VASCULAR DAMAGE IN SLE

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 (1)内皮型一氧化氮合酶(ENOS)基因多态性、血浆同型半胱氨酸水平、炎症标志物如血沉和C反应蛋白、氧化应激与系统性红斑狼疮(SLE)血管损伤的结构和功能指标有关。(2)选择超声检查颈动脉内膜中层厚度最高的患者，给予普伐他汀40 mg/d治疗3年。 特定目标： 1)验证以下假设：系统性红斑狼疮患者血管损伤的结构和功能指标比对照组更显著，eNOS基因多态性、血浆同型半胱氨酸浓度、炎症和氧化应激标志物与血管损伤的结构和功能指标相关。 2)验证假设，通过使用HMG辅酶A还原酶抑制剂治疗SLE患者，有可能改善血管损伤的结构和功能指标。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. (1) Endothelial nitric oxide synthase (eNOS) polymorphism, plasma homocysteine concetrations, markers of inflammationsuch as ESR and C-reactive protein, and oxidative stress are associated w/structural and functional measures of vascular damage in systemic lupus erythematosus (SLE). (2) Will select those patients w/the highest tertile of carotid intima-media thickness as determined by ultrasound scan and treat them w/pravastatin 40 mg daily for 3 years. SPECIFIC AIM: 1) To test the hypothesis that structural and functional measures of vascular damage are more marked in patients w/SLE than in matched controls and that eNOS polymorphism, plasma homocysteine concentrations, markers of inflammation and oxidative stress are associated w/structural and functional measures of vascular damage. 2) To test the hypothesis that it is possible to improve structural and functional measures of vascular damage in patients w/SLE through treatment w/an HMG coenzyme A reductase inhibitor.