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Colegio de Medicina Interna de México.

2008, Number 4

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Med Int Mex 2008; 24 (4)

Sepsis physiopathology: a molecular approach

Membreño MJP

Language: Spanish
References: 19
Page: 304-312
PDF size: 273.05 Kb.


ABSTRACT

Sepsis is a main cause for morbidity in intensive therapy units. Its mortality goes from 20 to 50%, according to the associated illness. This condition has not only an infectious origin, but causes several clinical and biochemical manifestations determined by its physiopathology. Inflammation and coagulation are usually studied as independent phenomenon; nevertheless, its participation in sepsis is interdependent. Sepsis is a proinflammatory and procoagulation process that with fibrinolysis decrease causes thrombus formation and subsequent multiple organic dysfunction. When a pathogenic agent invades the organism there is a local initial monocyte-mediated response. Tissue factor detonate the coagulation cascade transforming the circulating prothrombin into thrombin, and fibrinogen into fibrin, and activating platelet aggregation. Thrombin has important functions in coagulation and inflammation, depending on its free state or in thrombin-thrombomodulin complex. Three anticoagulation systems constitute the organism: activated protein C, antithrombin III (AT III) and inhibitor of tissue factor. Most studied biomarkers derived from endothelial activation in septicemia are: adhesion molecules (E-selectine [ELAM-1], ICAM-1, VCAM- 1); thrombomodulin; Von Willebrand factor; tissue factor; thrombin receptors; IL-6; activated C protein, and antithrombin III. Some studies have evaluated relationship between these biomarkers with seriousness of systemic inflammation, sepsis and its prognosis.


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