre-defined equivalence as the limits of the 95% confidence intervals for difference between the two groups for change in pain at days 2–5 to be no more than 0.5 Likert units, based on a four-point Likert scale. Both studies found indometacin and etoricoxib to have an equivalent effect on pain over days 2–5. Both studies reported fewer drug-related adverse events in the etoricoxib group. There were no differences in overall adverse events.

The remaining seven studies were of generally poor quality. Only one [18] reported any differences in outcome; these were at one time point and unlikely to be of any clinical importance. Most of these studies were too small to detect any important differences.

Colchicine
We found one placebo-controlled trial of colchicine 1 mg initially, and then 0.5 mg every 2 h until resolution or toxicity occurred. After 24 h, 41% of the colchicine group and 9% of the placebo group had ≥50% reduction in pain since baseline (not significant). After 48 h, 73% of the colchicine group and 36% of the placebo group had ≥50% reduction in pain since baseline (P<0.05). Everyone in the colchicine group developed toxicity (median time to onset 24 h). In only 41% did ≥50% improvement occur before toxicity. Five of the control group experienced nausea [21].

Steroids and adrenocorticotrophic hormone
We found no placebo-controlled trials of steroids or related compounds. We found one poor quality study comparing intramuscular adrenocorticotrophic hormone with intramuscular triamcinolone acetonide [22]. Effect on pain was not reported. There was no difference in time to complete resolution between the two groups. However, this study is probably too small to detect any important differences.

Ice
There is some evidence from one small study, with poor quality allocation concealment, that local ice provides additional relief when added to systemic treatment [23].


   Prevention of recurrent gout
Top
 Abstract
 Introduction
 Method
 Treatment of acute gout
 Prevention of recurrent gout
Discussion
 Acknowledgements
 References
 
We found no randomized controlled trials of lifestyle interventions, such as a low purine diet, weight loss or advice to reduce alcohol intake, in patients with gout that had either the incidence of recurrent gout or changes in serum urate as an outcome. Nor did we find any randomized controlled trials of allopurinol for the prevention of recurrent gout or that reported its long-term effect on serum urate. One small (14 subjects) study, reported only as a conference abstract, suggested that although sulphinpyrazone reduces serum urate it does not affect incidence of recurrent gout [24]. However, this study is probably too small to detect any important differences.


   Discussion
Top
 Abstract
 Introduction
 Method
 Treatment of acute gout
 Prevention of recurrent gout
 Discussion
Acknowledgements
 References
 
The shortage of robust data for a common problem such as gout is surprising. Current regimens for the treatment and prevention of recurrent gout were developed several decades ago. It is possible that we have overlooked some relevant randomized controlled trials. Firstly, some early studies that have not been indexed would not be identified by our searches. However, extensive citation checking of review articles and included studies did not identify any additional included studies. Secondly, it is possible that there are unpublished randomized controlled trial data that were produced for licencing purposes. We did not have the resources to systematically identify any such studies from multiple manufacturers and regulatory authorities. We are re-assured that this has not introduced substantial bias into our findings because for some drugs, for example allopurinol [25, 26], naproxen [27], diclofenac [28] and etodolac [29], we identified contemporary papers reviewing the early experience of these drugs for gout; none reported relevant randomized studies.

Acute gout
There is only one small randomized controlled trial to support the use of NSAIDs for the treatment of acute gout. The size, quality and comparisons made in most of the studies comparing different NSAIDs are such that they cannot inform our management. The only robust conclusion that can be drawn from the available randomized data is that the pain-relieving properties of indometacin and etoricoxib are equivalent. However, in the absence of a placebo-controlled trial of either of these drugs for the treatment of gout, we can only speculate on the magnitude of their clinical effect. The high incidence of gastrointestinal and other side effects of the high dose of indometacin used to treat acute gout is well-documented [30]. Etoricoxib has fewer gastro-intestinal adverse events, but concerns about cardiovascular adverse events from COX-2 inhibitors mean that this cannot be assumed to be a safer option than indometacin (http://medicines.mhra.gov.uk/ourwork/monitorsafequalmed/safetymessages/ddlcox2170205.pdf). Likewise, although colchicine appears to be effective in one randomized controlled trial, it has too high an incidence of adverse reactions for routine use [21, 31].

