Expression profiling and disseminated intravascular coagulation: finding genes gone wild.

American Journal of Respiratory and Critical Care Medicine (Impact Factor: 13). 10/2007; 176(6):528-30. DOI: 10.1164/rccm.200706-923ED
Source: PubMed
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    ABSTRACT: In seven of 30 consecutive patients with the adult respiratory distress syndrome, disseminated intravascular coagulation (DIC) developed. Increasing respiratory dysfunction characterized by decreased effective static compliance and increased hypoxemia coincided with the development of DIC. Patients in whom DIC developed were characterized by a high incidence of bleeding, gangrene of the extremities, renal dysfunction, mortality and autopsy evidence of fibrin microthrombi in the lungs, kidney and skin. In 12 of 23 patients who did not meet the criteria for DIC, the platelet count decreased by at least 50 per cent of the initial values at some time during their illness. Fibrin microthrombi were found in the lungs in the majority of the patients subjected to autopsy. These data support the concept that depostion of platelet on damaged pulmonary capillary endothelium may be more common in the adult respiratory distress syndrome than the DIC syndrome.
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    ABSTRACT: Disseminated Intravascular Coagulation (DIC) is an acquired syndrome representing a hypercoagulable state, haemorrhagic symptoms and multiple organ failure. The clinical relevance of this syndrome is complicated since there is no established way of diagnosing DIC and it is difficult to distinguish whether clinical features are attributable to the underlying disease or DIC. Experimental studies, based on models of gram-negative sepsis and the Generalized Shwartzman Reaction, show that DIC is characterized by strongly enhanced inflammatory activity, activated coagulation and impaired fibrinolysis. In this review we propose that activated neutrophils play a pivotal role in the pathophysiology of DIC, particularly by contributing to inflammation and vascular injury. Additionally, a distinct role for granulocytes in fibrinolysis has also been suggested. Although the underlying procoagulant pathways of DIC and the important role of tissue factor have been unravelled, therapeutic interventions counteracting the mediators of these pathways proved mainly unsuccessful (with the positive exception of activated protein C). Dissecting the molecular interactions at the onset and progression of DIC might therefore help to elucidate the fundamental consequences of DIC, possibly contributing to better diagnostic tools and more effective therapeutic options.
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