RACIAL DIFFERENCES IN THE EPIDEMIOLOGY OF GOUT

痛风是中年男性最常见的炎症性关节炎， 并导致相当大的短期残疾和医疗保健 利用率。此外，最近基于人口的数据表明， 年痛风和无症状高尿酸血症(AHU)的患病率正在上升 美国。然而，对痛风的流行病学知之甚少。 和黑人的阿胡，而且还没有系统的种族比较 已执行。拟议的项目将1)估计痛风的发生率，2) 确定血浆尿酸水平的分布，以及3)确定风险 在黑人和白人男性的类似人群中，痛风和AHU的因素。 此外，最近的一项研究再次强调了可能的因果关系 痛风与冠心病(CAD)的关系数据 在这项拟议的研究中制定的也将被分析以确定 痛风在两个种族冠心病发病中的可能病因作用 组。 提议的项目将包括非并发和并发 前瞻性队列设计。白人男子是约翰斯派对的参与者 霍普金斯前体研究(JHPS)，他们是从 1957年至1964年(N=536)。黑人是Meharry的参与者 医学院队列研究(MCS，N=423)，他们被登记为医生 从1957年到1965年的学生。这两组人使用相同的仪器进行治疗 基线和随访资料收集在研究发病率中的应用 心血管结果。痛风病例将通过以下方法识别 医生的自我报告，并使用公布的标准进行验证。电浆 尿酸将在作为上述部分获得的标本上进行测量 正在进行的JHPS和MCS研究。数据将使用关联进行分析 密度比和生存分析技术，包括COX 比例风险模型。 这项研究将是第一个系统的前瞻性研究，比较 黑人和白人男性痛风的发病率和危险因素。 此外，这些队列提供了一个独特的机会来调查 痛风在黑人和黑人中作为冠心病独立危险因素的潜在作用 白人。提高对痛风和冠心病风险因素的了解，将 允许制定和/或改进痛风和 CAD。

Gout is the most common form of inflammatory arthritis in middle-aged men, and results in considerable short-term disability and health care utilization. Furthermore, recent population-based data suggest that the prevalence of gout and asymptomatic hyperuricemia (AHU) is increasing in the United States. However, little is known about the epidemiology of gout and AHU in blacks, and no systematic racial comparisons have been performed. The proposed project will 1) estimate the incidence of gout, 2) determine the distribution of plasma uric acid levels, and 3) identify risk factors for gout and AHU, in comparable populations of black and white men. In addition, a recent study has reemphasized the possible causal association between gout and coronary artery disease (CAD). The data developed in this proposed study will also be analyzed to determine the possible etiologic role of gout in the development of CAD in the two racial groups. The proposed project will include both a nonconcurrent and concurrent prospective cohort design. The white men are participants in the Johns Hopkins Precursors Study (JHPS), who were enrolled as medical students from 1957 to 1964 (N=536). The black men are participants in the Meharry Medical College Cohort Study (MCS, N=423), who were enrolled as medical students from 1957 to 1965. Both cohorts use identical instruments for baseline and follow-up data collection in studying incidence of cardiovascular outcomes. Cases of gout will be identified using physicians' self-report, and validated using published criteria. Plasma uric acid will be measured on specimens to be obtained as part of the above ongoing JHPS and MCS studies. Data will be analyzed using incidence density ratios and techniques of survival analysis, including Cox proportional hazards model. This study will be the first systematic prospective study comparing the incidence of, and risk factors for, gout in black and white men. Furthermore, these cohorts offer a unique opportunity to investigate the potential role of gout as an independent risk factor for CAD in black and white men. Improved understanding of risk factors for gout, and CAD, will allow development and/or refinement of prevention strategies for gout and CAD.