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

The Schilling examination remains a popular means of evaluating in vivo absorption of vitamin B12. When absorption is abnormally low, the test may be repeated with addition of exogenous intrinsic factor (IF) in order to correct the IF deficiency that characterizes pernicious anemia. A dual-isotope variation provides a means of performing both stages of the test simultaneously, thereby speeding up the test and reducing dependence on complete urine collection. The dual-tracer test depends on no exchange of B12 moieties on the IF molecule. In vitro studies suggest that this exchange does take place, in a manner dependent on time, temperature, and pH. Furthermore, in vivo studies indicate that, when administered simultaneously, the absorption of unbound B12 is elevated, and IF-bound B12 is reduced, in pernicious-anemia patients, relative to the classic two-stage examination. A number of clinical studies indicate significant difficulty in resolving clinical diagnoses with the dual-tracer test. The potential weaknesses of the test discussed herein can be overcome by temporally separating the administration of the two B12 doses and by treating secondary malabsorption where it exists. An algorithm is offered for selecting the most suitable variation of the Schilling test to improve the accuracy of test results and the ease of performance.
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PMID:Schilling evaluation of pernicious anemia: current status. 647 Aug 5

It has been recently shown that crystalline cyanocobalamin in exocrine pancreatic insufficiency is sequestered by R binders down to the proximal jejunum, and that bile inhibits the binding of cobalamin to intrinsic factor. In freshly collected human bile, we have found a single type of apo R binder, with a relative molecular mass of 128 100, a molecular radius of 4.65 nm, and a mean isoelectric point of 3.72. Salivary and biliary holo R binders were incubated with normal human gastric juice and intestinal juice from healthy subjects and patients having exocrine pancreatic insufficiency. No degradation of these two holo R binders occurs with normal gastric juice and intestinal juice from patients after four hours incubation time at 37 degrees C, but a partial degradation of salivary holo R binders and a complete loss of biliary Cbl binding capacity were observed with normal intestinal juice in the same in vitro conditions. We have confirmed in vivo, using a triple-lumened tube, that a part of the salivary and biliary holo R binders remains undegraded down to the distal ileum in two patients with exocrine pancreatic insufficiency. These findings strongly suggest that the enterohepatic circulation of cobalamin is effective in healthy subjects, whereas it is partially interrupted in the patients. They provide a proof that a part of endogenous and crystalline exogenous cobalamin is sequestered to R binders down to the distal ileum, and confirm that the failure to degrade the digestive R binders is responsible for the malabsorption of crystalline cobalamin in exocrine pancreatic dysfunction.
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PMID:Sequestration of crystalline and endogenous cobalamin by R binders down to the distal ileum in exocrine pancreatic dysfunction. 665 15

Acute nonlymphocytic leukemia developed in a 57-year-old woman following adjuvant therapy with melphalan for ovarian carcinoma. Maturation of differentiating marrow myeloid and erythroid precursors was megaloblastic. The serum vitamin B12 level was low, and Schilling test revealed vitamin B12 malabsorption correctable with intrinsic factor. Megaloblastic maturation of the marrow cells was converted to normoblastic following treatment with vitamin B12 and folic acid. However, blast cells persisted in the marrow, and cytogenetic analysis revealed aneuploidy and trisomy 18. In contrast to the marrow blast cells, there was a decline in circulating blast cells following vitamin replacement, suggesting that these cells were capable of maturation but required vitamin B12 for this purpose.
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PMID:Unusual case of acute leukemia. Coexisting acute leukemia and pernicious anemia. 673 67

The suppressive effects of cimetidine on acid, pepsin, and intrinsic factor secretion have been well documented; however, the effect of cimetidine on cobalamin absorption has not been assessed. The absorption of both unbound [57Co]cyanocobalamin and protein-bound [57Co]cyanocobalamin was evaluated in 12 patients with duodenal ulcer disease during and after discontinuation of cimetidine therapy. Cimetidine administration did not lead to malabsorption of unbound cobalamin but caused malabsorption of protein-bound cobalamin (0.22 +/- 0.08%, [mean +/- 1 SEM] versus 2.3 +/- 0.10% in control subjects, P less than 0.01). This malabsorption was reversible upon discontinuation of cimetidine. Patients on cimetidine therapy malabsorb protein-bound cobalamin and, during long-term treatment, are at risk for developing cobalamin deficiency. This malabsorption was reversible upon discontinuation of cimetidine. Patients on cimetidine therapy malabsorb protein-bound cobalamin and, during long-term treatment, are at risk for developing cobalamin deficiency. This malabsorption of protein-bound cobalamin is not detectable by the usual tests of cobalamin absorption which employ unbound cobalamin.
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PMID:Malabsorption of protein-bound cobalamin but not unbound cobalamin during cimetidine administration. 676 34

