Markers of endothelial damage in organ dysfunction and sepsis

被引:227
作者
Reinhart, K [1 ]
Bayer, O [1 ]
Brunkhorst, F [1 ]
Meisner, M [1 ]
机构
[1] Univ Jena, Dept Anesthesiol & Intens Care Med, D-6900 Jena, Germany
关键词
coagulation parameters; endothelium; interleukin-6; organ dysfunction; procalcitonin; sepsis;
D O I
10.1097/00003246-200205001-00021
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Objectives., 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. Data Extraction and Synthesis: 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.
引用
收藏
页码:S302 / S312
页数:11
相关论文
共 115 条
[1]   Endothelial apoptosis is induced by serum of patients after cardiopulmonary bypass [J].
Aebert, H ;
Kirchner, S ;
Keyser, A ;
Birnbaum, DE ;
Holler, E ;
Andreesen, R ;
Eissner, G .
EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY, 2000, 18 (05) :589-593
[2]  
ARDITI M, 1995, J IMMUNOL, V155, P3994
[3]   PLASMA-LEVELS OF SOLUBLE THROMBOMODULIN INCREASE IN CASES OF DISSEMINATED INTRAVASCULAR COAGULATION WITH ORGAN FAILURE [J].
ASAKURA, H ;
JOKAJI, H ;
SAITO, M ;
UOTANI, C ;
KUMABASHIRI, I ;
MORISHITA, E ;
YAMAZAKI, M ;
MATSUDA, T .
AMERICAN JOURNAL OF HEMATOLOGY, 1991, 38 (04) :281-287
[4]   Plasma levels of the three endothelial-specific proteins von Willebrand factor, tissue factor pathway inhibitor, and thrombomodulin do not predict the development of acute respiratory distress syndrome [J].
Bajaj, MS ;
Tricomi, SM .
INTENSIVE CARE MEDICINE, 1999, 25 (11) :1259-1266
[5]   Efficacy and safety of recombinant human activated protein C for severe sepsis. [J].
Bernard, GR ;
Vincent, JL ;
Laterre, P ;
LaRosa, SP ;
Dhainaut, JF ;
Lopez-Rodriguez, A ;
Steingrub, JS ;
Garber, GE ;
Helterbrand, JD ;
Ely, EW ;
Fisher, CJ .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (10) :699-709
[6]  
BLANN AD, 1992, CLIN EXP IMMUNOL, V90, P88
[7]   SUBSTITUTION THERAPY WITH AN ANTITHROMBIN-III CONCENTRATE IN SHOCK AND DIC [J].
BLAUHUT, B ;
NECEK, S ;
VINAZZER, H ;
BERGMANN, H .
THROMBOSIS RESEARCH, 1982, 27 (03) :271-278
[8]   SUBSTITUTION OF ANTITHROMBIN-III IN SHOCK AND DIC - A RANDOMIZED STUDY [J].
BLAUHUT, B ;
KRAMAR, H ;
VINAZZER, H ;
BERGMANN, H .
THROMBOSIS RESEARCH, 1985, 39 (01) :81-89
[9]   RETRACTED: Does age influence circulating adhesion molecules in the critically ill? (Retracted Article) [J].
Boldt, J ;
Muller, M ;
Heesen, M ;
Papsdorf, M ;
Hempelmann, G .
CRITICAL CARE MEDICINE, 1997, 25 (01) :95-100
[10]   RETRACTED: Normothermic versus hypothermic cardiopulmonary bypass: Do changes in coagulation differ? (Retracted article. See vol. 111, 2021) [J].
Boldt, J ;
Knothe, C ;
Welters, I ;
Dapper, FL ;
Hempelmann, G .
ANNALS OF THORACIC SURGERY, 1996, 62 (01) :130-135