OUTCOME OF SYSTEMIC LUPUS ERYTHEMATOSUS IN MINORITIES

描述(取自应用程序) 遗传和非遗传因素都会导致这种易感性、病程 系统性红斑狼疮(SLE)的转归。我们已经组成了一个 来自三个种族的229名SLE患者的队列(西班牙裔， 非裔美国人和白种人)在两个地理位置(阿拉巴马州和 得克萨斯)，以考察 儿童的社会经济-人口学、行为-文化和免疫遗传学特征 系统性红斑狼疮随时间推移的临床表现。在疾病发作时，我们发现 免疫遗传和种族因素是导致疾病的主要原因 系统性红斑狼疮的活动性和特定器官表现(肾脏、神经精神疾病 和心脏)。在研究报告中，拉美裔和非裔美国人展示了 疾病活跃度更高。缺乏私人保险，突然 发病、抗Ro抗体、缺乏人类白细胞抗原-DR3和异常疾病 行为，也预示着更大的疾病活动。进行了两年的研究， 预计无助、社会支持不足和缺乏医疗保险 在研究期间持续的疾病活动。不出所料， 作为单一因素的持续性疾病活动最能预测疾病 损坏。随着时间的推移，我们注意到了不同的损伤率 三个民族的发病率，非高加索人患病更多 相关后果，尽管差异还不是统计上的 意义重大。尽管如此，自我感觉的功能在 三组。特别值得注意的是，种族本身独立于 到目前为止测量的遗传因素以及社会经济-人口和 行为-文化因素，预测持续的疾病活动和 损伤，这表明其他遗传因素正在影响 SLE。 在本意见书中，我们建议：1)继续遵循目前的 队列：2)按顺序将现有队列从229名患者扩大到450名 为了提高我们发现三者之间有意义的差异的能力 3)检查其他MHC-和非MHC基因，这些基因也具有 与系统性红斑狼疮(TNF、MBP、IL1-RA、Bcl2)有关；4)提炼 对那些临床、行为-文化因素的评估发现 疾病活动性、损害和自我感觉的重要预测因子 5)研究疾病活动之间的关系， 这些患者的疾病损害和自我感觉功能 疾病的进展和预测它们的因素。有更长时间的随访 我们预计这种疾病的影响在不同的国家和地区会有很大不同 三个民族，随着新病人的增加，我们 希望有能力检测社会经济-人口统计，临床， 导致这些的免疫遗传和行为文化因素 不同之处。

DESCRIPTION (Taken from the application) Both genetic and nongenetic factors contribute to the predisposition, course and outcome of systemic lupus erythematosus (SLE). We have constituted a cohort of 229 SLE patients from three ethnic groups (Hispanics, African-Americans and Caucasians) at two geographic locations (Alabama and Texas) in order to examine the relative importance of socioeconomic-demographic, behavioral-cultural and immunogenetic features in the clinical manifestations of SLE over time. At disease onset, we found that immunogenetic and ethnic factors primarily accounted for disease activity and specific organ manifestations of SLE (renal, neuropsychiatric and cardiac). At study entry, Hispanics and African-Americans exhibited higher levels of disease activity. Lack of private insurance, abrupt disease onset, anti-Ro antibodies, lack of HLA-DR3 and abnormal illness behaviors, also predicted greater disease activity. Two years into a study, helplessness, poor social support and lack of health insurance predicted persistent disease activity over the study duration. As expected, persistent disease activity as a single factor best predicted disease damage. As more time passes, we are noticing a differential rate of damage accrual in the three ethnic groups, with non-Caucasians having more disease related consequences, although the differences are not yet statistically significant. Despite this, self-perceived functioning was similar in the three groups. Of particular note was that ethnicity per se, independent of genetic factors measured thus far, and socioeconomic-demographic and behavioral-cultural factors, predicted both persistent disease activity and damage, suggesting that other genetic factors are affecting the course of SLE. In this submission, we propose: 1) to continue following the present cohort: 2) to enlarge the present cohort from 229 to 450 patients in order to increase our ability to detect meaningful differences between the three ethnic groups; 3) to examine additional MHC-and non-MHC genes that have also been associated with SLE (TNF, MBP, IL1-RA, Bcl-2); 4) to refine the assessment of those clinical, behavioral-cultural factors found to be important predictors of disease activity, damage and self-perceived functioning thus far; 5) to study the relationship among disease activity, disease damage and self-perceived functioning in these patients as the disease progresses and the factors that predict them. With longer follow-up we expect the impact of the disease will be significantly different among the three ethnic groups and with the addition of new patient recruits we expect to have the power to detect the socioeconomic-demographic, clinical, immunogenetic and behavioral-cultural factors contributing to these differences.