Systemic corticosteroids for acute gout.

BACKGROUND: Gout is one of the most frequently occurring rheumatic diseases, worldwide. Given the well-known drawbacks of the regular treatments for acute gout (non-steroidal anti-inflammatory drugs (NSAIDs), colchicine), systemic corticosteroids might be safe alternatives. OBJECTIVES: To assess the efficacy and safety of systemic corticosteroids in the treatment of acute gout in comparison with placebo, NSAIDs, colchicine, other active drugs, other therapies, or no therapy. SEARCH STRATEGY: Searches were done in the following electronic databases: Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2007); MEDLINE (1966 to 2007) through PubMed; EMBASE (1974 to 2007); Web of Science (1975 to 2007); LILACS (1986 to 2007); and databases of ongoing trials (up to April 2007). SELECTION CRITERIA: Randomized controlled trials and controlled clinical trials investigating the use of systemic corticosteroids in the treatment of acute gout were included. DATA COLLECTION AND ANALYSIS: Two review authors decided independently which trials to include. The same review authors also collected the data in a standardised form and assessed the methodological quality of the trial using validated criteria. When possible, continuous and dichotomous data were summarised statistically. MAIN RESULTS: Three head to head trials involving 148 patients (74 systemic corticosteroids; 74 comparator drugs) were included. Placebo-controlled trials were not found. In the studies, different kinds of systemic corticosteroids and different kinds of control drugs were used, both administered in different routes. Intramuscular triamcinolone acetonide was compared respectively to oral indomethacine, and intramuscular adrenocorticotropic hormone (ACTH); oral prednisolone (together with a single intramuscular diclophenac injection) was compared to oral indomethacine (together with a single placebo injection). Outcome measurements varied: average number of days until total relief of signs, mean decrease of pain per unit of time in mm on a visual analogue scale (VAS) - during rest and activity. In the triamcinolone-indomethacine trial the clinical joint status was used as an additional outcome. Clinically relevant differences between the studied systemic corticosteroids and the comparator drugs were not found; important safety problems attributable to the used corticosteroids were not reported. The quality of the three studies was graded as very low to moderate. Statistical pooling of results was not possible. AUTHORS' CONCLUSIONS: There is inconclusive evidence for the efficacy and effectiveness of systemic corticosteroids in the treatment of acute gout. Patients with gout did not report serious adverse effects from systemic corticosteroids, when used short term.

[Gout not induced by diuretics in a case-control study in general practice]. / Jicht niet uitgelokt door diuretica in een patiënt-controleonderzoek in de huisartspraktijk.

OBJECTIVE: To determine the relation between diuretics and the development of gout, taking into account the possible confounding by hypertension and cardiovascular diseases. DESIGN: Case-control study. METHOD: With the aid of the data on morbidity and medication from the electronic medical files ofa dispensing general practitioner, all patients with a first gout registration during the period from October 1994 to September 2002 were identified as cases; in the same practice, for each patient, 3 controls of the same age and sex who were known not to have gout were selected at random. Conditional logistic regression analyses were carried out to estimate the odds ratio (OR) for gout in patients who had used diuretics for at least 3 months and in patients suffering from hypertension, heart failure, or myocardial infarction. The statistical interaction between variables was investigated after stratification for diuretic use. RESULTS: Via the medical files, 70 gout patients (59 men), with a mean age of 55.1 years (SD: 13.5) were identified, plus 210 matched controls. When assessed without correction, the use ofdiuretics seemed to be associated with a definite risk of gout: OR: 2.8 (95% CI: 1.2-6.6). But after adjustment for the cardiovascular variables hypertension, heart failure and myocardial infarction, the risk of gout associated with diuretic use disappeared: OR: 0.6 (95% CI: 0.2-2.0). An independent risk of gout was demonstrated for hypertension (OR: 3.9; 95% CI: 1.6-10.0), and to a lesser degree for myocardial infarction (OR: 1.5; 95% CI: 0-5-4.1). The risk of gout associated with heart failure was also calculated (OR: 40.1; 95% CI: 3.8-437.2), but diuretic independency could not be proven as all patients with heart failure were on diuretics and there was no heart failure among those not using diuretics. CONCLUSION: In this case-control study, the use of diuretics did not increase the risk of gout. The cardiovascular indications for prescribing diuretics were significant confounders.

Gout, not induced by diuretics? A case-control study from primary care.

