Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Folic acid is one of the 'younger' vitamins, yet it has attracted intensive study in the thirty years since the identification of pteroylglutamic acid and its polyglutamyl conjugates. The absorption and malabsorption of folates, natural, purified and synthetic, in disease has been studied more than any other vitamin and indeed folate absorption has become one clinical test of intestinal function. We know little about the release of folate from protein complexes, but we have learned, with the help of synthetic radiolabelled pteroylpolyglutamates that polyglutamyl folates are hydrolysed at or near the luminal border of the intestine and the released folate is efficiently absorbed. The rate limiting stage of folate absorption appears to be the transport of the monoglutamyl folate. In disease, and with drugs, folate malabsorption occurs primarily when monoglutamyl transport is depressed. The specific components of the folate transport system, listed in Table 4, are receiving increased attention. The mechanism of uptake is still a topic of controversy but a dual system including both a saturable and a diffusion component would explain most of the data. Reduction and methyl or formyl addition occur in the intestine but such metabolism is not obligatory for transport. The nature of folate binding within the cell and the function of specific folate binding proteins requires further study. At present we have little or no information about the mechanism of folate release from the epithelial cell to the circulation but this step also could influence the rate and specificity of overall process. The tools are now at hand to complete our understanding of the steps in folate absorption and metabolism. Such an understanding should facilitate the management of folate deficiency whenever it complicates gastrointestinal disease or drug therapy.
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PMID:Absorption and malabsorption of folates. 1 Jan 21

In a consecutive study of 216 outpatients with chronic inflammatory bowel diseases (CIBD) low serum and erythrocyte folate levels were found in 59% and 26%, respectively. In patients with low folate levels in both serum and erythrocytes, megaloblastic changes in the bone marrow ere found in 67% (29 out of 44). Their folate intakes were borderline. Absorption studies with tritiated folate showed low absorption values on repeated examinations in 23% of the patients with low folate values (9 out of 40), with no relationship to the intake of salazosulphapyridine. In patients with low folate values the reticulocyte count was elevated (related to the dose of salazosulphapyridine), and the 51Cr erythrocyte survival was decreased. It is suggested that folate deficiency in CIBD is of multiple origin: inadequate diet, malabsorption, and chronic drug-induced low-grade haemolysis. The clinical consequence of the findings remains to be evaluated.
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PMID:Folate deficiency in chronic inflammatory bowel diseases. 4 87

Fourteen patients with ileal dysfunction due to resection or bypass were encountered over an 18-month period. Symptoms had been present for a mean period of 1.8 years. Diarrhoea was a universal symptom, and varied from mild to incapacitating. Weight loss, due in part to malabsorption and in part to the patients' fear of eating, occurred in 10 of 14 patients. The chief metabolic abnormalities were steatorrhoea and hypokalaemia. Vitamin B12 deficiency, folate deficiency, anaemia, hypoalbuminaemia, hypocalcaemia, hypomagnesaemia, hyperoxaluria, and an abnormal prothrombin ratio were less frequently seen. Treatment with cholestyramine and/or long-chain fat restriction effectively reduced diarrhoea in every case, and this was supplemented by replacement of specific deficiencies. There was little added benefit from non-specific antidiarrhoeal agents. It was found that the major symptoms of ileal dysfunction are readily treated, but that attention should also be given to a number of nutritional deficiencies.
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PMID:Consequences of ileal dysfunction: an approach to management. 10 34

A young patient was hospitalized for megaloblastic anemia due to folate deficiency. Laboratory exams and functional tests demonstrated that the deficiency was due to hormonal contraception treatment on which the woman had been for the last consecutive 11 months. The disease subsided completely following withdrawal of oral contraception (OC), and normal hematological values were maintained after that, suggesting that no malabsorption was present. Cases of megaloblastic anemia in women on OC are rare, and the phenomenon may be related to prolonged and uninterrupted drug assumption.
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PMID:Megaloblastic anemia due to folic acid deficiency after oral contraceptives. 11 9

The authors report 12 cases of neurological syndromes due to folic acid deficiency, due in 8 cases to chronic alcoholism. In 5 cases there was polyneuritis, 3 cases had cerebellar atrophy, whilst 4 patients had subacute combined degeneration of the cord. Folic acid deficiency occurred alone in five cases out of twelve, as in 3 cases vitamin B1 deficiency was associated, and in four cases there was malabsorption of vitamin B12. A neuropathological study of these cases showed: 1) moderate involvement of the mamillary tubercles as observed in deficiency encephalopathies. 2) severe peripheral nerve involvement especially of axonal type. 3) involvement of the anterior horns of the spinal cord with appearances of central chromatolysis and a few atrophic neurones.
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PMID:[Role of folic-acid deficiency in deficiency diseases of the nervous system. Apropos of 12 cases including an anatomo-clinical case]. 19 44

