Hemostatic abnormalities and the severity of illness in patients at the onset of clinically defined sepsis. Possible indication of the degree of endothelial cell activation?
OBJECTIVE
To find out whether changes within the hemostatic system are related to the severity of illness and organ failure in patients at the onset of clinically defined sepsis and to find some indications for the contribution of endothelial cell activation or perturbation to the patient's status. The following measurements were undertaken: Acute Physiology and Chronic Health Evaluation (APACHE) II score, multiple organ failure (MOF) score, plasma levels of thrombin-antithrombin III complexes (TAT), antithrombin III (AT III), protein C antigen, factor XII, and plasminogen activator inhibitor type 1 antigen (PAI-1), neopterin, and interleukin 6 (IL-6).


METHODS
A prospective case series study.


METHODS
Intensive care unit (ICU) of the Department of Internal Medicine, Justus Liebig University, Giessen, Germany.


METHODS
28 consecutive patients (11 females, 17 males; mean age 58 years) with clinically defined sepsis. Eleven patients were admitted from the surgical ICU (9 after elective surgery, 2 after trauma surgery). The operations were done 1-26 days (mean 14 days) prior to the onset of sepsis.


RESULTS
At the onset of sepsis we found elevated plasma levels of TAT, PAI-1, neopterin, and IL-6, and lowered plasma levels of AT III, factor XII, and protein Cantigen. Neopterin, PAI-1, IL-6, and factor XII showed a statistically significant correlation with the APACHE II score. The MOF score is significantly correlated with IL-6 and neopterin. The extent of hemostatic abnormalities was related to increasing levels of IL-6.


CONCLUSIONS
Clinical evidence of a septic process is most likely to be preceded by activation of the hemostatic system, the vascular endothelium, and the monocyte/macrophage system. IL-6 may have a regulatory function for hemostasis in inflammation. Laboratory monitoring could be helpful in deciding whether to start early intensive therapy in patients at risk for sepsis.
Leithäuser
B
B
Klinik für Innere Medizin, Justus Liebig-Universität, Giessen, Germany.
Matthias
F R
FR
Nicolai
U
U
Voss
R
R
D000328:Adult; D000368:Aged; D000990:Antithrombin III / Q000378:metabolism; D001708:Biopterins / Q000031:analogs & derivatives / Q000097:blood; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000276:immunology*; D005260:Female; D006487:Hemostasis / Q000276:immunology*; D006801:Humans; D007249:Inflammation; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D019798:Neopterin; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011183:Postoperative Complications / Q000276:immunology* / Q000378:metabolism; D011446:Prospective Studies; D011486:Protein C / Q000378:metabolism; D018805:Sepsis / Q000276:immunology* / Q000378:metabolism; D012720:Severity of Illness Index
D015850:Interleukin-6; D017395:Plasminogen Activator Inhibitor 1; D011486:Protein C; D001708:Biopterins; D019798:Neopterin; D000990:Antithrombin III