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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin E (tocopherol) concentrations in blood plasma were determined in 48 infants and correlated with their nutritional status. Infants were divided into two groups as following: group I (n : 12) estimated well-nourished, and group II (n : 36) appreciated undernourished. Clinical nutritional status was evaluated according to their weight, height and skinfold thickness of triceps percentiles. Plasma vitamin E levels were analysed by a modification of the spectrophotometric micro-technique of Fabiank et al. (using 0.2 ml of plasma). There was difference in serum tocopherol levels between two groups: 1.21 (0.21) mg/dl: mean (+/- SEM) in group I in front of 1.84 (0.18) mg/dl in group II (0.10 greater than p greater than 0.05). On the other hand, vitamin E concentrations were correlated with the skinfold thickness of triceps percentiles by a logarithm curve: y = 2.25-0.31 1n X (r: 0.35, p less than 0.02). Probably, serum vitamin E levels do not reflect the tissue store status in undernourished infants without malabsorption.
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PMID:[Serum vitamin E in well-nourished and malnourished infants]. 366 50

Vitamin A is necessary to maintain the integrity and the differentiation of epithelia of the skin and adnexa. Evident deficiency of vitamin A in chronic diseases, malabsorption and liver affections may result in skin xerosis, follicular keratosis, and metaplasia of mucous membranes. The remarkable toxicity of vitamin A in high doses does not recommend its usage in dermatology. On the contrary the employ of retinoids, synthetic derivatives of vitamin A, brings to excellent results. These vitamin A compounds are much more effective, even if they show important side-effects. Etretinate and isotretinoin are widely used in psoriasis, keratinization disorders, and severe acne. Vitamin E functions in skin biology are not totally known. Vitamin E is used in the treatment of dermolytic recessive epidermolysis bullosa, with controversial results.
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PMID:[Vitamin A and vitamin E in dermatology]. 391 47

A 72-year-old man had severe malabsorption, progressive retinopathy, and spinocerebellar degeneration 32 years after gastric surgery, blind loop formation, and intestinal bacterial overgrowth. Clinical and pathologic features were typical of vitamin E deficiency; vitamin E was nearly undetectable in serum and profoundly low in adipose tissue. Vitamin E blood levels initially improved on treatment with antibiotics; after additional vitamin E supplementation, there was clinical improvement.
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PMID:Blind loop syndrome, vitamin E malabsorption, and spinocerebellar degeneration. 397 92

Vitamin E malabsorption and deficiency during chronic childhood cholestasis has been associated with a progressive ataxic neurologic syndrome. Hyporeflexia, the first sign of neurologic dysfunction, may begin prior to age 2 years, but severe symptoms do not develop until age 5 to 10 years. To establish the age of onset of neuropathologic lesions, we prospectively evaluated four young children with severe cholestasis. Malabsorption and deficiency of vitamin E were documented by low serum vitamin E concentrations, low serum vitamin E to total serum lipids ratios, elevated hydrogen peroxide hemolysis, and impaired absorption of a pharmacologic dose of alpha-tocopherol. Abnormal neurologic findings in two patients were limited to areflexia, ptosis, mild truncal ataxia, and hypotonia; two patients had minimal signs of neurologic dysfunction. Sural nerve histology at age 6 to 25 months revealed a degenerative axonopathy involving large-caliber myelinated fibers, but without quantitative axonal loss. Muscle histology and histochemistry tests yielded normal results. Our study suggests that neurologic injury may occur during the first two years of life in vitamin E-deficient children with cholestatic hepatobiliary disease, obligating aggressive attempts at correcting this deficiency state at a very young age.
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PMID:Vitamin E deficiency during chronic childhood cholestasis: presence of sural nerve lesion prior to 2 1/2 years of age. 630 96

