Thrombogenic alleles, Escherichia coli O157 : H7 infections, and hemolyticuremic syndrome

Hemolytic uremic syndrome (HUS) of childhood most commonly follows gastroin testinal 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 co agulation 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) o r the plasminogen activator inhibitor (PAI)-1 promotor (4G/5G) genotypes an d 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 correla te with the PAI-1 genotype. We conclude that the alleles studied are not ma jor risk factors for the acquisition of E. (C) 2001 Lippincott Williams & W ilkins.