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)

The possibility that the canine pancreas might have an important role in the physiologic absorption of cobalamin (vitamin B12) has been explored by determining the effect of exocrine pancreatic insufficiency on cobalamin absorption and by examining the subsequent influence of bovine pancreatic enzymes and canine pancreatic juice. Exocrine pancreatic insufficiency was induced by ligation of pancreatic ducts and confirmed by indirect assessment of exocrine pancreatic function. Cobalamin absorption was determined by oral administration of cyano[58Co]cobalamin and quantitation of radioactivity in blood, urine, and feces during 48 hours. Pancreatic duct ligation resulted in a significant (P less than 0.001) decrease in cobalamin absorption, which was not restored by oral administration of bovine pancreatic enzymes, despite considerable improvements in steatorrhea and in vivo proteolytic activities. In marked contrast, malabsorption of cobalamin was significantly (P less than 0.05) reversed by oral administration of canine pancreatic juice. These results indicate that pancreatic secretions have an important role in the normal absorption of cobalamin in the dog, a role that does not appear to be attributable to pancreatic enzymes, but is consistent with the existence of a pancreatic intrinsic factor in this species.
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PMID:Effect of exocrine pancreatic insufficiency on cobalamin absorption in dogs. 278 6

Three cases of adult coeliac disease with severe vitamin B12 deficiency not accompanied by folate or iron depletion are presented. Two of the patients had the extremely rare combination of coeliac disease and lack of intrinsic factor and autoimmune thrombocytopenic purpura. A close association between coeliac disease and autoimmunity is indicated by the development of autoimmune thyroiditis in the third patient. Vitamin B12 malabsorption caused by coeliac disease is emphasized as a pathogenetic mechanism of megaloblastic anaemia.
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PMID:Selective vitamin B12 malabsorption in adult coeliac disease. Report on three cases with associated autoimmune diseases. 324 90

Inherited disorders of vitamin B12 include those which involve the inability of the vitamin to be absorbed from the gut and transported to the appropriate tissues, and those in which the vitamin is not utilised by target cells. The former include intrinsic factor abnormalities, selective malabsorption of vitamin B12 with proteinuria, and deficiencies of transcobalamin I and transcobalamin II. The latter include a defect in the release of free vitamin B12 from lysosomes (cblF), and defects in the formation of both vitamin B12 cofactors (cblC, cblD) or of adenosyl-B12 (cblA, cblB) or methyl-B12 alone (cblE, CblE variant). This article reviews the major clinical manifestations of these diseases, and provides an approach to the diagnosis of transcobalamin II deficiency and the cbl mutations using cultured cells.
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PMID:Inherited disorders of vitamin B12 metabolism. 333 1

A case of pernicious anemia in a 30 years old men is described. This disease was typical for the hematologic, immunologic and medullary patterns, for his evolution, but the Schilling test, a dual tracer method, did not confirm the diagnosis. The contradictory of this result can be explained wether by the bias of the test itself, or by the intestinal malabsorption due to the vitamin B12 deficiency, or by other factors like bacterial overgrowth state (associated in the pernicious anemia) and a high level of antibodies to intrinsic factor.
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PMID:[The Schilling test in Biermer's disease, problems of false negative reactions. Apropos of a case]. 343 71

Patient records from January 1975 to December 1984 were analysed to assess the possible incidence of protein-bound vitamin B12 malabsorption. This condition is characterised by a low serum vitamin B12 level and a normal Schilling test but impaired absorption of vitamin B12 bound to protein. We found that 48 (25%) patients with a low serum cobalamin level unexplained by other causes had a normal Schilling test. Megaloblastic haemopoiesis was found in 25 of these. From this group, all 10 patients who had a test of protein-bound vitamin B12 absorption showed impaired absorption. Protein-bound vitamin B12 malabsorption may represent an early phase of pernicious anaemia when hypochlorhydria precedes intrinsic factor deficiency and should be tested for when the serum vitamin B12 level is decreased and the Schilling test is normal.
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PMID:Incidence and clinical significance of protein-bound vitamin B12 malabsorption. 359 8

