Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In both animals and humans, vitamin E deficiency is associated with platelet hyperaggregability. In six E-deficient children, thrombocytosis was associated with marked hyperaggregability of their platelets to ADP, epinephrine, and collagen. Platelet malonyldialdehyde (MDA) formation was used as an indicator of prostaglandin formation, and was found to be increased during the E deficiency state. Following E repletion, both platelet aggregation and platelet MDA formation returned to normal. The addition of vitamin E to platelets in vitro has been associated with inhibition of platelet release, aggregation, and MDA formation. Extending these in vitro observations further, six normal controls were given 1600 units of vitamin E orally daily for 2 weeks to elevate their plasma E levels and the E content of their platelets in vivo. Concomitant with the elevation in their plasma E levels, there was an inhibitory effect of 12--20% on platelet MDA formation following E ingestion. These studies suggest that E deficiency increases the in vivo synthesis of platelet endoperoxides and prostaglandins, and that E excess has the opposite effect, i.e., inhibition of the endoperoxide intermediates of prostaglandin synthesis.
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PMID:Vitamin E and platelet function. 39 95

An infant is described who presented with ptosis and periorbital oedema and was found to have infantile cortical hyperostosis with thrombocytosis, raised IgM, and vitamin E deficiency.
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PMID:Vitamin E deficiency and thrombocytosis in Caffey's disease. 77 66

The effect of a prophylactic treatment with tocopherol, early iron substitution and administration of polyunsaturated fatty acids in different quantities on the plasma concentration of vitamin E, hemolysis in the peroxide test and hematological parameters during the first two months of life was determined in 23 premature infants with birth weights of less than 1800 gms. In no patient in any of the different treatment groups a tocopherol deficiency (plasma concentration less than 0.50 mg/100ml) was observed and accordingly no hemolytic anemia attributable to E hypovitaminosis was found. The mean concentration of tocopherol at birth (0.51 mg/100 ml) was already above the critical limit, and no single value was found below the latter after the 10th day of life. For that reason, the amount of vitamin E included in formulas generally used in this country and its intestinal absorption have to be considered as adequate even for small premature children. The different treatments of the test groups had no significant influence on the clinical state or the hematological findings. The infants with vitamin E substitution and those without had similar hemoglobin levels. Almost all children had a distinct reticulocytosis and thrombocytosis during the second month of their life. This seems to occur naturally. The peroxide test proved to be no reliable indicator of a tocopherol deficiency in the individual case. It is not yet clear which additional factors cause vitamin E deficiency, infrequently seen in small premature infants.
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PMID:[Vitamin E deficiency and anaemia in premature infants (author's transl)]. 89 38

A 16-month-old infant with hepatic fibrosis, cholestasis, and chronic jaundice had signs of vitamin E deficiency, including mild acanthocytosis, thrombocytosis, increased peroxide haemolysis, and absent serum vitamin E. Abormal prothrombin consumption and platelet restocetin aggregation suggested the presence of defective platelet function, and correction studies indicated that this was due to a plasma defect. The abnormality was corrected by treatment with vitamin E, and the findings suggest a possible role of this vitamin in platelet reactions.
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PMID:Vitamin E deficiency and platelet functional defect in a jaundiced infant. 117 3

The use of elevated dosages of vitamin E in humans has led to the discovery of vitamin E deficiency syndromes in neurological areas. This evidence comes from careful clinical studies in which elevated vitamin E dosages were applied. In long-term studies it has now been established that retinal and neurological abnormalities are due to vitamin E deficiency and can be ameliorated by therapy with a large amount of the vitamin enterally or parenterally, which can possibly completely prevent the development of clinical manifestations if adequate treatment is given from an early age. It has also become clear that similar neurological and ocular lesions occur in other chronic fat malabsorptive states such as cholestatic liver diseases, cystic fibrosis, and extensive resection of the gut, with respect to an elevated dosage of vitamin E therapy. More recently, several patients with spinocerebellar degeneration from vitamin E deficiency without other evidence of malabsorption have been reported on in whom the progression of the diseases is cessated by the vitamin E therapy. Whether or not the use of elevated dosages of vitamin E should be recommended for certain diseases in premature infants is controversial. Previously, it has been thought that newborn infants, especially premature infants, suffer from vitamin E deficiency, because of their low plasma vitamin E concentrations and high susceptibility of erythrocytes to hydrogen peroxide hemolysis test. Furthermore, tocopherol deficiency has been implicated in four neonatal conditions: anemia of prematurity, retrolental fibroplasia (RLF), bronchopulmonary dysplasia (BPD), and intraventricular hemorrhage (IVH). A hemolytic anemia, associated with thrombocytosis and edema, which is responsive to vitamin E therapy, is not well recognized and occurs in a minority of preterm infants, who were given high amounts of polyunsaturated fatty acids in their formula. However, prophylactic use of an elevated dosage of vitamin E to prevent anemia in the majority of premature infants is controversial. There is no evidence for beneficial effects in BPD. In addition, the prophylactic use of pharmacological dosages of vitamin E for prevention of RLF and IVH has also had conflicting results. In the course of therapy with elevated dosages of vitamin E, administered either orally, intramuscularly, or intravenously, many problems arose in the infants, such as unexpected death, increased frequency of necrotizing enterocolitis (NEC) and sepsis, and the development of unusual symptoms including hepatic injuries.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use and safety of elevated dosages of vitamin E in infants and children. 250 8

Glutathione peroxidase activity in platelets increased stepwise in selenium-depleted rats that were repleted with graded levels of dietary sodium selenite. In a 3-phase depletion/repletion/depletion feeding study, glutathione peroxidase activity was similar in platelets and liver, which apparently contains the largest labile pool of selenium in the body. The activity of glutathione S-transferase (selenium-independent glutathione peroxidase) in platelets was low and was not affected by selenium deficiency, even though hepatic transferase was markedly elevated in selenium-deficient rats. Vitamin E deficiency did not affect activities of glutathione peroxidase or glutathione S-transferase in platelets or liver. Determination of glutathione peroxidase activity in platelets apparently is a promising technique for assessing selenium status and, possibly, for measuring selenium bioavailability.
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PMID:Platelet glutathione peroxidase activity as an index of selenium status in rats. 682 91

Evidence from the literature indicates that in vitamin E-deficient animals prostaglandin (PG) synthesis in platelets is enhanced while it is decreased in the muscle and testis. In the present study the effects of aspirin, a known inhibitor of PG biosynthesis, on vitamin E deficiency signs in the rat were investigated. Administration of aspirin to vitamin E-deficient rats had no protective effect on fetal mortality, incisor depigmentation, body weight gain or red blood cell peroxidative hemolysis. Aspirin prevented the anemia and thrombocythemia observed in vitamin E-deficient rats. Aspirin, salicylic acid and a carbazole prostaglandin inhibitor exacerbated testis degeneration in vitamin E-deficient animals. Addition of aspirin to the diet more than doubled the vitamin E requirement for reversal of necrotizing myopathy.
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PMID:Effects of aspirin and related drugs in vitamin E-deficient rats. 742 Feb 4