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

HELLP-syndrome is one of the most severe variants of liver failure in pregnancy. The incidence among pregnant patients is 0.5-0.9%, and in presence of severe preeclampsia and eclampsy the incidence is 10-20%. Pathogenesis of HELLP-syndrome has common features with pathogenesis of preeclampsia, DIC-syndrome and fatty hepatosis of pregnant, this is confirmed by pathomorphological changes of liver in women with HELLP-syndrome. Efficacy of conservative therapy (corticosteroids, magnesium sulphate, hypotensive therapy, hepatoprotectors) and disintoxication methods (plasmapheresis, MARS-therapy) is not evident. Difficulties of timely diagnosing, symptomatic nature of treatment, severity of complications lead to high rates of maternal (up to 25%) and perinatal (up to 34%) mortality. The only radical and efficient method of HELLP-syndrome treatment available is a timely delivery. That's why the revelation and consideration of the slightest clinical and laboratorial manifestations is very important in pregnancy.
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PMID:[Clinicopathologic characteristics of HELLP-syndrome]. 2140 Aug 2