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.

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。 溶血性尿毒症综合征(HUS)是由大肠杆菌O157：H7感染引起的。大约10%的受感染儿童会出现这种并发症。HUS发生在受感染儿童腹泻发作后约7或8天。太平洋西北部是这种感染的流行地区。一些儿童患上HUS的原因尚不清楚，而大多数儿童不会。同样，急性感染后导致HUS的一连串异常也没有得到很好的描述。对感染O157：H7大肠杆菌的儿童使用抗生素会增加患HUS的风险。我们已经证明，在HUS之前，存在严重的凝血异常。血管性血友病因子似乎也没有发挥病理生理作用，不像它在血栓性血小板减少性紫癜(TTP)的演变中的关键作用。内皮细胞被认为是HUS阐述的毒素的关键靶点，因为HUS首先是一种血栓性疾病。