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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Symptoms of Vitamin E deficiency can be generally attributed to derangement of processes depending upon the integrity of cellular and subcellular membranes, following the formation of tissue-damaging products of lipid peroxidation. Antioxidants modulate also the formation of products derived from long-chain polyunsaturated fatty acids, such as arachidonic acid--which are structural components of biological membranes--through oxidative reactions involving the cyclooxygenase and lipoxygenase systems. Vitamin E inhibits the aggregatory responses of blood platelets to aggregating agents "in vitro", after a preincubation period required for the uptake of the compound by the cells. The antiaggregatory activity of alpha-tocopherol, however, does not appear to be strictly dependent upon inhibition of the formation of thromboxane, the proaggregatory compound derived from arachidonic acid through be cyclooxgenase system. The effects of Vitamin E on platelet function may be of relevance in the control of thromboembolic processes of clinical importance.
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PMID:Biological actions and possible uses of vitamin E. 675 99

Vitamin E (alpha-tocopherol) has been credited with a variety of beneficial effects in the premature newborn infant. It has been thought that deficiency of vitamin E is at least partly responsible for the anemia which often occurs 4 to 6 wk after premature birth, and routine dietary supplementation with vitamin E is frequently recommended. However, critical analysis reveals that published controlled studies of vitamin E supplementation do not agree on the magnitude or even the existence of this protective effect against anemia. Analysis of commonly used feeding practices suggests that the dietary ratio of alpha-tocopherol to polyunsaturated fatty acids is generally sufficient to prevent manifestations of vitamin E deficiency without supplementation. Large parenteral doses of vitamin E have been purported to protect premature infants exposed to oxygen-enriched environments and mechanical ventilation from the complications of retrolental fibroplasia and bronchopulmonary dysplasia. Subsequent studies, however, have not yet substantiated encouraging early reports of these protective effects. At present, there seems to be no clearly established need for supplementing the premature infant's usual dietary intake of vitamin E.
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PMID:The role of vitamin E in the nutrition of premature infants. 678 56

Preincubating platelet-rich plasma (PRP) of vitamin E-deficient rats with RRR-alpha-tocopherol prior to the aggregation induced by collagen suspension resulted in inhibition of the formation of endoperoxide metabolites derived from endogenous arachidonic acid (AA). This inhibition was not dose dependent at concentrations above the plasma level of RRR-alpha-tocopherol of vitamin E-supplemented rats. Preincubating the vitamin E-deficient PRP with RRR-alpha-tocopherol did not affect the formation of 12-hydroxyeicosatetraenoic acid, the platelet lipoxygenase product. Concentrations of endoperoxide metabolites in diluted whole blood challenged with collagen suspension were significantly greater in the vitamin E-deficient group than the supplemented group. The level of AA in platelet or plasma phospholipids was not different between the two groups. However, blood platelet counts in the deficient group were significantly greater than those of the supplemented group. Concentrations of endoperoxide metabolites in PRP samples in which platelet concentrations were equalized were still greater in vitamin E-deficient group; however, the difference was not statistically significant. There was also no difference in the degree of maximal platelet aggregation between the two groups. These results indicated that vitamin E deficiency can slightly stimulate the formation of cyclooxygenase products derived from endogenous AA, but it did not affect the formation of lipoxygenase product in rat platelets.
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PMID:In vitro and in vivo effects of vitamin E on arachidonic acid metabolism in rat platelets. 680 55

