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)

Following a single, oral dose of Bacillus cereus (2 X 10(8) bacteria) in vitro intestinal absorption of D-glucose, D-galactose, L-arginine, L-histidine, L-ornithine and L-proline in young mice (aged 2--3 1/2 months) decreased. Malabsorption of D-glucose was dose- and time-dependent. Impaired absorption of D-glucose occurred throughtout the length of the small intestine, particularly distally. Following hydrolysis of D-maltose at the brush border, D-glucose absorption in infected mice and that of the untreated controls was similar. Using D-glucose, fluid transfer in the infected intestine and that of the controls was alike. Although slightly lower, fluid transfer in the infected intestine using the other solutes was not significantly different compared with the controls. Glucose-dependent and glucose-independent intestinal fluid transfer in infected animals was like that of the controls. Using old infected mice (aged 8--9 months) intestinal absorption of D-glucose and L-histidine was unchanged compared with young mice. The fresh small intestinal weight in infected mice and the controls was alike. Changes in the histology of the small intestine in young infected mice were small and inconsistent.
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PMID:Bacillus cereus-induced malabsorption in young mice. 9 13

Dietary deficiency of vitamin B-12 has been reported, yet most people ingesting vitamin-B12-deficient diets even for many years appear to achieve a balance that does not lead to overt signs and symptoms of deficiency. I present the case of a vegan of 25 years' duration who developed severe neurologic abnormalities due to vitamin-B12 deficiency. His diet provided 1.2 microgram of vitamin B12 daily at most. Despite normal Schilling test findings, he absorbed subnormal amounts of vitamin B12 given with ovalbumin. This poor absorption appeared to be related to his gastritis, achlorhydria, and subnormal intrinsic-factor secretion. Probably, vitamin-B12 deficiency in this patient resulted from both dietary restriction and the subtle malabsorption, neither of which would have sufficed alone to produce the clinical problem. Possibly such malabsorption may also be present in many of those vegans developing overt vitamin-B12 deficiency in whom Schilling test findings have been normal.
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PMID:Nutritional vitamin-B12 deficiency. Possible contributory role of subtle vitamin-B12 malabsorption. 64 50

1. Using mouse everted whole small intestine 7 days after a single dose of Phenoclor DP6 (hexachlorobiphenyl) at 1.0 g kg-1 body wt, absorption of D-glucose decreased significantly, probably owing to toxic traces of pentodicholobenzofuran in the PCB preparation and not its high chlorine content. D-glucose tissue accumulation decreased. The serosal fluid transfer also fell but not the gut fluid uptake. D-glucose absorption and fluid transfer remained unchanged following doses of other Phenoclor and Pyralene (PCB) compounds. 2. Using DP6, malabsorption of D-glucose and impaired serosal fluid transfer were not evident 7 days after a single dose of 0.1, 0.25 and 0.50 g kg-1 body wt. One to 21 days after a single dose (1.0 g kg-1 body wt) of DP6, D-glucose absorption and serosal fluid transfer decreased from 3 to 14 days but thereafter became normal. 3. Although absorption of D-galactose, D-glucose following membrane hydrolysis of D-maltose, and L-arginine, L-histidine, L-ornithine and L-proline decreased slightly 7 days after a single dose of Phenoclor DP6,the results were not significant, nor were changes in fluid transfer. 4. Following Phenoclor DP6-treatment, D-glucose malabsorption was abolished by an exogenous energy supply (D-mannose). DP6 affected intracellular metabolism and not the glucose carrier at the membrane brush border. 5. The body-weights and fresh small intestinal weights of mice treated with different PCBs remained unchanged after seven days. The histology of the small intestine showed minimal changes.
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PMID:Polychlorinated biphenyls (phenoclor and pyralene) and intestinal transport of hexoses and amino acids in mice. 82 75

A patient with diffuse eosinophilic gastroenteritis, associated with progressive chronic interstitial pulmonary fibrosis, was followed for 29 years. His major symptoms were recurrent gastrointestinal bleeding, anemia, diarrhea, malabsorption, and increasing respiratory insufficiency. Multiple jejunal biopsies revealed eosinophilic infiltration and extensive villous atrophy. Results of a lung biopsy and pulmonary function tests were consistent with chronic interstitial pulmonary fibrosis. His gastrointestinal symptoms responded to steroid therapy, but he died of progressive respiratory insufficiency. At autopsy, villous atrophy was noted to extend throughout the whole extent of the small intestine in association with multiple "pseudopolypoidal" inflammatory lesions.
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PMID:Eosinophilic gastroenteritis with malabsorption, extensive villous atrophy, recurrent hemorrhage and chronic pulmonary fibrosis. 108 12

A male infant with bilateral iris coloboma who had had repeated infections and malabsorption was studied. The levels of total lymphocytes and of T and B cells were normal or high, but IgA became undectable and IgG low, whereas IgM was normal. His lymphocytes did not respond to phytohemagglutinin (PHA), concanavalin A, pokeweed mitogen (PWM) or in mixed lymphocyte reactions (MLR), nor did they respond in vitro when thymosin was included in the test systems. He was skin-test-negative, even to dinitrochlorobenzene. His crudely isolated T lymphocytes and the supernatant of his PHA-stimulated lymphocytes inhibit the response of normal lymphocytes to PHA, PWM, and in MLR. During thymosin treatment skin test and lymphocyte reactivity to mitogen remained negative. He became faintly positive in MLR, and the suppressor activity in the supernatant of his PHA-stimulated lymphocytes no longer inhibited the response of normal lymphocytes to PHA, PWM, or in MLR. In parallel with thymosin treatment he showed quite marked clinical improvement.
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PMID:Suppressor cell activity in a male infant with T-and B-lymphocyte dysfunction treated with thymosin. 108 48

