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

A middle-aged patient with "brown bowel syndrome" or gastrointestinal ceroidosis manifested as malabsorption of undetermined cause is described. Autopsy revealed involvement of the entire gastrointestinal tract and unusual cardiac findings. Microscopically, the pigment responsible for the discoloration is a lipofuchsin that is deposited in the smooth muscle cells of the gastrointestinal tract. In all reported cases, ceroidosis was associated with some abnormality of the gastrointestinal tract--that is, malabsorption, steatorrhea, or gross local disease--with the possible exception of prolonged malnutrition. This case is also unusual because of the unexplained multifocal proliferative endocarditis. Vitamin E deficiency may be the common denominator of all these various disorders.
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PMID:Ceroidosis in the "brown bowel syndrome". 42 5

Two children, aged 11 years, who originally had jejunal atresia corrected in the neonatal period, developed massive dilatation of the proximal small intestine. This resulted in circular muscular hypertrophy with lipofuscin deposits giving the typical appearance of "brown bowel." The condition was associated with malnutrition and vitamin E deficiency. Because of relatively short bowel, the condition was treated by limited resection and extensive tapering of the dilated segment, end-to-end reanastomosis, vitamin E supplementation, and intensive nutritional support.
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PMID:Brown bowel syndrome: a late complication of intestinal atresia. 146 88

The association between plasma ferritin concentration and vitamin A and E status was studied in 17 children aged 15-72 months with severe oedematous malnutrition. The controls were 10 children of similar age who were apparently well and with no obvious signs of clinical malnutrition. Plasma ferritin concentration in the patients was significantly higher than that in the control children. Conversely, the plasma concentrations of beta-carotene, alpha-tocopherol and retinol in patients were significantly lower than those in plasma of control children. The median (interquartile range) plasma alpha-tocopherol concentration of patients, 6.03 (5.29-9.50) mumol/l, is below the threshold of vitamin E deficiency (11.6 mumol/l). Fifteen of 17 (88%) malnourished patients were found to have plasma tocopherol concentrations below the normal threshold. However, all the patients had a tocopherol: cholesterol ratio greater than 2.22, indicating adequate vitamin E status for the level of cholesterol present in plasma. Twelve of 17 patients (70.5%) had plasma retinol concentration less than 0.70 mumol/l, indicative of marginal vitamin A status, while 3 patients had plasma retinol concentrations less than 0.35 mumol/l, indicating vitamin A deficiency. The median (interquartile range) plasma retinol concentration of patients, 0.51 (0.41-0.93) mumol/l, is significantly less than that of control children, 0.96 (0.74-1.09) mumol/l; p less than 0.01 Mann Whitney U test. Furthermore, anaemia (Hb less than 110 g/l) was widespread in the patients. The results also indicate no significant correlation between elevated ferritin concentration and the concentrations of beta-carotene, retinol and alpha-tocopherol in the patients' plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma ferritin concentration in relation to vitamin A and E status of children with severe oedematous malnutrition. 171 50

Nerve tissue (as well as capillaries and cerebral microvessels) has a very high concentration in polyunsaturated fatty acids belonging to linoleic and alpha-linolenic series. Nerve tissue also requires large amounts of oxygen. Radical peroxidation of the polyunsaturated fatty acids represents a serious risk to the biochemistry and physiology of the membranes: it can be a cause of cellular death. During aging, the capillaries and cerebral microvessels undergo extensive modifications at the level of the polyunsaturated fatty acids: for example, the concentration of arachidonic acid decreases by half. In brain in general, vitamin E is very well protected: after oxidation, it is rapidly regenerated; it seems to undergo only slight degradation. In case of dietary deficiency, the brain loses much less vitamin E, and at a slower rate, than other non-nerve tissue. During aging, there is a relation between the content in vitamin E and the concentration of polyunsaturated fatty acids of the linoleic series, but not of the alpha-linolenic series. In addition, vitamin E deficiency also leads to a decrease in the enzymatic activities that protect against peroxidation of fatty acids.
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PMID:[Vitamin E: protection of membrane polyunsaturated fatty acids against radical peroxidation in the course of cerebral aging, particularly in cerebral capillaries and microvessels]. 180

The effect of a dietary deficiency of vitamin E on the concentrations of lipofuscin in the hippocampus and the supraoptic nucleus (SON) of the hypothalamus, and in adrenal cortical cells was assessed in male mice. The animals were fed either a control diet or the vitamin E deficient diet after 2 months of age for a period of 6 months. There was no significant difference in the growth curves of the 2 groups of animals over the period studied. Fluorescence microscopy and transmission electron microscopy were used to assess the effect of the diet on lipofuscin in the different tissues. Quantitative morphological techniques were used to determine the relative volumes of lipofuscin in the neurons from the SON and in the adrenal cortical cells. There was no significant difference in the concentration of lipofuscin in the SON neurons after vitamin E deficiency but there was a significant increase in the adrenal cortical cells. There was a clear difference in the effect of the deficiency on mitotic and fixed post-mitotic cells over the period investigated but further studies would be necessary to determine whether or not there was a critical period in the life span where vitamin E deficiency may induce changes in all cell types.
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PMID:The effect of vitamin E deficiency on the induction of age pigment in various tissues of the mouse. 362 52