Vitamin E and essential fatty acid status were examined in two groups of patients, one receiving fat-free total parenteral nutrition (TPN) with intravenous all-rac-alpha-tocopherol for vitamin E deficiency and the other receiving routine intravenous fat (Intralipid, 10%) emulsions with TPN to supply both fatty acid and vitamin E requirements. Initial evaluation of both groups revealed a 50% incidence of vitamin E deficiency, platelet hyperaggregation, or in vitro H2O2-induced hemolysis. Only platelet hyperaggregation correlated significantly with vitamin E deficiency. Supplementation with all-rac-alpha-tocopherol corrected platelet hyperaggregation and H2O2-induced hemolysis; daily dosage requirements of 25-50 mg (fat-free TPN) or more (with intravenous fat) suggest increased vitamin E requirements during TPN. Intravenous fat emulsion did not correct the platelet and red blood cell abnormalities, a result of either increased vitamin E requirements or low alpha-tocopherol-equivalent content of the emulsion. Essential fatty acid deficiency (EFAD) was observed in seven patients with an associated platelet hyperaggregation independent of vitamin E deficiency. Prolonged TPN for enterocutaneous fistulae in three patients was associated with persistent EFAD and platelet hyperaggregation despite up to 2.0 liters of intravenous fat emulsion weekly.
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PMID:Vitamin E and total parenteral nutrition. 681 20

Significant alterations in hemotologic function in cystic fibrosis are suggested by the observation that polycythemia is uncommon, even among cyanotic patients. To elucidate those factors that influence hematologic equilibrium, 39 stable patients with cystic fibrosis were evaluated with regard to hemoglobin, hematocrit, RBC indices, reticulocyte count, serum iron and total iron binding capacity, serum ferritin, vitamin E, and carboxyhemoglobin levels. Hemoglobin concentrations were below the 50th percentile for age in 90% of the patients, including the 23% who were cyanotic. Serum ferritin levels were below the mean for age in 85% and below 12 ng/mL in 33% of patients. Vitamin E levels were less than 5 micrograms/dL in 33%, indicating deficiency. Carboxyhemoglobin values were elevated in 64% of the patients. These data indicate that relative anemia is common in cystic fibrosis and suggest that iron and vitamin E deficiency may contribute to that anemia. Twenty-two patients with cystic fibrosis were then given 2 weeks of oral iron therapy followed by two to three additional weeks of iron and vitamin E. This therapeutic trial resulted in an increase in mean hemoglobin concentration from 13.87 to 14.50 g/dL (P less than 0.01) associated with a significant increase in levels of serum ferritin (P less than 0.001). The increase in hemoglobin occurred primarily during the second 2 weeks when patients were receiving both iron and vitamin E. However, we were unable to document evidence of increased hemolysis when patients were receiving iron therapy alone. This response to oral iron therapy is confirmation that iron deficiency contributes to the failure of some patients with cystic fibrosis to compensate hemotologically for hypoxia.
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PMID:Relative anemia and iron deficiency in cystic fibrosis. 683 67

In an attempt to confirm prior reports of vitamin E deficiency in Werdnig-Hoffmann disease, we assessed vitamin E nutritional status in 11 children and 6 adults with spinal muscular atrophy (SMA). Serum vitamin E levels (10.6 +/- 3.3 micrograms/ml for those less than 12 years old, 13.2 +/- 4.5 for those older than 12) and the ratio of serum vitamin E to total serum lipids were normal in all patients. Vitamin E nutritional status appears to be normal in SMA, and vitamin E therapy is not indicated.
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PMID:Normal vitamin E status in spinal muscular atrophy. 684 48

Vitamin E deficiency in rats increased the sensitivity of liver and muscle mitochondria to damage during incubation at various temperatures, irradiation with visible light, or steady-state respiration with substrates. In all cases, vitamin E-deficient mitochondria exhibited increased lipid peroxidation, reduced transmembrane potential, decreased respiratory coupling, and lower rates of electron transport compared to control mitochondria. Muscle mitochondria always showed greater negative inner membrane surface charge density, and were also more sensitive to damage than were liver mitochondria. Vitamin E-deficient mitochondria also showed slightly more negative inner membrane surface charge density compared to controls. The relationship observed between greater negative surface potential and increased sensitivity to damage provides for a new and sensitive method to probe further the role of surface charge in membrane structure and function. Implications of these new findings for the well-known human muscle myopathies and those experimentally induced by vitamin E deficiency in animals are discussed.
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PMID:Membrane effects of vitamin E deficiency: bioenergetic and surface charge density studies of skeletal muscle and liver mitochondria. 695 60

