PATHOPHYSIOLOGY OF HEMOLYTIC UREMIC SYNDROME

溶血性尿毒综合征的病理生理学

• 批准号: 7603521
• 负责人: SANDRA L. WATKINS
• 金额: $ 0.01万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-04-01 至 2007-09-16
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7603521
• 关键词: Acute; Antibiotics; Area; Child; Coagulation Process; Complication; Computer Retrieval of Information on Scientific Projects Database; Diarrhea; Disease; Endothelial Cells; Escherichia coli O157; Evolution; Functional disorder; Funding; Grant; Hemolytic-Uremic Syndrome; Infection; Institution; Pacific Northwest; Play; Research; Research Personnel; Resources; Risk; Role; Source; Targeted Toxins; Thrombotic Thrombocytopenic Purpura; United States National Institutes of Health; day; von Willebrand Factor

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. Hemolytic uremic syndrome (HUS) is a consequence of Escherichia coli O157:H7 infections. Approximately 10 percent of infected children develop this complication. HUS occurs approximately 7 or 8 days after the onset of diarrhea in infected children. The Pacific Northwest is an endemic area for this infection. The reasons why some children develop HUS and most do not is unknown. Similarly, the cascade of abnormalities leading to HUS following acute infection has also been poorly delineated. Antibiotics when administered to children infected with E. coli O157:H7 increase the risk of developing HUS. We have demonstrated that in advance of HUS, there are profound coagulation abnormalities. Von Willebrand Factor also does not appear to play a pathophysiologic role, unlike its critical importance in the evolution of thrombotic thrombocytopenic purpura (TTP). The endothelial cell is believed to be the critical target of the toxins elaborated by HUS because HUS is above all a thrombotic disorder.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 溶血性尿毒症综合征 (HUS) 是大肠杆菌 O157:H7 感染的结果。 大约 10% 的受感染儿童会出现这种并发症。 HUS 发生在感染儿童腹泻后大约 7 或 8 天。 太平洋西北地区是这种感染的流行地区。 有些儿童患上溶血性尿毒症综合症（HUS）而大多数儿童没有患上溶血性尿毒症综合症（HUS）的原因尚不清楚。 同样，急性感染后导致 HUS 的一系列异常现象也不清楚。 感染大肠杆菌 O157:H7 的儿童使用抗生素会增加患 HUS 的风险。 我们已经证明，在 HUS 发生之前，就存在严重的凝血异常。 与血管性血友病因子在血栓性血小板减少性紫癜 (TTP) 演变中的至关重要性不同，它似乎也没有发挥病理生理作用。 内皮细胞被认为是 HUS 产生的毒素的关键目标，因为 HUS 首先是一种血栓性疾病。