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 introduction of a simple method for analysis of 14CO2 in breath allowed a more widely application of breath-tests in the diagnosis of gastroenterological diseases. During a breath-test a 14C-labelled compound is administered orally and 14CO2 is subsequently measured in breath by discontinuous samplings of 14CO2 by virtue of a trapping solution (hyamine hydroxide). Most helpful tests in gastroenterology are the 14C-glycyl-cholate breath test for detecting increased deconjugation of bile acids due to small intestinal bacterial overgrowth or bile acid malabsorption in ileal resection or Crohn's disease of the ileum, the 14C-lactose breath test in lactase deficiency, whereas the 14C-tripalmitin test seems less helpful in the diagnosis of fat malabsorption. A 14C-aminopyrine breath test may turn out to be a simple and valuable liver function test. Oral loading tests with breath analysis of H2 have shown to be helpful in the diagnosis of carbohydrate malabsorption, determination of intestinal transit time and intestinal gas production. Due to technical reasons (gas-chromatographie analysis) H2-breath analysis is still limited to research centers. Despite low radiation doses after oral administration of 14C-labelled compounds oral loading tests with H2- or 13C-analysis might be preferable in the future.
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PMID:[Breath-analysis tests in gastroenetrological diagnosis]. 77 14

This study examines the effects of nonsteroidal antiinflammatory drugs on the small intestine in humans. Using an 111In-leukocyte technique in patients with rheumatoid arthritis (n = 90) and osteoarthritis (n = 7), it appears that nonsteroidal antiinflammatory drugs cause small intestinal inflammation in two-thirds of patients on long-term treatment and on discontinuation, the inflammation may persist for up to 16 mo. The prevalence and magnitude of the intestinal inflammation was unrelated to the type and dose of nonsteroidal drugs and previous or concomitant second-line drug treatment. There was a significant inverse correlation (r = -0.29, p less than 0.05) between fecal 111In excretion and hemoglobin levels in patients treated with nonsteroidal antiinflammatory drugs. The kinetics of fecal indium 111 excretion in patients treated with nonsteroidal antiinflammatory drugs was almost identical to that of patients with small bowel Crohn's disease. Eighteen patients on nonsteroidal antiinflammatory drugs underwent a radiologic examination of the small bowel and 3 were found to have asymptomatic ileal disease with ulceration and strictures. Nineteen patients on nonsteroidal antiinflammatory drugs, 20 healthy controls, and 13 patients with Crohn's ileitis underwent a dual radioisotopic ileal function test with tauro 23 (75Se) selena-25-homocholic acid and cobalt 58-labeled cyanocobalamine. On day 4, more than half of the patients with rheumatoid arthritis had evidence of bile acid malabsorption, but the ileal dysfunction was much milder than seen in patients with Crohn's ileitis.
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PMID:Nonsteroidal antiinflammatory drug-induced intestinal inflammation in humans. 360 58

Abdominal gamma-counting after oral administration of 23-selena-25-homocholyltaurine (75SeHCAT) was carried out on 23 healthy volunteers and 66 patients: 33 with distal ileum resections, 3 with Crohn's disease of the ileum, 17 suffering from various intestinal diseases but with normal ileum, and 13 with chronic diarrhea syndrome but without evident intestinal or extraintestinal pathology. The percentage value of 75SeHCAT abdominal retention was assessed by analysis of the activity versus time curve, obtained by single exponential least-squares fit in five consecutive measurements (time zero and 1, 3, 5, and 7 days after 75SeHCAT administration) and directly by the gamma-camera countings on days 3, 5, and 7. The percentage values obtained from the curve on the third day were found to be the most suitable for differentiating between the groups, giving the 75SeHCAT test a 94% sensitivity and a 100% specificity. Our data show that this test is a valid indicator of bile acid loss: actually, it gave evidence of idiopathic malabsorption of bile salts in 6 patients with diarrhea of unknown origin who responded to cholestyramine and showed a correlation (correlation index = 0.585) with the residual ileum of the last meter in resected patients. Moreover, the 75SeHCAT test is easy to perform in any hospital with gamma-counting facilities and has negligible radiation risk.
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PMID:Use of 23-selena-25-homocholyltaurine to detect bile acid malabsorption in patients with illeal dysfunction or diarrhea. 371 57

