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

We studied intestinal absorption of vitamin E in 26 adults with primary biliary cirrhosis (PBC) and 6 control subjects. Seven (27%) PBC patients were vitamin E-deficient based on the ratio of serum vitamin E to serum total lipid concentrations. An oral vitamin E tolerance test was performed in all patients and control subjects using a loading dose of 2000 IU alpha-tocopheryl acetate with measurement of serial serum vitamin E concentrations over 24 h. Vitamin E absorption was expressed as the maximal rise in serum vitamin E above baseline, the area under the oral tolerance test curve, and these two values divided by the fasting total serum lipid concentration. Absorption of vitamin E was significantly impaired in all PBC patients vs. control subjects (p less than 0.01), in vitamin E-deficient vs. vitamin E-sufficient PBC patients (p less than 0.05 to p less than 0.01), and in PBC patients with serum vitamin E levels below 10 micrograms/ml vs. those with serum vitamin E levels above 10 micrograms/ml (p less than 0.01). Vitamin E absorption was inversely related to stage of PBC, serum cholylglycine, total bilirubin, cholesterol, alkaline phosphatase, aspartate aminotransferase, and prothrombin time. Patients with serum vitamin E below 10 micrograms/ml, serum total bilirubin above 3 mg/dl, serum cholylglycine above 600 micrograms/dl, or serum alkaline phosphatase above 1000 IU/L had severe malabsorption of vitamin E and would be at high risk for the development of vitamin E deficiency. Therefore, vitamin E supplementation should be considered not only in patients in whom overt vitamin E deficiency is present, but also in PBC patients meeting these criteria.
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PMID:Intestinal malabsorption of vitamin E in primary biliary cirrhosis. 291 Jul 63

Experiments were conducted to examine the effects of dietary zinc (Zn) upon plasma vitamin E (E) concentrations to test the hypothesis that there may be a significant dietary interaction between these two nutrients. Weanling female Sprague-Dawley rats were fed diets that were (i) Zn-deficient (less than 0.9 micrograms Zn/g diet) ad libitum; (ii) Zn-adequate (50.9 micrograms Zn/g diet), pair-fed to the Zn-deficient group; and (iii) Zn-adequate (50.9 micrograms Zn/g diet) ad libitum. Plasma E in Zn-deficient animals (4.02 +/- 1.20 micrograms/ml) was significantly reduced (P less than or equal to 0.05) compared with results in both Zn-adequate pair-fed (9.21 +/- 0.70 micrograms/ml) and Zn-adequate ad libitum-fed (9.47 +/- 0.90 micrograms/ml) animals. Zn deficiency in this model system also resulted in significant (P less than or equal to 0.05) reductions in femur and plasma Zn concentrations as well as in plasma retinol, plasma triglyceride, and plasma cholesterol concentrations. Plasma albumin and total plasma protein concentrations were normal in Zn-deficient animals. With dietary Zn deficiency, the decrease in plasma E appeared to be out of proportion to associated decreases in plasma triglyceride and plasma cholesterol concentrations. Since E is associated with plasma lipoproteins, these data suggest that lipid and/or E malabsorption may be a consequence of Zn deficiency. In response to increased dietary intake of E, increments of plasma E were lower in Zn-depleted than in Zn-adequate, pair-fed animals. These findings suggest that dietary Zn deficiency possibly may increase the nutritional requirement for E necessary to maintain adequate plasma concentrations.
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PMID:Dietary zinc deficiency decreases plasma concentrations of vitamin E. 292 52

The interaction between malabsorption syndrome (MAS) and dietary vitamins A and D was studied in broiler chicks reared in floor pens for 4 weeks. The chicks were naturally infected with MAS, whereas hatchmates fed the same diets but in a separate facility (battery brooder) did not exhibit signs of MAS and, therefore, were considered controls. MAS significantly reduced body weights, bone ash, serum calcium and phosphorus concentrations, and liver lipids and increased the incidence of skeletal abnormalities (tibial dyschondroplasia and rickets). Rather than ameliorating the effects of MAS, vitamin A caused a further reduction in body weight and bone ash. A possible nutrient interaction between vitamin A and vitamin D or vitamin E in birds with MAS may account for the exacerbative effect of vitamin A.
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PMID:Exacerbative effect of vitamin A on malabsorption syndrome in chicks. 299 37

