Home > Medical Reference > Patient EducationServices at Maryland GeneralA complete list of inpatient and outpatient healthcare services at MGH.Gout - Causes and Risk Factors
DescriptionAn in-depth report on the causes, diagnosis, treatment, and prevention of gout.Alternative NamesHyperuricemia Causes and Risk Factors:Gout is classified as either primary or secondary, depending on what causes the high levels of uric acid in the blood (hyperuricemia). More than 99% of primary gout cases are referred to as idiopathic, meaning that the cause of the hyperuricemia cannot be determined. Primary gout is most likely the result of a combination of genetic, hormonal, and dietary factors. Secondary gout is caused by drug therapy or by medical conditions other than a metabolic disorder. The following factors increase your risk for gout:
Each risk factor is discussed in more detail below. AgeMiddle-Aged Adults. Gout usually occurs in middle-aged men, peaking in the mid-40s. It is most often associated in this age group with obesity, high blood pressure, unhealthy cholesterol levels, and heavy alcohol use. Elderly. Gout can also develop in older people, when it occurs equally in men and women. In this group, gout is most often associated with kidney problems and the use of diuretics. It is less often associated with alcohol use. Children. Except for rare inherited genetic disorders that cause hyperuricemia, gout in children is rare. GenderMen. Men are significantly at higher risk for gout. In males, uric acid levels rise substantially at puberty. In about 5 - 8% of American men, levels exceed 7 mg/dL (indicating hyperuricemia). However, gout typically strikes after 20 - 40 years of persistent hyperuricemia, so men who develop it usually experience their first attack between the ages of 30 and 50. Women. Before menopause, women have a significantly lower risk for gout than men, possibly because of the actions of estrogen. This female hormone appears to facilitate uric acid excretion by the kidneys. (Only about 15% of female gout cases occur before menopause.) After menopause the risk increases in women. At age 60 the incidence is equal in men and women, and after 80, gout occurs more often in women. Family HistoryA family history of gout is present in close to 20% of patients with this condition. Three genetic locations have been associated with the body's uric acid handling and gout. Some people with a family history of gout have a defective protein (enzyme) that interferes with the way the body breaks down purines. ObesityResearchers report a clear link between body weight and uric acid levels. In one Japanese study, overweight people had two to more than three times the rate of hyperuricemia as those who maintained a healthy weight. Children who are obese may have a higher risk for gout in adulthood. MedicationsThiazide diuretics are "water pills" used to control hypertension. The drugs are strongly linked to the development of gout. A large percentage of patients who develop gout at an older age report the use of diuretics. Several other medications can increase uric acid levels and raise your risk for gout. These include:
AlcoholDrinking excessive amounts of alcohol can raise your risk of gout. Beer is the kind of alcohol most strongly linked with gout, followed by spirits. Moderate wine consumption does not appear to increase the risk of developing gout. Alcohol use is highly associated with gout in younger adults. Binge drinking particularly increases uric acid levels. Alcohol appears to play less of a role among elderly patients, especially among women with gout. Alcohol increases uric acid levels in the following three ways:
Lead ExposureChronic occupational exposure to lead is associated with build-up of uric acid and a high incidence of gout. Organ TransplantsKidney transplantation poses a high risk for renal insufficiency and gout. In addition, other transplantation procedures, such as heart and liver, increase the risk of gout. The procedure itself poses a risk of gout, as does the medication (cyclosporine) used to prevent rejection of the transplanted organ. Cyclosporine also interacts with indomethacin, a common gout treatment. The kidneys are responsible for removing waste from the body, regulating electrolyte balance and blood pressure, and stimulating red blood cell production. ![]() Other IllnessesTreatment of several other conditions can cause significant elevations of uric acid in the blood, and therefore a gout attack. These conditions include:
Resources
ReferencesChoi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57(1):109-15. Dehghan A, Köttgen A, Yang Q, et al. Association of three genetic loci with uric acid concentration and risk of gout: a genome-wide association study. Lancet. 2008;372(9654): 1953-1961. Huang HY, Appel LJ, Choi MJ et al. The effects of vitamin C supplementation on serum concentrations of uric acid: results of a randomized controlled trial. Arthritis Rheum. 2005 Jun;52(6):1843-7. Keith MP, Gilliland WR. Updates in the management of gout. Am J Med. 2007;120(3):221-224. Krishnan E, Baker JF, Furst DE, Schumacher HR. Gout and the risk of acute myocardial infarction. Arthritis Rheum. 2006 Aug;54(8):2688-96. Underwood M. Diagnosis and management of gout. BMJ. 2006;332(7553):1315-9. Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1301-11. Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1312-24. Zhang YQ, Chaisson CE, Chen CA, McAlindon TE, Hunter DJ. High Humidity and High Temperature Increase the Risk of Recurrent Gout Attacks: The Online Case-crossover Gout Study. Presentation Number 707. American College of Rheumatology Annual Scientific Meeting, Washington, DC, November 2006.
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