OBJECTIVE: To estimate the incidence of and examine risk factors for the development of gout in black and white male physicians. METHODS: Data from 2 cohorts of former medical students, 352 black men in the Meharry Cohort Study and 571 white men in the Johns Hopkins Precursors Study, were analyzed. Cases of gout were identified by self-report. Baseline variables and incident hypertension were examined as risk factors for the development of gout in both cohorts. RESULTS: The incidence of gout was 3.11 and 1.82 per 1,000 person-years in the black men and the white men, respectively (P < 0.05); the cumulative incidence was 10.9% and 5.8%, respectively (P = 0.04). The relative risk (RR) for gout among the black men was 1.69 (95% confidence interval [95% CI] 1.02-2.80). This excess risk persisted after adjustment for baseline systolic blood pressure (adjusted RR = 1.96 [95% CI 1.14-3.38]). Incident hypertension was independently associated with the development of gout in univariate analysis (RR = 3.78 [95% CI 2.18-6.58]); when this variable was included as a time-dependent covariate in a Cox model, the excess risk for gout in black men was reduced and no longer significant (adjusted RR = 1.30 [95% CI 0.77-2.19]). CONCLUSION: The approximately 2-fold excess risk for gout among black men is explained, in part, by a greater risk of incident hypertension.
OBJECTIVE: To estimate the incidence of and examine risk factors for the development of gout in black and white male physicians. METHODS: Data from 2 cohorts of former medical students, 352 black men in the Meharry Cohort Study and 571 white men in the Johns Hopkins Precursors Study, were analyzed. Cases of gout were identified by self-report. Baseline variables and incident hypertension were examined as risk factors for the development of gout in both cohorts. RESULTS: The incidence of gout was 3.11 and 1.82 per 1,000 person-years in the black men and the white men, respectively (P < 0.05); the cumulative incidence was 10.9% and 5.8%, respectively (P = 0.04). The relative risk (RR) for gout among the black men was 1.69 (95% confidence interval [95% CI] 1.02-2.80). This excess risk persisted after adjustment for baseline systolic blood pressure (adjusted RR = 1.96 [95% CI 1.14-3.38]). Incident hypertension was independently associated with the development of gout in univariate analysis (RR = 3.78 [95% CI 2.18-6.58]); when this variable was included as a time-dependent covariate in a Cox model, the excess risk for gout in black men was reduced and no longer significant (adjusted RR = 1.30 [95% CI 0.77-2.19]). CONCLUSION: The approximately 2-fold excess risk for gout among black men is explained, in part, by a greater risk of incident hypertension.
Authors: José M A Wijnands; Wolfgang Viechtbauer; Kristof Thevissen; Ilja C W Arts; Pieter C Dagnelie; Coen D A Stehouwer; Sjef van der Linden; Annelies Boonen Journal: Eur J Epidemiol Date: 2014-07-27 Impact factor: 8.082
Authors: H J E M Janssens; E H van de Lisdonk; M Janssen; H J M van den Hoogen; A L M Verbeek Journal: Ann Rheum Dis Date: 2005-11-16 Impact factor: 19.103