In human malabsorption syndromes, lipofuscin accumulation has been reported to occur exclusively within the muscle layers of the intestine. It has been widely speculated that this lipofuscin deposition is related to vitamin E deficiency. To determine whether vitamin E deficiency leads to the same pattern of intestinal lipofuscin accumulation as that seen in many human malabsorption syndromes, the duodenums of rats that had been fed a vitamin E-deficient diet for 17 or 34 wk were examined for the presence of lipofuscin. Lipofuscin did not appear in the muscle layers of the duodenum until 34 wk, at which time occasional fibers containing large amounts of lipofuscin were present. An earlier and more pronounced deposition of lipofuscin occurred within connective tissue cells of the intestinal villi. After 17 wk, many fibroblastlike cells in the lamina propria of the villi contained large amounts of lipofuscin. By 34 wk, the numbers of these lipofuscin-containing cells in the lamina propria had increased substantially, and scattered cells containing lipofuscin were also seen in the submucosa. The difference in intestinal lipofuscin distribution between vitamin E-deficient rats and humans with malabsorption syndromes suggests that other factors, in addition to vitamin E, probably play important roles in regulating lipofuscin accumulation in the intestine.
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PMID:Localization of lipofuscin in the duodenums of vitamin E-deficient rats. 299 23

A 41-yr-old woman with primary biliary cirrhosis developed weakness and wasting in proximal muscles, areflexia, and decreased proprioceptive and vibratory sensation. Investigations revealed law serum levels of vitamin E and electromyographic and muscle biopsy changes consistent with a neuropathy. Sural nerve histology demonstrated axonal dystrophy with patchy demyelination. These features closely resemble a neurologic syndrome associated with chronic cholestatic liver disease and vitamin E deficiency in children. Adults with chronic cholestasis may also be susceptible to neurologic damage from prolonged malabsorption of vitamin E.
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PMID:Neurologic syndrome associated with low levels of vitamin E in primary biliary cirrhosis. 301 81

Selenium (Se) is a metalloid with chemical properties closed to those of sulfur, but they can not substitute for one another in vivo. Se body content reflected soil Se content (13 to 20 mg in North Americans, 3 to 6 in New Zealand residents). The daily intake recommended is 50 to 200 micrograms. In the diet Se occurs in mineral or organic forms, the bioavailability of these latter is better. Se as selenocysteine is incorporated in specific proteins such as glutathione peroxidase (GSH-Px). Se is metabolized in H2Se by reductive pathways. H2Se is methylated and methylated compounds are excreted in the urines. The Se urinary excretion represents the principal known process of Se regulation. Se bound to GSH-Px participates to free radical destruction and cellular membrane protection. Its role is complementary of vitamin E effect. Se also seems indispensable to appropriate immune response. It can chelate various metals allowing their detoxication. Se metabolism can be studied by Se assay in serum, whole blood, urine (reference values must be performed for each studied population) and by GSH-Px activity determination in erythrocytes or platelets. Vitamin E assay completes estimation of the antioxidative status of organism. Few Se intoxications have been recognized but Se deficiencies often happen. They can lead to a cardiomyopathy (Keshan disease), increase the risk of cardiovascular diseases or cancer. Se deficiencies are found in chronic renal failure, malnutrition malabsorption, long term parenteral nutrition. At the present time it is not known how Se deficiency interfers with chronic infections which often go with these diseases. A better knowledge of Se requirements and Se role could allow an appropriate supplementation in various diseases.
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PMID:[Selenium: physiologic role and value in human pathology]. 305 85