Experiments were performed to determine the effects of dietary selenium and/or vitamin E deficiency on cell-mediated cytotoxicity in the mouse. Natural killer cell-mediated cytotoxicity (NKCC) was depressed after 8 wk on diets deficient in selenium and/or vitamin E. In contrast, antibody-dependent cell-mediated cytotoxicity (ADCC) was not affected by 8 wk of dietary deficiency of selenium and/or vitamin E. T-lymphocyte-mediated cytotoxicity (TCMC) was found to be depressed by combined selenium-vitamin E deficiency after 7 weeks on diets.
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PMID:Antioxidant effects on cell-mediated immunity. 387 76

Relatively high proportions of long-chain, polyunsaturated fatty acids seem to be required in rod photoreceptor membranes in order to provide the precise microenvironment for the proper function of the visual pigment rhodopsin. At the same time, such high levels of lipid unsaturation put the photoreceptor membranes at a high risk for autoxidation. The antioxidant vitamin E which can minimize autoxidation of polyunsaturated fatty acids is found in rather high concentrations in the outer segment membranes. Dietary deficiency in vitamin E induces disintegration of rod outer segment membranes, probably by increasing autoxidation. Also, it greatly accelerates the accumulation of aging pigments in the retinal pigment epithelium, probably because these lipofuscin granules do indeed represent the end products of lipid peroxidation. Vitamin E supplements, up to threefold normal levels, appear to provide no significant protection of the retina from light damage produced either by short but acute or by long-term, low level exposures to light. This is not consistent with current theories which implicate lipid peroxidation in the destruction of rod outer segments in light damaged retinas; more work is needed before any relation between retinal light damage and vitamin E levels can be assessed. Surprisingly, the amount of lipofuscin granule accumulation in the retinal pigment epithelium is influenced dramatically by dietary levels of vitamin A. Even retinas lacking a source of polyunsaturated fatty acids from rod outer segments still may accumulate massive lipofuscin if dietary vitamin A is provided. Perhaps vitamin A, which has such a dynamic relationship with the retinal pigment epithelium, becomes oxidized, and then contributes to the formation of a lipofuscin-like pigment. Centrophenoxine, a drug claimed to be effective in reversing the accumulation of age-related lipofuscin in the central nervous system, has no obvious effect in the eye or uterus in removing the lipofuscin granules induced by vitamin E deficiency. Microperoxisomes are abundant in the retinal pigment epithelium, and may be associated with rapid lipid turnover and/or utilization of lipid soluble vitamins. Their potential roles, however, need further documentation and clarification. Recently developed techniques and new discoveries in lipid research open the way for many fruitful studies on the interactions and precise roles of lipids and lipid-soluble vitamins in vision.
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PMID:The roles of vitamin E and unsaturated fatty acids in the visual process. 610 Nov 34

Copper deficiency anemia occurs in some specific situations if supplemental copper is not given: low birth-weight premature infants fed milk only, protracted total parenteral nutrition, chronic diarrhea with severe malnutrition. Severe neutropenia precedes the onset of sideroblastic anemia. Iron therapy is ineffective. Diagnosis is established by the low serum copper concentrations, the delayed osseous anomalies, and the dramatic response to copper therapy. Low serum vitamin E concentrations may be found in low birth-weight premature infants aged six to ten weeks with hemolytic anemia. In such cases, vitamin E therapy is effective. This condition occurs more often in infants fed milk formulas without supplemental copper and in infants given high doses of iron. Whether vitamin E deficiency causes anemia is still an open question. Preventive vitamin E supplementation is only partly effective.
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PMID:[Rare nutritional deficiency anemia: deficiency of copper and vitamin E]. 630 91

Brown bowel syndrome is a rare intestinal disorder associated with the deposition of lipofuscin pigment in the smooth muscle cells. We report two such cases presenting with intestinal pseudo-obstruction, abdominal pain, and body weight loss. Both cases had malabsorption and fatty liver. Exploratory laparotomy revealed brownish discoloration of the small bowel wall and enlargement of mesenteric lymph nodes. Light microscopy, autofluorescence and ultrastructure studies confirmed the deposition of lipofuscin pigments in the intestinal muscle cells and reticuloendothelial cells of mesenteric lymph nodes. In addition, the calf muscle biopsy of case 1 displayed myopathy and fatty replacement. Skeletal muscle strength of both patients was partially restored after parenteral and oral vitamin E supplement and other conservative treatment, but gastrointestinal symptoms of both patients continued to deteriorate. Thus, brown bowel syndrome associated with prolonged and severe malnutrition and possibly vitamin E deficiency appears only partially responsive to vitamin E supplementation.
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PMID:Brown bowel syndrome: report of two cases. 791 59

Three infants are described with cystic fibrosis (CF) and malnutrition leading to severe anemia beginning as early as 6 weeks of age. Laboratory studies demonstrated high reticulocyte counts, negative Coombs' tests, abnormal peroxide hemolysis test results, and biochemical evidence of vitamin E deficiency. Oral administration of alpha-tocopherol resulted in rapid correction of the in vitro hemolysis and improvement of in vivo hematologic indices. Investigation of these patients supports the conclusion that the hemolytic anemia of infancy in CF is caused by vitamin E deficiency and should be treated promptly with 50 IU/day of vitamin E. Because two of the three patients were identified in a CF screening/surveillance program, we can estimate that the frequency of clinically significant anemia in CF infants is 4%. Our observations demonstrate a potential advantage of CF neonatal screening for individual patients susceptible to vitamin E-deficient hemolytic anemia and suggest that confirmatory follow-up diagnostic studies, such as sweat tests, should be performed by 4 to 6 weeks of age.
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PMID:Severe hemolytic anemia associated with vitamin E deficiency in infants with cystic fibrosis. Implications for neonatal screening. 815 23


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