Certain owl monkeys (AOT) develop spontaneous hemolytic anemia that responds to vitamin E. The anemia is associated with red blood cell lipid peroxidation and altered red blood cell membrane lipid composition. To investigate these changes, plasma lipid and lipoprotein profiles were characterized in anemic, anemia-susceptible, and anemia-resistant AOT. The plasma vitamin E and vitamin A concentrations were assessed as an index of fat absorption and the effect of corn oil supplementation and vitamin E-selenium injection were measured. Anemia-susceptible AOT had depressed plasma levels of vitamin E and A and an altered lipoprotein metabolism characterized by elevated ratios of low/high density lipoprotein cholesterol and free to esterified cholesterol in these lipoproteins. Vitamin E-selenium injection in anemia-susceptible AOT increased the plasma vitamin E, and vitamin E and corn oil supplements reduced the high density lipoprotein free to esterified cholesterol ratio. The data suggest that the AOT suffer from fat malabsorption and that the consequences (including tocopherol deficiency) result in altered cholesterol metabolism.
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PMID:Altered lipoprotein metabolism in spontaneous vitamin E deficiency of owl monkeys. 641 97

Evidence that vitamin E is important for normal neurological function in humans is presented. First, in abetalipoproteinaemia early therapy with vitamin E delays and may prevent the development of the neurological complications, and in patients with established lesions treatment can arrest or reverse the neuropathy. Second, in other chronic disorders of fat absorption with severe vitamin E deficiency, neurological manifestations which are very similar to those described in untreated abetalipoproteinaemia can be improved by vitamin E. Vitamin E supplementation is therefore advisable for all patients with chronic fat malabsorption who have low serum vitamin E concentration. Serum vitamin E concentrations should also be measured in patients with spinocerebellar disorders, whatever the aetiology.
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PMID:Vitamin E and neurological function: abetalipoproteinaemia and other disorders of fat absorption. 655 2

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

Vitamin E levels were measured in the plasma of infants and children with various neuromuscular disorders. Seven of 8 infants with Werdnig-Hoffmann disease (WHD) had a significantly lower plasma vitamin E level (p less than 0.01) than age-matched normal controls, children with congenital myopathies, or children with muscular dystrophy. Vitamin E deficiency in WHD is not caused by malabsorption. A therapeutic trial of vitamin E in 3 patients with WHD did not change the natural course of the disease. Vitamin E deficiency may play a role in the pathogenesis of WHD.
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PMID:Vitamin E deficiency in Werdnig-Hoffmann disease. 729 34

We report a 44-year-old woman in whom intestinal bypass for obesity at age 23 resulted in chronic malabsorption. After hysterectomy for menorrhagia due to atypical endometrial hyperplasia, the finding of myometrial lipofuscinosis led to a demonstration of vitamin E deficiency. Vitamin E supplementation led to an unexpected improvement in the unsteadiness of gait and slurring of speech of which she had also complained. We suggest that supplementation with vitamin E should be routine in all patients with persistent severe steatorrhoea.
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PMID:Symptomatic vitamin E deficiency diagnosed after histological recognition of myometrial lipofuscinosis. 765 82

1. A vicious cycle of malabsorption and malnutrition has been implicated in the pathogenesis of protracted diarrhoeal disease in infancy. Vitamin E deficiency is common in malnourished infants with protracted diarrhoea. We have studied the effects of chronic vitamin E deficiency on small-intestinal secretion and absorption in the rat. 2. Weanling rats were fed vitamin E-sufficient or -deficient diets for 21 weeks. Jejunal function was studied in vitro in an Ussing chamber after this period. 3. Steady-state isotopic flux experiments in unstimulated tissues demonstrated net Na+ and Cl- secretion in vitamin E-deficient jejuna but net Na+ and Cl- absorption in vitamin E-sufficient jejuna. 4. Basal intestinal short-circuit current was the same in both groups. 5. Cyclic nucleotide and maximal non-neuronal acetylcholine-mediated electrogenic secretion were increased in vitamin E-deficient jejuna. 6. Exogenous 5-hydroxytryptamine (serotonin) induced a smaller increment in electrogenic secretion in vitamin E-deficient jejuna. 7. Vitamin E-deficient jejuna were less responsive to exogenous noradrenaline, resulting in a smaller alpha 2-adrenergic-mediated decrease in intestinal short-circuit current. 8. Fasting for 72h produced a greater increment in intestinal short-circuit current in vitamin E-deficient jejuna. 9. Chronic vitamin E deficiency is prosecretory in the small intestine and may predispose to the perpetuation of protracted diarrhoeal diseases.
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PMID:Modulation of small-intestinal secretion and absorption in chronic vitamin E deficiency: studies in rat jejunum in vitro. 828 52


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