The gastric pentagastrin-stimulated secretions of acid (peak acid output) and of unsaturated intrinsic factor in eight cystic fibrosis patients (1.4 +/- 0.5 mEq/kg/h and 0.27 +/- 0.12 nmol/kg/h, respectively) were significantly enhanced (p less than 0.05) when compared with six normal controls (0.27 +/- 0.16 mEq/kg/h and 0.10 +/- 0.02 nmol/kg/h, respectively). Despite the gastric hypersecretion of intrinsic factor, no significant physicochemical modification of this glycoprotein was observed in cystic fibrosis when using gel filtration and isoelectrofocusing. Haptocorrin (a cobalamin glycoproteic binder that does not promote the assimilation of cobalamin) also increased in gastric juice after stimulation. Since the sequestration of cobalamin to haptocorrin is pH dependent, the gastric acid hypersecretion observed in cystic fibrosis may explain that the malabsorption of crystalline cobalamin is much more frequent in cystic fibrosis than in chronic pancreatitis.
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PMID:Gastric intrinsic factor hypersecretion stimulated by pentagastrin in cystic fibrosis. 368 75

Three siblings presented in their second year of life with megaloblastic anemia that responded to parenteral cobalamin (Cbl). Schilling tests were less than 1%, correcting to 5 to 15% after addition of hog intrinsic factor (IF). Gastric acid analysis and gastric biopsies were normal by light and electron microscopy. Gastric juice contained less than 3 pmol/ml of Cbl-binding ability due to IF (normal, 10-34 pmol/ml) and less than 2 pmol/ml of IF when measured with a radioimmunoassay (RIA) using normal human IF-[57Co]Cbl and rabbit anti-human IF serum (normal, 17-66 pmol/ml). However, RIA employing rabbit anti-hog IF serum gave values of 4-13 pmol/ml of IF (normal, 11-33 pmol/ml). This material had an apparent molecular weight of 40,000 (normal IF = 70,000). The IF from gastric biopsies appeared normal in terms of Cbl-binding ability, ileal binding, molecular weight, and both RIAs. This IF differed from normal mucosal IF, in that it lost its Cbl-binding ability when incubated at 37 degrees C at acid pH or in the presence of pepsin or trypsin. This loss was retarded when [57Co]Cbl was bound to the IF before these incubations. The stabilizing effects of neutralization and Cbl were also demonstrated in vivo. Schilling tests for the siblings of 0.4, 0.5, and 1.0% increased to 2.7, 5.7, and 4.3% (P less than 0.05), respectively, when the Schilling tests were repeated with the addition of NaHCO3 and cobinamide (which allows Cbl to bind immediately to IF). We conclude that Cbl malabsorption in these children is due to an abnormal IF that is markedly susceptible to acid and proteolytic enzymes which cause a decrease in its molecular weight and Cbl-binding ability and a loss of antigenic determinants that are recognized by the anti-human IF serum.
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PMID:Cobalamin malabsorption in three siblings due to an abnormal intrinsic factor that is markedly susceptible to acid and proteolysis. 390 80

The first case of megaloblastic anemia due to selective malabsorption of vitamin B(12) and vitamin B(12)-intrinsic factor is described in an otherwise normal female adult, in whom pernicious anemia had previously been diagnosed.
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PMID:Selective malabsorption of vitamin B12 and vitamin B12-intrinsic factor with megaloblastic anemia in an adult. 405 72

A 68-year-old man presenting with chronic intermittent diarrhea and progressive ataxia was found to have idiopathic hypoparathyroidism. Intrinsic factor-resistant vitamin B(12) malabsorption was demonstrated. Both the diarrhea and vitamin malabsorption were reversed by correction of hypocalcemia.His neurological profile was a combination of peripheral nerve, posterior column and cerebellar deficits. He had calcifications in the dentate nuclei of the cerebellum. Possible etiological factors such as vitamin B(12) deficiency, folic acid deficiency and steatorrhea have been excluded. Posterior column and cerebellar abnormalities improved with treatment. It is postulated that hypocalcemia causes functional, reversible spinal cord and cerebellar dysfunction.
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PMID:Idiopathic hypoparathyroidism with impaired vitamin B 12 absorption and neuropathy. 433 89

Two siblings with megaloblastic anemia responsive to parenteral vitamin B(12) were studied to elucidate the cause of the B(12) deficiency. Gastric juice from both contained acid and functional intrinsic factor. Serum contained transcobalamin II and lacked antibodies to intrinsic factor. Schilling tests showed vitamin B(12) malabsorption uncorrected by hog intrinsic factor or pancreatic extract. Other parameters of small intestinal function were normal. Proteinuria was initially present in both but cleared in one following treatment with B(12). These patients with "familial selective vitamin B(12) malabsorption" are the first reported from Canada. Only 37 cases have been reported in the world literature to date.
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PMID:Selective vitamin B12 malabsorption in two siblings. 481 48


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