In a survey of 46 randomly selected diabetic patients on biguanide therapy, 30% had malabsorption of vitamin B12. Withdrawal of the drug resulted in normal absorption in only half of those with malabsorption. In most patients with persistent malabsorption, the results of absorption tests with exogenous intrinsic factor suggested the diagnosis of coincidental intrinsic factor deficiency. Further considerations, however, led to the concept that biguanides can induce malabsorption by two different mechanisms. One of these is temporary and unrelated to intrinsic factor secretion and the other is permanent and mediated by depression of intrinsic factor secretion.
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PMID:Malabsorption of vitamin B12 and intrinsic factor secretion during biguanide therapy. 682 78

The conventional method of measuring vitamin B12 absorption using a whole-body counter normally involves a delay of fourteen days before complete faecal excretion of unabsorbed B12 tracer can be assumed. A modified technique has been used which reduces the delay to four days. A non-absorbable tracer, 51Cr-chromic chloride, was administered firstly with 58Co-labelled vitamin B12 and then three hours later with 57Co-labelled vitamin B12 and then three hours later with 57Co-labelled vitamin B12 plus 50 mg hog intrinsic factor which normalises B12 malabsorption in patients with pernicious anaemia. Three days later, the residual whole-body activities of the three radionuclides were measured. The retention of 51Cr indicated the efficiency of faecal excretion of unabsorbed B12 tracer and could be used to quantify vitamin B12 absorption before complete excretion of unabsorbed B12 tracer. Vitamin B12 absorption values were measured at four days by this technique and compared with the corresponding values at fourteen days in 38 tests on 33 subjects, 16 of whom had pernicious anaemia. Excellent correlations between the results obtained at four and 14 days were obtained for both B12 tracers.
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PMID:A fast method of measuring vitamin B12 absorption using a whole-body counter. 683 44

The physiological absorption of vitamin B12 is a complex process which requires the interaction of several macromolecules. Mediated by the glycoprotein, intrinsic factor (IF), this process requires formation of a primary complex between vitamin B12 and IF (IF-B12), the recognition and binding of this complex to specific ileal receptors and the transport of vitamin B12 across the ileal cell. As a measure of this overall process, the vitamin B12 absorption test has helped to identify abnormal vitamin B12 absorption in patients with exocrine pancreatic insufficiency and familial vitamin B12 malabsorption (Immerslung-Grasbeck syndrome). Progress into understanding the role of proteolytic enzymes in promoting vitamin B12 absorption as well as the molecular events of vitamin B12 transport across the ileal cell has been brought about by recent investigation based upon this determination.
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PMID:Intrinsic factor mediated cobalamin absorption. 700 31

Several vitamins have been demonstrated to interfere with the pathogenesis of some metabolic diseases, mainly by three different mechanisms: 1) vitamin malabsorption, 2) errors in vitamin metabolism, 3) vitamin dependent syndromes. The latter is due to a deficiency of the apoenzyme whose coenzyme is the vitamin itself. In this case pharmacological, instead of nutritional doses of the vitamin may be needed. The vitamins which interfere with inborn metabolic errors are reviewed; for each vitamin the corresponding diseases which may be treated are indicated. The vitamins are: 1) thiamine (leucinosis); b) nicotinic acid (hyperlipoproteinemia); c) biotin (beta-methyl-crotonyl-glycinuria, propionic aciduria); d) pyridoxine (infantile convulsions, familial pyridoxine responsive anemia, homocystinuria, cystathioninuria, xanthurenicaciduria); e) cobalamins (congenital intrinsic factor deficiency, cobalamin malabsorption, transcobalamin deficiency, methylmalonic aciduria) f) folic acid (congenital folic acid malabsorption, formimino-transferase deficiency, methylenetetrahydrofolic reductase deficiency, Lesch-Nyhan syndrome); g) vitamin D (phosphatic diabetes, Prader's type rickets, Albright's syndrome; essential hereditary hypophosphatemia, etc). It is noteworthy that the vitamin therapy of these diseases, not only corrects the metabolic errors, but can also promote the healing or the amelioration of the psycho-physical growth, of central nervous system alterations and of other lesions.
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PMID:[Vitamins in metabolic diseases]. 702 68

A 71-year-old patient presented with failing vision. She was a life-long smoker who had suffered from Crohn's disease for at least 13 years and had vitamin B12 malabsorption which failed to correct with intrinsic factor. It is suggested that toxic amblyopia be considered in any patient with visual impairment associated with terminal ileal disease.
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PMID:Toxic amblyopia associated with Crohn's disease. 707 Jul 64

Classic pernicious anemia with abnormal Schilling test results developed in a previously described vegan patient who had coexisting subtle cobalamin malabsorption (demonstrable by abnormal ovalbumin-cobalamin absorption test results but normal Schilling test results). This suggests that the ovalbumin-cobalamin absorption test or a modified version may serve as a prodromal phenomenon to identify patients at risk for developing pernicious anemia. The patient's transformation was also accompanied by the appearance of serum anti-intrinsic factor antibody. A modified assay retrospectively detected this antibody a year earlier than did the standard assay, indicating that such modification enhances the sensitivity of this useful test.
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PMID:Subtle cobalamin malabsorption in a vegan patient: evolution into classic pernicious anemia with anti-intrinsic factor antibody. 713 69


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