VASCULAR DAMAGE IN SLE

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 (1)内皮型一氧化氮合酶（eNOS）多态性、血浆同型半胱氨酸浓度、炎症标志物如ESR和C反应蛋白以及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相关。 (2)将选择超声扫描确定的颈动脉内膜中层厚度最高三分位数的患者，并接受普伐他汀40 mg/d治疗3年。 具体目标： 1)为了验证以下假设：SLE患者的血管损伤的结构和功能指标比匹配的对照组更显著，eNOS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)检验HMG辅酶A还原酶抑制剂治疗可能改善SLE患者血管损伤的结构和功能指标的假设。

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.