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)

A dual isotope vitamin B12 absorption test in which vitamin B12 is given both in aqueous solution and bound to protein (chicken serum), was evaluated in 26 controls and 68 patients with subnormal serum vitamin B12 concentrations (19 with pernicious anaemia, 13 with iron deficiency, seven after partial gastrectomy, seven with malabsorptive states, five with folate deficiency, four with chronic alcoholism and 13 in whom no cause was apparent). In control patients protein bound absorption decreased with age; isotope excretion was 1.0% or over in those aged under 60 and 0.5% or over in those aged 60 and above. Malabsorption of protein bound vitamin B12 with normal aqueous absorption occurred in five patients with iron deficiency, three with alcoholism, two after partial gastrectomy, two with folate deficiency and in one with a malabsorptive state. In alcoholics abstinence produced an improvement in protein bound absorption. All patients in the group for whom no cause could be found for the subnormal serum vitamin B12 concentration had normal aqueous absorption but four had malabsorption of protein bound vitamin. Although the dual isotope test gave reproducible results and was consistent with the standard Schilling test some anomalies were detected; nine patients had reduced aqueous absorption with normal protein bound absorption. Despite this the dual test may prove useful in determining the importance of a subnormal vitamin B12 concentration where the cause is not clinically apparent. Further development is needed before it can be considered for routine use.
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PMID:Experiences with dual protein bound aqueous vitamin B12 absorption test in subjects with low serum vitamin B12 concentrations. 361 94

Nonhuman primates fed folic acid-deficient diets +/- 30% kcal ethanol were used to determine alcohol effects on megaloblastic anemia development and folate bioavailability. Lower hemoglobin (Hb) and red blood cell (RBC) counts and higher mean corpuscular volume (MCV) occurred after 13 wk in alcohol-fed monkeys, later in controls. Plasma, RBC, and liver folate declined and urinary formiminoglutamic acid (FIGLU) was elevated in both groups with FIGLU increasing more among alcohol-fed monkeys at 38 wk. After 40 wk, the bioavailability of oral 3H-folic acid was investigated and showed increased fecal and reduced urinary tritium excretion in alcohol-fed monkeys compared with controls while plasma uptake and liver and whole body tritium retention were similar in both groups. These observations demonstrate that chronic alcohol consumption impairs folate coenzymes, accelerates appearance of hematologic indices of megaloblastic anemia, and causes possible malabsorption of enterohepatically circulated folates in folate deficiency even when other essential nutrients are provided.
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PMID:Intestinal absorption, liver uptake, and excretion of 3H-folic acid in folic acid-deficient, alcohol-consuming nonhuman primates. 363 Sep 68

Folic acid absorption was studied in 12 elderly subjects with atrophic gastritis and 10 elderly normal controls using tritium-labeled pteroylmonoglutamic acid. Two folic acid absorption tests were carried out on each subject with 120 ml of either water or 0.1 N HCl. Folic acid absorption was significantly lower in subjects with atrophic gastritis than in normal controls (31% vs. 51%, respectively; p less than 0.01). In subjects with atrophic gastritis, folic acid absorption rose significantly to 54% (p less than 0.001) when administered with acid, but did not change in normal controls (50%). Serum folate levels were normal in all subjects. Proximal small intestinal pH was higher in atrophic gastritis subjects than in normal controls (7.1 vs. 6.7, respectively; p less than 0.05), as were bacterial counts of small intestinal fluid (p less than 0.01). Bacteria cultured from the aspirates of subjects with atrophic gastritis were able to synthesize folate in vitro when incubated in a folate-free medium. Atrophic gastritis results in folic acid malabsorption but not in folate deficiency, possibly due to increased bacterial synthesis of folate in the small intestine.
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PMID:Folic acid malabsorption in atrophic gastritis. Possible compensation by bacterial folate synthesis. 377 Mar 72

A patient with megaloblastic anaemia due to nutritional folate deficiency is described. Partial villous atrophy and malabsorption of xylose showed progressive improvement to normal with folic acid therapy.
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PMID:Partial villous atrophy in nutritional megaloblastic anaemia corrected by folic acid therapy. 555 80

Of eight patients with Paget's disease one had diarrhoea, steatorrhoea, impaired xylose absorption, and macrocytic anaemia due to folic acid deficiency, while another had diarrhoea and very low xylose absorption. In both patients jejunal biopsy was normal, and they responded to folic acid therapy with considerable increase in xylose absorption. Low xylose excretion was seen in three more patients, one of whom also had steatorrhoea. Thus malabsorption may be a systemic complication of Paget's disease of bone, possibly due either to secondary folate deficiency or to relative ischaemia of the bowel.
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PMID:Malabsorption syndrome in Paget's disease of bone. 568 70