BACKGROUND: It is taken for granted that diuretics may induce gout, but there is a general lack of evidence on this topic. OBJECTIVES: To determine the incidence of gout in patients who use diuretics, taking into account concurrent hypertension and cardiovascular diseases. METHODS: A case-control study was designed. From a primary care population all patients with a first gout registration (59 men, 11 women; mean (SD) age 55.1 (13.5)) were identified as cases. To relate the occurrence of gout to diuretic use a matched reference series of three controls for each case was compiled. Conditional logistic regression analyses were applied to estimate incidence rate ratios (IRRs) of gout, and 95% confidence intervals (CIs), in subjects with and without diuretic treatment, hypertension, and cardiovascular diseases. Additional stratification analyses were made, particularly in the subjects not using diuretics. RESULTS: The IRRs of gout in subjects with v those without diuretic treatment, hypertension, heart failure, and myocardial infarction were 2.8 (95% CI 1.2 to 6.6), 2.6 (95% CI 1.2 to 5.6), 20.9 (95% CI 2.5 to 173.8), and 1.9 (95% CI 0.7 to 4.7), respectively. After adjustment, the IRR of gout for diuretic use dropped to 0.6 (95% CI 0.2 to 2.0), while the IRRs of gout for hypertension, heart failure, and myocardial infarction were still >1. This was also the case for subjects with hypertension or myocardial infarction, who had not used diuretics. CONCLUSION: The results suggest that diuretics do not actually increase the risk of gout. Cardiovascular indications for treatment may have confounded previous inferences.

Gout, just a nasty event or a cardiovascular signal? A study from primary care.

OBJECTIVE: Our aim was to examine the relationship between gout on the one hand and cardiovascular diseases and cardiovascular risk indicators on the other. METHODS: A case-control study was carried out in an aggregate primary care population of approximately 12 000 patients from four Dutch general practices, with follow-up of the cases free of cardiovascular diseases at the time of the first registered episode of gout. The subjects comprised 261 patients with a first episode of gout, 170 of whom were without prevalent cardiovascular diseases, and two control patients for each case matched for age, sex and practice. In the case-control study, the main outcome measures were the prevalence of cardiovascular morbidity (angina pectoris, myocardial infarction, heart failure, cerebrovascular accident, transient ischaemic attack, peripheral vascular disease), hypertension, diabetes mellitus, obesity and hypercholesterolaemia; in the follow-up study, the main outcome measure was the incidence of cardiovascular morbidity. RESULTS: Thirty-five percent of 261 gout patients and 26% of 522 controls had one or more prevalent cardiovascular diseases. Compared with controls, patients had a higher prevalence of hypertension (43% versus 18%), hypercholesterolaemia (14% versus 6%) and obesity (56% versus 30%). A total of 170 gout patients without prevalent cardiovascular diseases (compared with 340 controls) had a higher prevalence of hypertension (39% versus 14%), hypercholesterolaemia (8% versus 4%), diabetes mellitus (5% versus 1%) and obesity (52% versus 27%). The first occurrence of a cardiovascular disease (real end-point) was seen in 26% of the patients free of cardiovascular morbidity and in 21% of the controls. This difference was not significant. In a Cox proportional hazard model, controlling for the cardiovascular risk indicators, gout did not prove to be an independent determinant for the development of cardiovascular disease. CONCLUSION: Gout was found to be associated with cardiovascular diseases and with cardiovascular risk indicators, without evidence of it being an independent risk indicator itself. A gout attack should be an incentive to assess the cardiovascular risk profile, when a patient seeks medical help.

[The Dutch College of General Practitioners' "Gout" Standard: a response from general practitioners]. / De standaard 'Jicht' van het Nederlands Huisartsen Genootschap; reactie vanuit de huisartsengeneeskunde.

Although gout has a long nosological history, there are still many uncertainties regarding its pathophysiology, causative factors and most common therapies. Therefore, composing an evidence-based guideline on gout is a challenge. There is a lack of good clinical research, especially in primary care populations where most gout patients are diagnosed and treated. Far more insight is required into the mechanisms which underlie increasing and decreasing serum uric acid levels which, via the blood-synovium barrier, should increase or decrease urate crystals with inflammatory potency. In view of this lack of information, it would have been more appropriate for the Standard not to contain unproven facts and therapeutic recommendations. Guidelines should be kept simple until good clinical research proves the opposite.