Rat lung and liver microsomes were used to examine the effects of dietary vitamin E deficiency on membrane lipid peroxidation. Microsomes from vitamin-E-deficient rats displayed increased lipid peroxidation in comparison to microsomes from vitamin-E-supplemented controls. The extent of lipid peroxidation, as determined by measurement of thiobarbituric acid reacting materials, was enhanced by addition of reduced iron and ascorbate (or NADPH). Rats fed a vitamin-E-supplemented diet and exposed to 3 ppm NO2 for 7 days did not exhibit increases in microsomal lipid peroxidation compared to air-breathing controls. However, increase were found in microsomes prepared from rats fed a vitamin-E-deficient diet and exposed to NO2. Lung microsomes from vitamin-E-fed rats contained almost 10 times as much vitamin E as liver microsomes when expressed in terms of polyunsaturated fatty acid content. The extent of lipid peroxidation was, in turn, considerably less in lung than in liver microsomes. Lipid peroxidation in lung microsomes from vitamin-E-deficient rats comparable to liver microsomes from vitamin-E-supplemented rats as was the content of vitamin E in these respective microsomal samples. A combination of vitamin E deficiency and NO2 exposure resulted in the greatest increases in lung and liver microsomal lipid peroxidation with the largest relative increases occurring in lung microsomes. An inverse relationship was found between the extent of lipid peroxidation and vitamin E content. Most of the peroxidation in lung microsomes appeared to proceed nonenzymatically whereas peroxidation in liver was largely enzymatic. Vitamin E appears to be assimilated by the lung during oxidant inhalation, but with dietary vitamin E deprivation, the margin for protection in lung may be less than in liver.
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PMID:Influence of vitamin E and nitrogen dioxide on lipid peroxidation in rat lung and liver microsomes. 707 57

The mechanisms and consequences of Vitamin E deficiency were studied in 12 children presenting with chronic cholestasis. Preliminary results indicate that: (1) Vitamin E serum levels are lowest in children with the long-lasting cholestasis and in children in whom fat malabsorption is deepest. (2) Signs of neurologic dysfunction involving peripheral nerves, cerebellum, eye movements and retina were present in 7 children. (3) In vitro study of RBC showed increased hemolysis with oxidating agents and in physiological saline. Degree of hemolysis was inversely related to the serum level of vitamin E. (4) Increased platelet aggregation was observed in 8 patients; 6 of these also had low levels of serum Vitamin E.
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PMID:[Vitamin E and cholestasis in children]. 714 9

In 63 patients with malabsorption syndromes, 16 with congenital biliary atresia (BA) and 47 with cystic fibrosis (CF), axonal dystrophy in the gracile nucleus (ADG) was studied. Of the 16 patients with BA, ADG of considerable severity was observed in all 10 over one year of age. Of the 47 patients with CF, it was observed in 32, 61 and 80% of the cases in the first, second, and third decades, respectively. Evidence is presented that there has been a substantial decrease in the incidence of ADG in CF patients in recent years and that the decreased incidence is attributable to vitamin E (Aquasol E) therapy. The beneficial effect of vitamin E supplementation in CF patients is proffered as strong evidence that ADG in BA and CF is related to vitamin E deficiency. The present study indicates that BA and CF patients require vitamin E supplementation to maintain a normal integrity of axons related to the gracile and perhaps other sensory nuclei. Critical neurological evaluation for possible dysfunction of the sensory nuclei in these patients with malabsorption syndromes is advised.
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PMID:Axonal dystrophy in the gracile nucleus in congenital biliary atresia and cystic fibrosis (mucoviscidosis): beneficial effect of vitamin E therapy. 721


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