The incidence of gout is highest in the elderly population [32], who may be frail, and it is particularly common in those with cardiovascular disease [33]. It is in this group, who are at high risk of serious adverse events, that we are using drugs of known toxicity in the absence of randomized controlled trials of their effectiveness.

There is a need to re-appraise how we treat acute gout. This re-appraisal needs to consider the risks and benefits of the drugs we use to treat a condition that usually improves spontaneously even without treatment [34]. For example, does a treatment with analgesics or oral steroids and ice packs [23] provide an improved balance between risks and benefits compared with routine treatment with non-selective NSAIDs, COX-2 inhibitors or colchicine for most patients with acute gout?

Prevention of recurrent gout
Allopurinol is the mainstay of recurrent gout prevention. In 2002–03, 2 423 000 allopurinol prescriptions, at a cost of £6 848 000, were dispensed in England (http://www.publications.doh.gov.uk/stats/pca2003.htm). Making a very crude assumption that each person on prophylactic allopurinol has 12 prescriptions per year, then at least 200 000 people in England are on regular allopurinol.

The absence of long-term data on the effect of allopurinol on either incidence of recurrent gout or serum urate is surprising, particularly as it has well-recognized, rare but serious side effects [9, 35]. A number of studies show that it does reduce serum urate, at least in the short term [36] and there is a well-documented relationship between serum urate and the incidence of acute gout [32]. These data, and extensive clinical experience, suggest that allopurinol is effective in preventing recurrent gout.

There is a need to re-appraise how we use allopurinol and sulphinpyrazone. For example, what are the risks and benefits of allopurinol/sulphinpyrazone? At what levels of urate and frequency of attacks is it worth considering allopurinol/sulphinpyrazone?

Although there are no randomized controlled trials of dietary changes for the prevention of recurrent gout, there are now good-quality observational data showing the relationship between diet and alcohol intake, and a first attack of gout [5, 6]. These data suggest that practical lifestyle changes may be an alternative to drug treatment. The role of lifestyle advice for the prevention of recurrent gout also needs to be re-assessed.

What is already known on this topic:

  • Gout is a common disorder.
  • Non-steroidal anti-inflammatory drugs or colchicine are common treatments for acute gout. Allopurinol or sulphinpyrazone are commonly used to prevent recurrence.
  • All of the drugs used in the management of gout can have potentially serious side effects.

What this study adds:

  • The efficiency of drugs commonly used to treat gout has not been established.
  • The balance of risks and benefits from these drugs is unknown.
  • Current approaches to the treatment of gout need to be re-assessed.


   Acknowledgements
Top
 Abstract
 Introduction
 Method
 Treatment of acute gout
 Prevention of recurrent gout
 Discussion
 Acknowledgements
References
 
This article is based on dissertations submitted by S.S. and R.K. as part of an intercalated B Med Sci., supported by bursaries from the Research Advisory Board. Translation of de la Torre [11] was originally provided by Clinical Evidence for their review of gout. We are grateful to Yu Mei Chang for translation of Chinese papers and Nancy Schumann for translation of German and Portuguese papers.

S.S. and R.K. jointly designed and carried out the study with M.U.'s guidance. S.S. wrote the first draft of this article. R.K. and M.U. commented on successive drafts. M.U. had the original idea for this study, supervized all stages of the work and is the guarantor. M.U. has received speaker fees from Pfizer, the manufacturers of valdecoxib and celecoxib, and from Menarini Pharmaceuticals, the manufacturers of ketoprofen and dexketoprofen. M.U. has received fees for speaking from Menarini Pharmaceuticals and from Pfizer. The other authors have declared no conflicts of interest.


   References
Top
 Abstract
 Introduction
 Method
 Treatment of acute gout
 Prevention of recurrent gout
 Discussion
 Acknowledgements
 References
 

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Submitted 16 October 2005; revised version accepted 7 February 2006.
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