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Query: UMLS:C0024523 (
malabsorption
)
7,319
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The role of vitamin E in human nutrition was studied by investigation of patients with cystic fibrosis (CF) and associated pancreatic insufficiency.
Vitamin E
status was assessed by measurement of the plasma concentration of the principal circulating isomer, alpha-tocopherol. Results of such determinations in 52 CF patients with pancreatogenic steatorrhea revealed that all were deficient in the vitamin. The extent of decreased plasma tocopherol varied markedly but correlated with indices of
intestinal malabsorption
, such as the serum carotene concentration and percentage of dietary fat absorbed. Supplementation with 5-10 times the recommended daily allowance of vitamin E in a water-miscible form increased the plasma alpha-tocopherol concentrations to normal in all 19 CF patients so evaluated. Studies on the effects of vitamin E deficiency focused on possible hematologic alterations. An improved technique was developed to measure erythrocyte hemolysis in vitro in the presence of hydrogen peroxide. While erythrocyte suspensions from control subjects demonstrated resistance to hemolysis during a 3-h incubation, all samples from tocopherol-deficient CF patients showed abnormal oxidant susceptibility, evidenced by greater than 5% hemoglobin release. The degree of peroxide-induced hemolysis was related to the plasma alpha-tocopherol concentration in an inverse, sigmoidal manner. The possibility of in vivo hemolysis was assessed by measuring the survival of (51)Cr-labeled erythrocytes in 19 vitamin-E deficient patients. A moderate but statistically significant decrease in the mean (51)Cr erythrocyte half-life value was found in this group. Measurement of erythrocyte survival before and after supplementation of 6 patients with vitamin E demonstrated that the shortened erythrocyte lifespan could be corrected to normal with this treatment. Other hematologic indices in deficient subjects, however, were normal and did not change upon supplementation with vitamin E. It is concluded that CF is invariably associated with vitamin E deficiency, provided that the patient in question has pancreatic achylia and is not taking supplementary doses of tocopherol. Concomitant hematologic effects consistent with mild hemolysis, but not anemia, occur and may be reversed with vitamin E therapy. Patients with CF should be given daily doses of a water-miscible form of vitamin E to correct the deficiency.
...
PMID:The occurrence and effects of human vitamin E deficiency. A study in patients with cystic fibrosis. 87 86
Vitamin E
includes eight naturally occurring fat-soluble nutrients called tocopherols and dietary intake of vitamin E activity is essential in many species. alpha-Tocopherol has the highest biological activity and the highest molar concentration of lipid soluble antioxidant in man. Deficiency of vitamin E may cause neurological dysfunction, myopathies and diminished erythrocyte life span. alpha-Tocopherol is absorbed via the lymphatic pathway and transported in association with chylomicrons. In plasma alpha-tocopherol is found in all lipoprotein fractions, but mostly associated with apo B-containing lipoproteins in man. In rats approximately 50% of alpha-tocopherol is bound to high density lipoproteins (HDL). After intestinal absorption and transport with chylomicrons alpha-tocopherol is mostly transferred to parenchymal cells of the liver were most of the fat-soluble vitamin is stored. Little vitamin E is stored in the non-parenchymal cells (endothelial, stellate and Kupffer cells). alpha-Tocopherol is secreted in association with very low density lipoprotein (VLDL) from the liver. In the rat about 90% of total body mass of alpha-tocopherol is recovered in the liver, skeletal muscle and adipose tissue. Most alpha-tocopherol is located in the mitochondrial fractions and in the endoplasmic reticulum, whereas little is found in cytosol and peroxisomes. Clinical evidence from heavy drinkers and from experimental work in rats suggests that alcohol may increase oxidation of alpha-tocopherol, causing reduced tissue concentrations of alpha-tocopherol. Increased demand for vitamin E has also been observed in premature babies and patients with
malabsorption
, but there is little evidence that the well balanced diet of the healthy population would be improved by supplementation with vitamin E.
...
PMID:Absorption, transport and metabolism of vitamin E. 187 54
Vitamin E
is the term used for eight naturally occurring fat-soluble nutrients called tocopherols. alpha-Tocopherol is essential, has the highest biological activity and predominates in many species. In humans vitamin E is the most important lipid soluble antioxidant and deficiency may cause neurological dysfunction, myopathies and diminished erythrocyte life span. alpha-Tocopherol is absorbed via the lymphatic pathway and transported in association with chylomicrons. In plasma, alpha-tocopherol is found in all lipoprotein fractions but mostly is associated with apo B-containing lipoproteins. alpha-Tocopherol is associated with very-low-density lipoprotein when it is secreted from the liver. In the rat, about 90% of total body mass of alpha-tocopherol is recovered in the liver, skeletal muscle and adipose tissue. Most alpha-tocopherol is located in the mitochondrial fractions and in the endoplasmic reticulum, whereas little is found in cytosol and peroxisomes. New clinical evidence from heavy drinkers and from experimental work in rats suggests that alcohol may increase oxidation of alpha-tocopherol. Increased demand for vitamin E has also been observed in premature infants and patients with
malabsorption
, but there is little evidence that the healthy population requires supplementation of vitamin E to a well-balanced diet.
