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

The case of a 59 year old white man who had chronic malabsorption and selective IgA deficiency with severe iron deficiency is reported. In addition, he was deficient in vitamin E and selenium, important antioxidants which protect against lipid peroxidation. He was intolerant of oral iron and when treated with iron-dextran developed symptoms suggestive of polymyositis with evidence of rhabdomyolysis. It is suggested that free iron within iron-dextran activated free radicals, initiating lipid peroxidation and leading to polymyositis, rhabdomyolysis, and myoglobulinuria.
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PMID:Rhabdomyolysis after intramuscular iron-dextran in malabsorption. 201 14

The intestinal absorption of vitamin E is often thought to be closely correlated to that of fatty acids, but the biochemical mechanisms involved in the process are still not clear. For this reason, the present study aimed to assess the absorption of triglycerides and vitamin E, following oral administration, in 11 children with suspected malabsorption syndromes. Intestinal biopsy in 9 children showed the presence of a flat mucosa, whereas no changes were present in 2 patients. The results confirm the inverse correlation between the absorption of triglycerides and vitamin E, as if tocopherols used an independent system of transport. These findings contrast with those reported in the literature perhaps due to the low level of precision of colorimetric techniques previously used to assay vitamin E.
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PMID:[Intestinal absorption of vitamin E in children with atrophy of the jejunal mucosa]. 208 27

The essential effects of Tocopherol are based on its antioxidative capacity. Tocopherol, however, is just one in a group of antioxidants, which are important for the organism. Established indication for therapeutical application of vitamin E in infancy is only vitamin-E-malabsorption in connection with chronic cholestasis, pancreatic insufficiency (cystic fibrosis) and short bowel syndrome. In emergency therapy vitamin E is suggested with high dosage in case of shock lung and haemolytic-uraemic syndrome. Positive effects of daily vitamin E application in connection with prophylaxis of retinopathy prematurity, bronchopulmonary dysplasia and intraventricular encephalorrhagia of premature infants of severe underweight are not established. Very questionable therapeutic or prophylactic efficiency is opposed to the risk of higher incidence of severe complications in caring for premature infants of severe underweight, such as enterocolitis necroticans and neonatal septicaemia.
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PMID:[The use of vitamin E in childhood]. 209 6

Over the past decade it has become apparent that vitamin E is an essential nutrient for maintaining the structural and functional integrity of the developing human nervous system, skeletal muscle, and the retina. The clinical and histologic resemblance of the human neuromuscular disorder associated with chronic fat and vitamin E malabsorption to that observed in experimental vitamin E-deficient animal models is striking. Because of chronic malabsorption of vitamin E, children with CF, chronic cholestasis, abetalipoproteinemia, and short bowel syndrome are at risk for the development of neurologic deficits caused by vitamin E deficiency. Correction of the vitamin E deficiency state prevents, reverses, or, at least, stabilizes the neurologic dysfunction in susceptible individuals. Advances in stable isotope technology permit study of the hepatic discrimination among the various stereoisomers and forms of vitamin E. Investigations into the cause of the primary form of vitamin E deficiency, the isolated vitamin E deficiency syndrome, promise to delineate the normal physiologic processes involved in absorption, transport, and tissue delivery of vitamin E. Studies in progress are addressing the optimal route and form of vitamin E therapy to be used in each predisposing condition. One major task remaining is to better define the mechanism by which vitamin E deficiency leads to neurologic injury.
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PMID:Vitamin E and neurologic deficits. 217 58

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.
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PMID:Absorption, transport and distribution of vitamin E. 218 Oct 82