In normal subjects, the folic acid absorption (TRIFA test) was independent of age and sex. Among 53 geriatric patients with nutritional folate deficiency, impaired absorption of folic acid was present in 19 (36%). After treatment with folic acid for 4 weeks, the absorption returned to normal. It is concluded that folate deficiency per se can produce a malabsorption syndrome resulting in further depletion of folate. Protein deficiency and weight loss alone do not impair the absorption of folic acid.
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PMID:Reversible malabsorption of folic acid in the elderly with nutritional folate deficiency. 81 51

Red cell anisocytosis as assessed using the Coulter Channelyzer C-1000 showed an increase with progressive anaemia in 25 patients with macrocytosis due to B12 and/or folate deficiency. In deficiency of a single factor, the degree of anisocytosis increased with progressive anaemia. In five cases with B12 and folate deficiency combined, anisocytosis was markedly increased out of proportion to the degree of anaemia present. Iron stores were also reduced in four of these cases. It is suggested that objective measurement of anisocytosis is of early diagnostic value in the assessment of multiple haematinic factor deficiency, for example, in macrocytic anaemia associated with malabsorption states and unexpected multiple deficiency states.
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PMID:Anisocytosis and the C-1000 Channelyzer in macrocytic anaemia. 95 53

The restless legs syndrome could represent a folate responsive disorder in both patients with acquired-folate deficiency and those with familial symptomatology. Patients with acquired folate-deficiency could be divided into two subgroups. (i) those with minor neurological signs (restless legs syndrome, vibration sense impairment and tactile hypoesthesia in both legs with diminished ankle jerks and a prolonged or assymetrical Achilles-reflex time) and (ii) those with major neurological signs (subacute combined degeneration with or without neuropathies). In some of these patients the classical triad of the malabsorption syndrome is replaced by another triad, constipation, abnormal jejunal biopsy and abnormal d-xylose absorption. A low folic serum acid level could induce minor neuropsychiatric symptoms while an additional low CSF folate could induce major neurological symptoms in spite of the presence of a normal erythrocyte folate level and in the absence of frank anemia. Possible further studies are described.
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PMID:Folate deficiency and neurological disorders in adults. 95 35

To identify potentially remediable abnormalities in Crohn disease, 63 patients had evaluations performed for anemia, electrolyte deficiencies, defects of carbohydrate, fat, nitrogen, and vitamin B12 absorption, and jejunal bacterial overgrowth. Ninety percent of the group had two or more potentially correctable defects. More than 50% had anemia associated with iron or folate deficiency of vitamin B12 malabsorption; 33% had low levels of serum sodium, potassium, calcium, or magnesium either singly or in combination; 22% had lactose intolerance, fat malabsorption was persent in 31%; 75% had evidence of disturbed protein metabolism; and bacterial overgrowth of the upper part of the small bowel was identified in 30% of 47 patients.
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PMID:Remediable defects in Crohn disease: a prospective study of 63 patients. 105 64

Since 1964, 41 patients with strictly defined, severe primary (dietetic) protein malnutrition have been studied under metabolic ward conditions during prolonged periods, initially on a low (20 g) and later on a high (100 g) protein diet. Clinical, nutritional, hematological, intestinal absorptive and histological studies were performed in the malnourished state, during and after protein repletion. Classical signs and symptoms of malnutrition, lasting for at least 4 months, were present in most patients. Mild diarrhea was frequent. All were normoblastically anemic, hypoproteinemic, and hypocholesterolemic; serum folate values were normal or low but serum B12 values were normal or high. Liver biopsy showed fatty liver in the cases where it was performed. Mild malabsorption was detected in over one-half of the patients, with moderate intestinal radiological abnormalities. Malabsorption was independent of concomitant folate deficiency. All the clinical, absorptive and histological abnormalities reversed with treatment consisting only of a high protein diet. In addition to protein lack, another factor has to be invoked in the pathogenesis of the intestinal abnormalities present in severely malnourished adults from rural areas in the tropics.
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PMID:Enteropathy in adult protein malnutrition: a review of the Cali experience. 114 51


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