Human jejunal brush border folate conjugase (EC 3.4.22.-) was partially purified and characterized. Three drugs known to be associated with clinical folate deficiency were tested for inhibition of the partially purified enzyme. Using jejunal mucosa from obese patients undergoing intestinal bypass surgery, brush border folate conjugase was purified 50-80-fold by centrifugation, Triton X-100 solubilization and DEAE-Sephadex and Sephacryl S-200 chromatography. Using synthetic pteroyldiglutamyl[14C]glutamate as substrate, the enzyme was found to have a pH optimum of 6.5 and an apparent Km of 1.6 micro M. Incubation of the enzyme with synthetic pteroyl[14C]glutamylhexaglutamate resulted in a spectrum of shorter-chain 14C-labeled pteroylglutamates at 60 min. Pteroyl[14C]glutamate was the major product at 120 min, with quantitative recovery of free glutamate in the incubation medium. Salicylazosulfapyridine was a competitive inhibitor of the enzyme (Ki = 0.13 mM), while ethanol, diphenylhydantoin and salicylazosulfapyridine metabolites had no effect. These data suggest that brush border folate conjugase is an exopeptidase which progressively hydrolyzes glutamyl units from pteroylpolyglutamate, leaving pteroylmonoglutamate as the folate form available for intestinal transport. Inhibition of brush border folate conjugase by salicylazosulfapyridine provides a mechanism for folate malabsorption and deficiency in chronic users of this drug.
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PMID:Human jejunal brush border folate conjugase. Characteristics and inhibition by salicylazosulfapyridine. 611 48

A 57-year-old woman developed dementia and peripheral neuropathy 16 years after a partial gastrectomy (Billroth II). Serum cobalamin was 198 pmol/l (reference interval 150-550), and the vitamin B12 absorption test (Schilling) showed decreased absorption (1.7% without and 2.2% with intrinsic factor). In spite of 20 months' therapy with vitamin B12, the neurological symptoms progressed. Folate deficiency was suggested by a very low erythrocyte folate and a slightly abnormal FIGLU test. There were no other signs of general malabsorption. A few months' treatment with folic acid significantly improved the massive neurological manifestations which were verified neurophysiologically as well as histologically. A common role of vitamin B12 and folate in the development of neuropathy is suggested.
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PMID:Reversible dementia and neuropathy associated with folate deficiency 16 years after partial gastrectomy. 625 53

This review focusses on research performed by the author and coworkers. The absorption, turnover and excretion of cobalamin and the pathogenesis of cobalamin deficiency states are described and the laboratory tests used to diagnose these states are discussed. Topics dealt with in detail include: overall turnover, daily need, enterohepatic circulation and excretion of cobalamin and other corrins . The soluble proteins mediating cobalamin transport and their cellular receptors are described and their nomenclature, isolation, structure and mode of action, the role of calcium in the membrane transport, the evolution of these systems and the analogies with transport systems for other substrates are discussed together with deficiency states, especially fish tapeworm anemia and familial selective vitamin B12 malabsorption with proteinuria. Folate deficiency is a relatively rare cause of megaloblastic anemia in Scandinavia but common in North America and explanations for this difference are suggested. The methods of assaying cobalamin in serum and plasma and the performance of radiovitamin B12 absorption tests are critically evaluated. The measurement of intrinsic factor in gastric juice, serum, amniotic fluid and urine is described.
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PMID:Biochemistry and clinical chemistry of vitamin B12 transport and the related diseases. 632 50

The risk of developing folate deficiency is greatest in patients who have a poor diet and malabsorption secondary to disease of the jejunal mucosa or drugs which interfere with its metabolism. In contrast to cobalamin deficiency, in which body stores delay the onset of major metabolic complications, folate deficiency may develop in a matter of months. It is frequently possible to predict these deficiencies and always possible to reverse them by supplementation.
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PMID:Importance of vitamin B12 and folate metabolism in malabsorption. 634 65

Patients with subnormal serum vitamin B12 concentrations were tested for absorption of protein bound vitamin B12 and compared with controls. Absorption of the protein bound vitamin appeared to decrease with increasing age in healthy subjects. Differences between the result of this test and the result of the Schilling test in patients who had undergone gastric surgery were confirmed; such differences were also seen in some patients who had iron deficiency anaemia, an excessive alcohol intake, or folate deficiency. Defective absorption was also found in six patients with an adequate dietary intake of vitamin B12, normal Schilling test results, low serum vitamin concentrations, and tissue changes responding to treatment with vitamin B12. Malabsorption of the vitamin from protein bound sources, which is not detected by the Schilling test, may produce vitamin B12 deficiency of clinical importance.
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PMID:Malabsorption of protein bound vitamin B12. 642 28


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