Markers of endothelial damage in organ dysfunction and sepsis.
OBJECTIVE
To review the literature on direct and indirect markers of endothelial activation and damage in patients with sepsis and systemic inflammation and to assess their clinical usefulness for diagnosis and outcome. Various markers derived from or activated by endothelial cells are described, such as adhesion molecules, thrombomodulin, von Willebrand factor, parameters of the coagulation system, and interleukin-6. Furthermore, the association of these markers with the severity of sepsis, systemic inflammation, and outcome is evaluated.


METHODS
Published research and review articles related to these parameters, with special emphasis on clinical studies.


CONCLUSIONS
Endothelial activation and damage occur early during sepsis and play a major role in the pathophysiology of systemic inflammation. Various markers of endothelial activation are increased during sepsis and systemic inflammation, and in most studies, the level of markers such as soluble intercellular adhesion molecule, vascular cell adhesion molecule, and E selectin correlate well with the severity of inflammation and the course of the disease. However, to date, it remains unclear whether adhesion molecules and coagulation parameters are superior in this respect to interleukin-6 and procalcitonin, as direct comparisons are lacking. In addition, it is evident that markers of endothelial activation and coagulation parameters lack specificity for infection-induced endothelial damage and organ dysfunction.
Reinhart
Konrad
K
Department of Anesthesiology and Intensive Care Medicine, Friedrich Schiller University, Jena, Germany.
Bayer
Ole
O
Brunkhorst
Frank
F
Meisner
Michael
M
D015415:Biomarkers; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism*; D006801:Humans; D012720:Severity of Illness Index; D012772:Shock, Septic / Q000097:blood / Q000378:metabolism*; D018746:Systemic Inflammatory Response Syndrome / Q000175:diagnosis / Q000378:metabolism / Q000503:physiopathology; D018180:Thrombomodulin / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism*
D015415:Biomarkers; D015815:Cell Adhesion Molecules; D018180:Thrombomodulin; D014841:von Willebrand Factor