| Literature DB >> 18491973 |
Erik I Tucker1, David Gailani, Sawan Hurst, Qiufang Cheng, Stephen R Hanson, András Gruber.
Abstract
Anticoagulation is a rational approach to the treatment of sepsis-associated consumptive coagulopathy, but its application is limited because of the risk of excessive bleeding. Factor XI (FXI) contributes substantially to pathological blood coagulation (thrombosis), whereas it contributes only modestly to normal hemostasis. We found that FXI-deficient mice have reduced coagulopathy and increased survival relative to FXI-expressing wild-type mice during cecal ligation and puncture-induced acute peritonitis/sepsis. This finding suggests that FXI contributes to coagulopathy and/or inflammation during sepsis and that pharmacologic inhibition of FXI activity may alter the course and outcome of some infections.Entities:
Mesh:
Substances:
Year: 2008 PMID: 18491973 PMCID: PMC2654284 DOI: 10.1086/589514
Source DB: PubMed Journal: J Infect Dis ISSN: 0022-1899 Impact factor: 5.226