Alcohol consumption as a trigger of recurrent gout attacks.

Boston University Clinical Epidemiology Research and Training Unit, the Department of Medicine at Boston Medical Center, Boston, Mass 02118, USA.
The American journal of medicine (Impact Factor: 5.3). 09/2006; 119(9):800.e13-8. DOI: 10.1016/j.amjmed.2006.01.020
Source: PubMed

ABSTRACT Alcohol consumption has long been considered a trigger for recurrent gout attacks; however, this hypothesis has not been formally tested.
We conducted an Internet-based case-crossover study to assess several putative risk factors, including alcohol consumption, thought to trigger recurrent gout attacks. Subjects who had an attack within the past year were recruited online and asked to provide access to medical records pertaining to their gout. Data were obtained on the amount and type of alcoholic beverage consumed on each day over the 2-day period before a gout attack and on each day over a 2-day period during the intercritical period. We examined the amount and type of alcohol consumption and the risk of recurrent gout attacks using a conditional logistic regression adjusting for diuretic use and purine intake.
A total of 197 subjects were recruited online over a 10-month period. Of those, 179 (91%) fulfilled the American College of Rheumatology Criteria for gout. Compared with no alcohol consumption, odds ratios for recurrent gout attacks were 1.1, 0.9, 2.0, and 2.5 for 1 to 2, 3 to 4, 5 to 6, and 7 or more drinks consumed over the 2-day period, respectively (P<.005). A dose-response relationship of risk of gout attacks was more evident for alcohol consumed over the last 24 hours. An increased risk of recurrent gout attacks was found for each type of beverage consumed.
Alcohol consumption triggers recurrent gout attacks. This effect was likely to occur within 24 hours after its consumption.

1 Bookmark
  • [Show abstract] [Hide abstract]
    ABSTRACT: Introduction: Gouty arthritis and hyperuricemia have ailed humans for centuries. Recent advances in understanding of the mechanism(s) of their development have changed our perception of the disease process. Despite these gains, the treatment options available are limited. The FDA approval of febuxostat for the treatment of hyperuricemia in gout has been a significant step forward. Since its approval in 2009, febuxostat has proven to be safe and efficacious although concerns remain regarding its long-term effects and superiority to other uricosuric agents, such as allopurinol. Areas covered: A comprehensive literature review of PubMed and Ovid examining clinical trials and post-marketing studies yielded congruent findings on efficacy and safety in elderly populations and those with mild-to-moderate renal/hepatic impairment. A lack of literature and clinical studies was found with regard to comparison of febuxostat to FDA-approved high-dose allopurinol (> 300 mg), the safety of febuxostat in the treatment of severe renal/hepatic impairment and the benefit in the treatment of secondary cases of hyperuricemia. Expert opinion: Febuxostat is effective in the treatment of mild-to-moderate renal/hepatic impairment with dramatic effects on the serum urate level. It can be used safely in patients with hypersensitivity reactions to allopurinol. Further research is needed to determine the long-term benefits and risks.
    Expert Opinion on Drug Metabolism &amp Toxicology 04/2014; · 2.94 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Gout has been amply described from the times of Galen and it continues to be a public health problem that causes important morbidity in the world population. The treatment of acute gout has not changed in the last years, but a current review and actualization of the medical literature is necessary since there are continuous flaws in the management of this illness, not only in the actual indication of specific drugs, but also in the attentive care required due to the potential development of side effects from the traditional medications used in the treatment.
    Revista Med. 06/2009; 17(2):252-263.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The clinical manifestations of gout occur as a result of immune responses to monosodium urate crystals. Elevated serum levels of urate (hyperuricemia) are a prerequisite for the development of gout with reduced fractional renal excretion of uric acid (FEUA) an important cause. In New Zealand, Mãori and Pacifi c Island people have inherently raised urate levels with one consequence a higher prevalence of more severe gout. One characteristic metabolic eff ect of fructose, present in sugar-sweetened beverages (SSB), is raised urate from hepatic processing of fructose. Here we discuss, and place in a biological context evidence, linking consumption of SSB with hyperuricemia and gout, including the fi rst review of recent ecological and clinical studies of the impact of fructose and SSB exposure in Pacifi c Island people. Both increased serum urate and increased FEUA are observed in clinical studies examining the eff ects of an acute fructose load. In contrast, chronic exposure to increased fructose in the diet also leads to increased serum urate concentrations, but reduced FEUA. Epidemiological studies have consistently associated SSB consumption with increased serum urate levels and increased risk of gout. Non-additive interaction of SSB consumption with a genetic variant of a uric acid transporter in serum urate levels and gout risk emphasizes the causality of SSB in gout. Taken together these data demonstrate the hyperuricemic eff ect of SSB and fructose, with biochemical pathways reasonably well understood. The evidence that dietary fructose increases urate is strong. The evidence summarized here is of suffi cient weight to recommend reduction of SSB consumption, particularly in Pacifi c Island and Mãori people, to reduce the burden of gout.
    Pacific health dialog: a publication of the Pacific Basin Officers Training Program and the Fiji School of Medicine 03/2014; 20(1):31.

Full-text (2 Sources)

Available from
Jun 2, 2014