Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An evaluation of the coagulation system has been conducted in vitamin E and/or selenium deficient swine. The partial thromboplastin time, plasma fibrinogen concentration, platelet lipid peroxides, as well as the fibrinogen/fibrin degradation products were not found to be significantly affected by either vitamin E deficiency, selenium deficiency, or deficiency of both. With selenium deficiency, the prothrombin time was shortened (p less than 0.05). The platelet count and platelet turnover were greatly decreased by both vitamin E (p less than 0.001) and selenium deficiency (p less than 0.005). Further-more, the survival of platelets labelled with 75Se-selenomethionine and the per cent isotope incorporated into platelets were reduced (p less than 0.05 and p less than 0.005) in association with vitamin E deficiency, but not with selenium deficiency. These results were interpreted as evidence of a platelet production defect and possibly a platelet function defect in vitamin E deficient animals. Selenium deficiency were also associated with decreased (p less than 0.05) survival of fibrinogen labelled with 75Se-selenomethionine and increased (p less than 0.05) turnover of fibrinogen. From these fibrinogen kinetic findings, it was considered that chronic low grade disseminated intravascular coagulation possibly occurs in selenium deficient animals, probably in relation to the development of hepatosis dietetica or widespread microvascular damage. However, other possibilities such as increased fibrinogenolysis in relation with hepatosis dietetica or an intrinsic fibrinogen defect due to selenium deficiency also need to be taken into consideration and have not been ruled out in the present study.
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PMID:Studies on vitamin E and selenium deficiency in young pigs. IV. Effect on coagulation system. 83 91

Vitamin E pretreatment significantly prevented E. coli-induced Disseminated Intravascular Coagulation (DIC) in rats (1). DIC, a reduction in fibrinogen and a falling platelet count and diffuse haemorrhage are part of the clinical features of Haemorrhagic Shock Encephalopathy Syndrome (HSES), recognised as a disease entity in the 1980s (2). At the SIDS Conference 1974 Reisinger described the effect of Escherichia coli (E. coli) endotoxin on the rabbit (3). An early effect was a reduction in fibrinogen and a falling platelet count, resulting in the release of relatively large amounts of the neuro-transmitter serotonin, stored in platelets (3, 4). Fibrinogen inhibited the release of serotonin from platelets (24). Serotonin is released from platelets during platelet aggregation (14). Platelet aggregation is inhibited by vitamin E (1). Serotonin is a neuro-transmitter associated with deep sleep, respiratory movements and cardiovascular collapse (3). Death at a later stage involved vascular permeability, edema and haemorrhage. After fibrin-platelet clots had formed DIC was present in lungs, kidneys and other organs (3). Medical researchers in Australia linked almost half of SIDS victims with a poisonous strain of intestinal E. coli bacteria (5). Dietary selenium in the intestinal villous tip is considered a daily modulator of cytochrome P450-dependent metabolism of drugs and toxins absorbed by intestinal mucosa (6). Villous atrophy occurs in HSES (2).
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PMID:Sudden infant death syndrome (SIDS) and the immune response. 146 Nov 72

This review describes the role of oxidative stress caused by endotoxin challenge in sepsis or septic shock symptoms. We observed that endotoxin injection resulted in lipid peroxide formation and membrane damage (near 60-150 kDa) in the livers of experimental animals, causing decreased levels of scavengers or quenchers of free radicals. The administration of alpha-tocopherol completely prevented injury to the liver plasma membrane caused by endotoxin, and suggested that lipid peroxidation by free radicals might occur in a tissue ischemic state, probably by disseminated intravascular coagulation (DIC), in endotoxemia. In mice, depression of Ca(2+)-ATPase activity in the liver plasma membrane may contribute to the membrane damage caused by endotoxin, and the increase of [Ca(2+)](i) in the liver cytoplasm may partially explain the oxidative stress that occurs in endotoxemia. It seems that endotoxin-induced free radical formation is regulated by Ca(2+) mobilization. Moreover, we have suggested that the oxidative stress caused by endotoxin may be due, at least in part, to the changes in endogenous zinc or selenium regulation during endotoxemia. Interestingly, the extent of TNF-alpha-induced oxidative stress may be the result of a synergism between TNF-alpha and gut-derived endotoxin. It is likely that bacterial or endotoxin translocation plays a significant role in TNF-alpha-induced septic shock. On the other hand, although nitric oxide (NO) has been implicated in the pathogenesis of vascular hyporesponsiveness and hypotension in septic shock in our experimental model, it is unlikely that NO plays a significant role in liver injury caused by free radical generation in endotoxemia.
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PMID:Oxidative stress and septic shock: metabolic aspects of oxygen-derived free radicals generated in the liver during endotoxemia. 1683 Dec 3