The relation between faecal DL-lactate and intestinal inflammation or malabsorption was evaluated in 100 nonselected inpatients at a referral center for gastrointestinal disorders. Twenty-one (21%) had DL-lactate concentrations (range, 8-95 mmol/l) above the 95% limit (6.1 mmol/l) in healthy individuals. Inflammatory bowel disease with active proctitis was associated with increased faecal DL-lactate in 11 of 15 patients (73%) (mean, 32 mmol/l; range, 8-95 mmol/l) and in the 1 patient with pouchitis (8 mmol/l), whereas only 1 of 8 patients (13%) with active inflammatory bowel disease without proctitis had L-lactate elevation (25 mmol/l). Among 26 patients with malabsorption and quiescent or noninflammatory bowel disease, 3 of 17 (18%) with preserved colonic function and 3 of 9 (33%) with jejunostomy had increased faecal lactate. Only 2 of 50 (4%) patients with neither active inflammatory bowel disease nor malabsorption had faecal DL-lactate elevation. In vitro bacterial fermentation of most dietary polysaccharides did not cause accumulation of lactate, corresponding to a lack of correlation between faecal carbohydrate excretion and lactate accumulation. An isolated increase in faecal L-lactate was observed in 6 of 13 patients with inflammatory bowel disease, whereas D-lactate was not increased without a simultaneous increase of the L-lactate isomer. In conclusion, the faecal lactate concentration was frequently increased in patients with inflammatory bowel disease and proctitis, occasionally increased in patients with severe malabsorption, and often normal in patients with quiescent inflammatory bowel disease or localized Crohn's ileitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Faecal DL-lactate concentration in 100 gastrointestinal patients. 820 86

Bile acid malabsorption has been shown to be associated with diarrhea in cases such as ileal resection Crohn's disease of the ileum, and radiation enteritis. The mechanisms of bile acid-induced diarrhea are not fully understood. Although the induction of colonic chloride secretion in response to bile acids has been extensively investigated, to date the direct effect of bile acids on intestinal chloride absorption has not been well defined. Therefore, the current studies were undertaken to investigate the effect of bile acids on the apical Cl(-)/OH(-) exchange process utilizing Caco2 monolayers as an in vitro cellular model. Cl(-)/OH(-) exchange activity was measured as DIDS-sensitive pH gradient-driven (36)Cl uptake. The results are summarized as follows: (i) short-term exposure (20 min) of Caco2 cells to taurodeoxycholate (TDC; 200 microM) and glycochenodeoxycholate (GCDC; 200 microM) acids significantly inhibited apical Cl(-)/OH(-) exchange (by approximately 60-70%); (ii) the Ca(2+) chelator BAPTA-AM blocked the inhibition by TDC; (iii) the reduction in Cl(-)/OH(-) exchange by TDC was reversed by the PKC inhibitor, chelerythrine chloride; (iv) functional and inhibitor studies indicated that TDC induced inhibition of Cl(-)/OH(-) exchange was mediated via the activation of the PKC beta I isoform; (v) the effect of TDC on apical Cl(-)/OH(-) exchange was completely blocked by the PI3 kinase inhibitor LY294002 (5 microM); and (vi) the PKA inhibitor, RpcAMP, had no effect on TDC induced inhibition of Cl(-)/OH(-) exchange. In conclusion, our studies provide direct evidence for inhibition of human intestinal apical Cl(-)/OH(-) exchange activity by bile acids via Ca(2+)-, PI3 kinase-, and PKC beta I-dependent pathways in Caco2 cells.
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PMID:Taurodeoxycholate modulates apical Cl-/OH- exchange activity in Caco2 cells. 1738 13

Bile acid malabsorption (BAM) is a common but an underestimated and often neglected sign of inflammatory bowel diseases (IBDs), especially those affecting the distal ileum. Clinically relevant BAM is most often present in patients with Crohn's ileitis and particularly in ileal-resected Crohn's disease patients. However, deterioration of bile acid (BA) metabolism occurs also in patients with IBD without ileal disease or in those in clinical remission, and the role of BAM in these patients is not well appreciated by clinicians. In a majority of cases, BAM in IBD is caused by impaired conjugated BA reabsorption, mediated by apical sodium/BA cotransporting polypeptide, localized at the luminal surface of the ileal enterocytes. As a consequence, numerous pathological sequelae may occur, including the malfunction of lipid digestion with clinical steatorrhea, impaired intestinal motility, and/or significant changes in the intestinal microflora environment. In this review, a detailed description of the pathophysiological mechanisms of BAM-related diarrhea is presented. Although BAM is present in a significant number of patients with Crohn's disease, its laboratory assessment is not routinely included in diagnostic workups, partially because of costs, logistical reasons, or the unavailability of the more sophisticated laboratory equipment needed. Simultaneously, novel findings related to the effects of the BA signaling pathways on immune functions (mediated through TGR5, cell membrane G protein-coupled BA receptor 1, nuclear farnesoid X receptor, nuclear pregnane X receptor, or nuclear vitamin D receptor) are discussed along with intestinal metabolism in its relationship to the pathogenesis of IBD.
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PMID:Bile acid malabsorption in inflammatory bowel disease. 2524 1