Thrombogenic alleles, Escherichia coli O157:H7 infections, and hemolytic uremic syndrome.
Thrombogenic alleles, Escherichia coli O157:H7 infections, and hemolytic uremic syndrome.
复制标题
血栓形成等位基因、大肠杆菌 O157:H7 感染和溶血性尿毒症综合征。
DOI：
10.1097/00001721-200106000-00009
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Tarr,PI
中科院分区：
文献类型：
--
作者：
Sprouse,JT;Wong,CS;Chandler,WL;Williams,GD;Watkins,SL;Tarr,PI
Hemolytic uremic syndrome (HUS) of childhood most commonly follows gastrointestinal infection with Escherichia coli O157: H7. This pathogen elaborates Shiga toxins that are believed to cause microvascular injury and to trigger a thrombogenic response. The exact mechanisms leading to variable disease manifestations are unknown. Allelic variation in genes encoding selected coagulation factors and inhibitors of fibrinolysis were examined to determine whether or not a causal relationship exists between hypercoagulability and the development of HUS. No correlation between the thrombogenic factor V (G1691A), factor II (G20210A), methylenetetrahydrofolate reductase (C677T), or the plasminogen activator inhibitor (PAI)-1 promotor (4G/5G) genotypes and the risk of infection with E. coli O157: H7, or the risk of development of HUS among infected patients, was found. Serum PAI-1 levels did not correlate with the PAI-1 genotype. We conclude that the alleles studied are not major risk factors for the acquisition of E. coli O157: H7 infection, or of E. coli O157: H7-related HUS.
