Thrombogenic alleles, Escherichia coli O157:H7 infections, and hemolytic uremic syndrome

J. T. Sprouse, C. S. Wong, W. L. Chandler, G. D. Williams, S. L. Watkins, P. I. Tarr

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)283-288
Number of pages6
JournalBlood Coagulation and Fibrinolysis
Volume12
Issue number4
DOIs
StatePublished - 2001

Keywords

  • Factor V Leiden
  • Hemolytic uremic syndrome
  • Methylenetetrahydrofolate reductase gene
  • Plasminogen activator inhibitor-1 promoter
  • Prothrombin gene

ASJC Scopus subject areas

  • Hematology

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