A 58 year old Chinese male, one week after arriving in Canada from Hong Kong, presented with acute abdominal pain and diarrhoea which was rapidly followed by Escherichia coli infection causing septicaemia and meningitis. His past history revealed bronchial asthma for 15 years treated with steroids. At laparotomy, 7 days after the onset of symptoms, he was found to have extensive haemorrhagic infarction of the small bowel and right colon. Examination of the fibrosed mesenteric vessels revealed numerous filariform larvae of Strongyloides stercoralis, within the walls, and in all layers of bowel wall. The role of the parasite in the production of obliterative arteritis in this fatal case of haemorrhagic enteropathy is discussed. Clinical strongyloidiasis, in uncomplicated cases, varies from mild to severe with gastroenteritis, nausea, colicky abdominal pain, electrolyte imbalance and symptoms of malabsorption syndrome (MARCIAL-ROJAS, 1971). In malnourished individuals and patients with debilitating infections, either newly acquired or asymptomatic latent infection with S. stercoralis can assume severe dimensions (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). Similarly, in patients on steroid (CRUZ et al., 1966; WILLIS and MWOKOLO, 1966; NEEFE et al., 1973) and immunosuppressive therapy for lymphomatous diseases or deficient in immune response (ROGERS and NELSON, 1966; RIVERA et al., 1970), systemic strongyloidiasis is often fatal. The increased frequency of auto-infection in such patients with a breached immune barrier is, however, unclear. Further complications of this infection due to severe enterocolitis result in sepsis, bacteraemia and meningitis (BROWN and PERNA, 1958; HUGHTON and HORN, 1959). This paper presents a fatal case of S. stercoralis infection which illustrates an uncommon if not unique, mechanism in its production of haemorrhagic enteropathy leading to sepsis and death.
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PMID:Fatal bowel infarction and sepsis: an unusual complication of systemic strongyloidiasis. 122 84

Carnosinase, the dipeptidase which hydrolyses carnosine and other histidine-containing dipeptides, was assayed in mucosal tissues of the human and of the rat gut. Kinetic properties of the intestinal enzyme were found to be similar to carnosinase of other animal tissues. Little or no activity was detected in human gastric or colonic mucosa, and the levels were lower in duodenal than jejunal mucosa. The distribution of carnosinase is similar to that of the disaccharidases. Mean carnosinase activity was 8-8 units/g weight in 15 patients with histologically normal mucosa compared with 5-7 units in five with villous atrophy. The enzyme levels increased with histological improvement of the mucosa in patients with coeliac disease on a gluten-free diet. Tolerance curves for carnosine and its constitutent amino acids showed malabsorption of the dipeptide in a patient with carnosinase deficiency. It is concluded that the intestinal mucosa has much less hydrolase activity for carnosine than for glycylglycine and other dipeptidases, and the relatively slow hydrolysis appears to be the rate-limiting step in the total absorptive process.
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PMID:Carnosinase activity of human gastrointestinal mucosa. 123 44

This 54-year-old Korean coal miner suffered from continuous watery diarrhea and weight loss after corticosteroid treatment (beta-methasone, 4 mg daily for 1 week) due to hip-bone fracture in January 1991. Except for the short therapy of steroid, no other histories were contributory. The malabsorption syndrome was aggravated while the case was treated under the impression of amebiasis or intestinal tuberculosis. AIDS antibody test by EIA was negative and quantitative analysis of serum immunoglobulins was in normal ranges. Nine months after the onset of symptoms, the case was diagnosed as malabsorption syndrome caused by complexed and aggravated infection by Strongyloides stercoralis, Isospora and cytomegalovirus in the small intestine, which were proved by stool examination and duodenal biopsy. His clinical course became worse even after high-dosed and prolonged albendazole treatment for strongyloidiasis with supportive fluid therapy. The patient was discharged in hopeless status in November, 1991 and died after one week at home.
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PMID:[A case of fatal malabsorption syndrome caused by strongyloidiasis complicated with isosporiasis and human cytomegalovirus infection]. 131 69

Seven cases of arthritis related to coeliac disease have been described in the English literature, all with features of malabsorption. We describe a patient with an acute inflammatory oligoarthritis and little evidence of intestinal malabsorption who was subsequently found to have asymptomatic coeliac disease on intestinal biopsy. His arthritis responded to gluten free diet and is now in remission. A greater awareness of the association between coeliac disease and arthritis is needed, especially because both these conditions are potentially curable.
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PMID:Oligoarthritis--a presenting feature of occult coeliac disease. 844 25

To investigate the cause of low serum histidine in rheumatoid arthritis (RA) single oral and intravenous doses of L-histidine were administered to patients with active RA, and to an equal number of age and sex matched control subjects. In the first study 13 patients and their controls received a 100 mg kg-1 dose of L-histidine as an aqueous slurry. Significant differences were seen in body weight, predose baseline serum histidine concentration, Cmax, t1/2, and area under curve, AUC0-infinity. In a second study six patients and six controls each received a 50 mg kg-1 dose of L-histidine both orally and intravenously on two separate occasions. The patients with RA had a lower baseline serum histidine concentration, a lower volume of distribution, and a shorter plasma half life than the controls, but these differences were not statistically significant. No difference was seen in bioavailability or clearance. Low serum histidine in RA is unlikely to be due to malabsorption from the gut, uptake by abnormal gut flora, or increased metabolism.
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PMID:Kinetic investigations into the possible cause of low serum histidine in rheumatoid arthritis. 334 4


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