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 Follower
  • 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.
    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.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The forthcoming post-Millennium Development Goals era will bring about new challenges in global health. Low- and middle-income countries will have to contend with a dual burden of infectious and non-communicable diseases (NCDs). Some of these NCDs, such as neoplasms, COPD, cardiovascular diseases and diabetes, cause much health loss worldwide and are already widely recognised as doing so. However, 55% of the global NCD burden arises from other NCDs, which tend to be ignored in terms of premature mortality and quality of life reduction. Here, experts in some of these 'forgotten NCDs' review the clinical impact of these diseases along with the consequences of their ignoring their medical importance, and discuss ways in which they can be given higher global health priority in order to decrease the growing burden of disease and disability.
    BMC Medicine 10/2014; 12(1):200. DOI:10.1186/s12916-014-0200-8 · 7.28 Impact Factor

Full-text (2 Sources)

Available from
Jun 2, 2014