Coagulation in sepsis: all bugs bite equally.
Sepsis almost invariably leads to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation. There is compelling evidence from clinical and experimental studies that disseminated intravascular coagulation is involved in the pathogenesis of microvascular dysfunction and contributes to organ failure. Data from the PROWESS phase III clinical trial of recombinant activated protein C in patients with severe sepsis confirm this notion and demonstrate that the vast majority of patients with severe sepsis have increased markers for systemic coagulation activation, decreased physiological anticoagulant proteins and depressed fibrinolysis. There is no correlation between the type of microorganism that has caused the infection and the presence or severity of the coagulation disorder.
Levi
Marcel
M
Department of Medicine, Academic Medical Center, University of Amsterdam, The Netherlands. m.m.levi@amc.uva.nl
van der Poll
Tom
T
D015415:Biomarkers / Q000032:analysis*; D001780:Blood Coagulation Tests; D017326:Clinical Trials, Phase III as Topic; D004211:Disseminated Intravascular Coagulation / Q000097:blood / Q000175:diagnosis*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis; D011379:Prognosis; D011486:Protein C / Q000627:therapeutic use; D011994:Recombinant Proteins / Q000627:therapeutic use; D018805:Sepsis / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology; D012720:Severity of Illness Index
D015415:Biomarkers; D011486:Protein C; D011994:Recombinant Proteins; C421124:drotrecogin alfa activated