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)

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 study examines whether vitamin E deficiency has any role in the hypercoagulability of neonatal blood. Blood was collected from mothers and their full-term placental cords. Vitamin E was measured by high-pressure liquid chromatography and whole blood clotting time was measured by recalcification. Cord plasma had significantly lower vitamin E (P < 0.0001) compared with maternal plasma. Whole blood clotting time of cord blood was significantly (P < 0.002) shorter compared with the clotting time of maternal blood. There was a significant correlation between plasma vitamin E and whole blood clotting time (r = 0.54, P < 0.04) of cord blood. The addition of standard vitamin E to cord blood in vitro resulted in prolongation of whole blood clotting time. This suggests that a deficiency of plasma vitamin E can shorten whole blood clotting time in newborns, which may have a role in the disseminated intravascular coagulation frequently experienced by newborn infants.
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PMID:Vitamin E and the hypercoagulability of neonatal blood. 808 11