...
PMID:Absorption, transport and distribution of vitamin E. 218 Oct 82
Exocrine pancreatic insufficiency with varying severity must be anticipated in 85-95% of CF patients. It leads to fat maldigestion and
malabsorption
of the liposoluble vitamins - A, D, E, K - and fecal loss of fat. In general, supplementation with fat-soluble vitamins is recommended in CF patients. In this study an oral vitamin E tolerance test (100 mg/kg bodyweight) was performed in 5 healthy adult volunteers to elaborate a vitamin E absorption kinetics and additionally in CF patients on medication with pancreatic enzymes to evaluate the absorption of vitamin E. 19 CF patients (ages 4 to 19 years) were studied after cessation of any additional vitamin E supplementation for 7 days.
Vitamin E
serum concentrations were sampled over a 72 hour period. Serum vitamin E determinations were performed with a HPLC-fluorescence technique. The kinetics of
Vitamin E
in healthy volunteers can be described with an open 2 compartment model. CF patients revealed consistently an altered kinetics of absorption of vitamin E, which was not compatible with this model. Baseline (c*) and maximal serum concentrations (cmax) of vitamin E as well as the area outer the oral absorption curve (AUC) correlated with the nutritional status expressed by bodyweight percentiles in CF patients. The results of this study show that in normal weight CF patients on pancreatic enzymes medication vitamin E depletion is unlikely.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Effect of nutritional status on absorption kinetics of vitamin E in mucoviscidosis]. 231 1
Extensive brownish discoloration of the small bowel is rare and has been described mainly in association with
malabsorption
disorders. It is related to deficiency of the fat soluble vitamin E.
Vitamin E
is an antioxidant substance that prevents peroxidation of unsaturated fatty acids. Vitamin E deficiency may result in oxidized lipids, which when polymerized with polysaccharides form the brown, PAS-positive pigment termed ceroid or lipofuscin. The deposition of pigmented granules in the effected tissues accounts for the brownish discoloration. We present three patients ultimately found to have "brown bowel syndrome (BBS)," in which the symptoms, preoperative findings, and respective diagnoses were different. In all three patients, serum
Vitamin E
levels were found to be extremely low.
...
PMID:Brown-bowel syndrome. 277 66
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.
...
PMID:Intestinal malabsorption of vitamin E in primary biliary cirrhosis. 291 Jul 63
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.
...
PMID:[Selenium: physiologic role and value in human pathology]. 305 85
A progressive neurological syndrome with cerebellar signs, abnormal proprioception, areflexia and Babinski response was observed in a child with chronic
intestinal malabsorption
. There was no ophtalmoplegia or retinitis pigmentosa. Electromyography and biopsy showed no axonopathy or myopathy. Two other members of the family were also affected. The serum
Vitamin E
corrected the serum
Vitamin E
levels within a few months and led to secondary neurological improvement. The authors underline the importance of searching for Vitamin E deficiency and its cause in patients, especially children, with signs of spino cerebellar degeneration. Substitative therapy may have a favorable influence on the neurological condition even when administered late.
...
PMID:[Neurological manifestations in relation to vitamin E deficiency, caused by a defect of biliary acid synthesis]. 320 25
We report the cases of two adult patients with cystic fibrosis affecting the pancreas and liver, who also had severe vitamin E deficiency and neurologic disease. The most prominent clinical features were abnormal eye movements, diminished reflexes, decreased vibratory and position sense, ataxia, and muscle weakness. Treatment with intramuscular injections of vitamin E partially corrected the neurologic deficits.
Vitamin E
absorption tests documented severe
malabsorption
, which was later alleviated by the addition of dessicated ox bile to the regimen of alpha-tocopheryl acetate. These studies suggest that a decreased intraluminal concentration of bile salts is an important factor in the development of severe vitamin E deficiency and in the poor response to oral replacement therapy that is seen in some patients with cystic fibrosis.
...
PMID:Vitamin E deficiency and neurologic disease in adults with cystic fibrosis. 359 48
Four patients had accumulation of ceroid in smooth muscle (lipofuscinosis), which indicated severe or uncontrolled
malabsorption
, with confirmed vitamin E deficiency in three cases. The distribution of the pigment was systematic, and there seemed to be an association between
malabsorption syndrome
and vitamin E deficiency.
Vitamin E
supplementation seems to be indicated in such patients, and it is suggested that studies of smooth muscle function should be made in cases of heavy accumulation of ceroid.
...
PMID:Accumulation of ceroid in smooth muscle indicates severe malabsorption and vitamin E deficiency. 362 1
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