During the recent resurgence of interest in the clinical uses of vitamin E, one of the major foci of attention has been the neurologic role of vitamin E in humans. Studies in patients with secondary vitamin E deficiency, caused by fat malabsorption disorders and total parenteral nutrition lacking an adequate supply of vitamin E, have elucidated a clinical disorder and histologic lesions of the nervous system and muscle that closely resemble those of experimental vitamin-E-deficient animal models. Investigations of the primary form of human vitamin E deficiency, the isolated vitamin E deficiency syndrome, have further substantiated the relationship between neurologic dysfunction and human vitamin E deficiency. It is now clear that vitamin E is an essential nutrient necessary for the optimal development and maintenance of the integrity and function of the human nervous system and skeletal muscle. The task for future study is to determine the mechanism by which vitamin E deficiency causes degeneration of selective regions of the nervous system and to investigate possible benefits of vitamin E supplementation in other neurologic disorders. In addition, further study of the isolated vitamin E deficiency syndrome promises to teach us more about normal physiologic mechanisms of vitamin E absorption and transport in humans.
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PMID:Vitamin E deficiency and neurologic disease. 306 Jan 70

We studied plasma vitamin E levels in children/adolescents 3-19 years of age (10.9 +/- 4.5; mean +/- 1 SD) with chronic renal failure treated conservatively, on hemodialysis, on continuous ambulatory peritoneal dialysis and after renal transplantation. In all 4 groups of patients vitamin E levels (0.66-0.90 mg/dl) were within the normal range (0.76 +/- 0.19 mg/dl). The lowest levels of vitamin E (0.59 +/- 0.1 mg/dl) were found in nonuremic patients with a good functioning renal transplant. These data do not support the notion that uremia is accompanied by vitamin E malabsorption.
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PMID:Plasma vitamin E levels in uremic children and adolescents. 307 4

Home parenteral nutrition (HPN) provides long-term nutritional support for persons whose absorptive capacity is compromised by a variety of intestinal malabsorption problems. However, the presence of vitamin and mineral deficiency syndromes that normally would not have time to develop in the hospitalized patient receiving total parenteral nutrition has been reported in patients receiving HPN. This study entails a longitudinal survey of plasma concentrations of vitamins A, E, and 1,25-dihydroxyvitamin D, as well as the minerals zinc, copper, and selenium, in patients receiving HPN. Plasma samples from eight patients who had been on HPN for 1-92 months before the study began were obtained once a month over a 12-month period. The blood was drawn immediately before their evening infusion of TPN in order to approximate fasting plasma nutrient concentrations. Patient values were compared to fasting control values and to published norms. Values for vitamin A, 1,25-dihydroxyvitamin D, and zinc all were within the normal range, and there was no evidence of metabolic bone disease. Plasma vitamin E and copper concentrations exceeded the normal range for most of the 12-month period. Of all of the nutrients studied, only plasma selenium concentrations were consistently in the low-normal to below-normal range. Selenium levels in patients on HPN should be monitored regularly, and supplementation may be necessary if clinical conditions warrant.
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PMID:Plasma vitamin and mineral status in home parenteral nutrition patients. 311 95

The total and free fatty acid composition of plasma and lipid peroxide concentrations was studied in 32 cholestatic children with syndromatic paucity of interlobular bile ducts (Alagille's syndrome). The mean lipid peroxide value in these patients was 8.80 +/- 3.70 nmol/ml, nearly 4 times higher than the mean control value. Compared to the control group, the patients exhibited significant variations in total fatty acids, and in particular a relative decrease in linoleic acid (from 29.5 +/- 6.1% in the controls to 19.1 +/- 8.03% in the patients) compensated by an increase in saturated and monounsaturated fatty acids. The plasma lipid peroxide levels were inversely correlated with the unsaturated/saturated fatty acids ratio in total fatty acids, and with the vitamin E status (vitamin E/total lipids). Most of the total and free fatty acid variations observed were largest in patients with severe jaundice. Dietary fat malabsorption and the increase in lipid peroxidation partly explain these results. Furthermore, in free fatty acids, we observed a marked increase in arachidonic acid (from 1.43 +/- 0.85% in the controls to 4.27 +/- 2.24% in the patients), suggesting abnormal eicosanoid synthesis.
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PMID:Plasma fatty acid composition and lipid peroxide levels in children with paucity of interlobular bile ducts. 319 90


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