Sibling cases of familial vitamin E deficiency accompanied by ataxia, polyneuropathy and mental retardation were reported. Case 1 was a 37-year-old male who developed progressive gait disturbance, deformity of the feet and head tremor from childhood, after normal delivery and development of early childhood. On physical examination, he had cataract, high arched palate and pes cavus. Neurological examination revealed mental retardation (WAIS 68), scanning speech, muscular atrophy of the face and extremities with predominance in the lower limbs, absent Achilles tendon reflex, disturbance of superficial and deep sensation predominant in distal limbs, and marked gait ataxia. Ataxia was both cerebellar and sensory in nature. Laboratory data of the blood showed no significant abnormalities including blood glucose and vitamin B12 except a markedly low level of serum vitamin E. The brain CT scan revealed severe cerebellar atrophy and marked dilatation of the cisterna magna and the subarachnoid space around the cerebellum. Motor nerve conduction velocity in the leg was decreased. Biopsy specimen from the quadriceps muscle showed neurogenic atrophy. Sural nerve biopsy revealed decrease in large myelinated fibers with axonal degeneration and regeneration. Oral administration of alpha-tocopherol acetate, 600 mg per day, diminished ataxia significantly. Based on lysosomal enzyme activity in leukocytes, clinical and laboratory examination, lipidosis or spinocerebellar degeneration was excluded. Chronic lipid malabsorption or beta lipoprotein deficiency which can cause decrease in vitamin E absorption, was not recognized. On oral loading with 2 g of alpha-tocopherol acetate, the decrease rate of serum vitamin E was normal. Consequently the low vitamin E was considered to have resulted from selective impairment of vitamin E absorption.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Familial idiopathic vitamin E deficiency associated with cerebellar atrophy]. 226 7

A 52-year-old man, suffering for years from malabsorption due to endemic sprue, developed progressive bowel dysfunction, ie, recurrent ileus and intestinal pseudo-obstruction. Because of partial volvulus formation, ileocecal resection was performed. Histopathologic examination of the resected specimen revealed signs of advanced brown bowel syndrome, with excessive deposits of ceroid-lipofuscin in, and a considerable loss of, smooth-muscle cells and myofibrils. The patient died after surgery, and at autopsy a systemic ceroid lipofuscinosis of smooth-muscle cells was detected. Neuronal ceroid lipofuscinosis was not observed. Serious and eventually fatal bowel dysfunction is rarely seen in brown bowel syndrome, but may occur in advanced stages. Since treatment with vitamin E appears to exert a favorable effect, early diagnosis of brown bowel syndrome seems to be very important.
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PMID:Fatal intestinal pseudo-obstruction in brown bowel syndrome. 229 70

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)
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PMID:[Effect of nutritional status on absorption kinetics of vitamin E in mucoviscidosis]. 231 1

Thirteen patients with adult-onset vitamin E deficiency due to fat malabsorption were investigated clinically and electrophysiologically. These patients had slightly or moderately decreased serum vitamin E (1.7-4.8 micrograms/ml, normal less than 6.0) or vitamin E/cholesterol ratio (0.21-0.31 mg/g, normal less than 0.35). Only one patient had typical neurological manifestations of vitamin E deficiency, which improved with supplementary vitamin E. The pathological findings in this patient were also compatible with vitamin E deficiency. This patient had poorly controlled diabetes mellitus due to advanced chronic pancreatitis. Reviewing previously reported cases of vitamin E deficiency with diabetes mellitus in chronic pancreatitis, the duration of deficiency until the onset of symptoms was shorter than in those cases without complications. Although adult patients with early, slight deficiency of vitamin E are generally asymptomatic, patients with diabetes mellitus tend to have early neurological symptoms. The vitamin E tolerance test should be used, because even in some patients with vitamin E deficiency due to malabsorption, the deficiency can be overcome by large oral doses of vitamin E.
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PMID:Vitamin E deficiency in acquired fat malabsorption. 235 33

Serum pancreatic secretory trypsin inhibitor (PSTI) was measured by radioimmunoassay in 5 patients with malabsorption syndrome. The serum level of PSTI was elevated to 123.8 +/- 25.8 ng/ml (Mean +/- SE) in patients with malabsorption syndrome, which was significantly higher than the 16.6 +/- 0.7 ng/ml level seen in 116 healthy control subjects. Serum PSTI levels in 5 patients with malabsorption syndrome showed inverse correlations with serum levels of cholesterol, cholinesterase and amylase, and not with serum levels of vitamin E, carotene, apoprotein A-IV, albumin, nor with immunoreactive elastase 1, respectively. These results suggest that elevated levels of serum PSTI represent a state of malnutrition due to impaired intestinal absorption.
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PMID:Elevated levels of serum pancreatic secretory trypsin inhibitor (PSTI) in patients with malabsorption syndrome. 243 66


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