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)

Current requirements for the lactose breath hydrogen test (LBHT) include serial expired air samplings and multiple hydrogen (H2) determinations. One hundred thirty-two consecutive LBHTs were evaluated to determine whether multiple samplings are indeed necessary for detection of lactose malabsorption. Expired air samples were collected at 0, 30, 60, 90, 120, 150, and 180 min following ingestion of lactose. Fifty-five LBHTs were positive for lactose malabsorption. All tests showed abnormally elevated breath H2 concentrations at 120 min. The mean value of the change in parts per million (delta ppm) of H2 at 120 min (51.1 +/- 4.7 SEM) was higher than at any other time point. If only the 120-min samples were examined without subtracting the initial concentrations, four of the 77 negative tests (5.2%) would have been falsely positive. Thus, the values of H2 at 0 and 120 min were sufficient to define lactose malabsorption in all cases. We conclude that just as a single blood sample now suffices for determining xylose malabsorption, so expired air sampling at only 0 and 120 min during the LBHT is a reliable method for detecting lactose malabsorption and diminishes the need for acquiring and analyzing multiple samples.
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PMID:Two-hour lactose breath hydrogen test. 394 36

Magnesium deficiency may play a role in the pathogenesis of atherosclerosis, cardiac arrhythmias, and coronary spasm. Because less than 1% of magnesium (Mg) is extracellular, the serum magnesium (sMg) does not always accurately reflect intracellular Mg stores. To determine the frequency of Mg deficiency in patients with cardiovascular disease, we measured blood mononuclear cell Mg content (mMg) and sMg concentrations in 104 unselected patients admitted to our intensive cardiac care unit (CCU). Twenty-seven normal healthy controls and 33 hypomagnesemic patients with chronic alcoholism and/or malabsorption syndrome served as reference groups. The sMg concentration in the CCU patients was 2.05 +/- 0.03 mg/dl (mean +/- SEM), and did not differ from normal controls (mean 2.01 +/- 0.03 mg/dl). Only 8 of 104 CCU patients were hypomagnesemic (7.7%). mMg in the CCU patients, however, was significantly lower than in the normal controls (1.15 +/- 0.02 micrograms/mg protein and 1.34 +/- 0.02 micrograms/mg protein respectively, p less than 0.001). Fifty-three percent (55 of 104) of CCU patients had mMg contents less than 1.119 micrograms/mg protein, i.e., below that of the lowest normal control. mMg was significantly lower in those patients with congestive heart failure (mMg = 1.08 +/- 0.03 micrograms/mg protein) when compared to those patients without congestive heart failure (1.23 +/- 0.02 micrograms/mg protein, p less than 0.001). We conclude that the incidence of intracellular Mg deficiency in patients with cardiovascular disease is much higher than the sMg would lead one to suspect, and may contribute to clinical cardiovascular morbidity.
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PMID:Low blood mononuclear cell magnesium in intensive cardiac care unit patients. 395 55

A technique was developed to quantitate the absorption of ingested carbohydrate by means of continuous measurements of pulmonary H(2) excretion. This technique is based on the observation that H(2) is produced in the colon when carbohydrate is fermented by colonic bacteria, and this H(2) is then excreted by the lungs. The quantitative relationship of pulmonary H(2) excretion to unabsorbed carbohydrate was studied in nine subjects. After ingestion of 6.5, 13, and 26 g of lactulose (a nonabsorbable disaccharide), H(2) excretion increased linearly, averaging (+/-1 SEM) 13+/-3.5, 23+/-7.2, and 49+/-7 ml per 2 hr. Because of consistent individual differences in H(2) excretion per gram of lactulose, the variability of this linear response was less in a given subject, with the H(2) excretion after 6.5 g and 26 g lactulose dosages averaging 55+/-4.2% and 214+/-16% of that observed after the 13 g dose. It was further demonstrated with fecal homogenates, as well as in rats after direct intracecal instillation of carbohydrate, that there was no significant difference in the rate of H(2) formation from lactulose as compared with the normally ingested sugars. Thus, a subject's H(2) excretion after a 13 g dose of lactulose can be used as a standard to convert H(2) excretion after ingestion of other carbohydrates into grams of carbohydrate not absorbed. Application of this technique to seven partially gastrectomized patients indicated all subjects malabsorbed a portion of a 100 g dose of glucose whereas six of seven completely absorbed a 25 g dose. Malabsorption of physiologic quantities of various carbohydrates was clearly demonstrated in one subject. This technique appears to provide quantitative information on carbohydrate malabsorption not readily obtained by presently available techniques.
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PMID:Use of pulmonary hydrogen (H 2 ) measurements to quantitate carbohydrate absorption. Study of partially gastrectomized patients. 502 Apr 34

There is evidence for both humans and rats that malnutrition frequently occurs when ethanol is chronically ingested. Small bowel 14C-labelled glucose absorption was measured with an ex vivo system in which the small bowel of the rat was surgically removed and then arterially perfused with an artificial medium. Glucose absorption for a control group of seven rats was 248 +/- 8 microM/min/gm dry weight of small bowel (mean +/- SEM). This was significantly greater than the value 112 +/- 12 microM/min/gm dry weight (P less than 0.005) for a group of five rats in which a competitive inhibitor of glucose absorption, phlorizin (0.2 mM), was added to the bowel lumen. In the presence of 3% ethanol within the gut lumen of five rats, glucose absorption was also reduced (to 131 +/- 12 microM/min/gm dry weight) compared to absorption in the control group (P less than 0.005). The calculated amount of glucose absorbed was corrected for metabolism to lactate and carbon dioxide. We conclude that both phlorizin and ethanol inhibit glucose absorption in the isolated and perfused small bowel of rats and that probably at least part of the malnutrition in ethanol-fed rats is due to glucose malabsorption.
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PMID:Ethanol inhibition of glucose absorption in isolated, perfused small bowel of rats. 641 May 24

Endogenous steatorrhea has only been evaluated in patients with non-pathological digestive tract. We decided, therefore, to study this parameter in 22 consecutive patients submitted to total parenteral nutrition for severe gastrointestinal diseases. The determination of steatorrhea, creatorrhea, and fecal clearance of alpha 1-antitrypsin was performed by three days stool collections. After 10 days of parenteral nutrition, 13 of the 22 patients still had measurable stool losses and 106 fecal collections were done. In these 13 patients, fecal weight was 610 +/- 130 g.d-1, (mean +/- SEM), steatorrhea was: 3.1 +/- 0.4 g.d-1, creatorrhea was: 1.7 +/- 0.6 g.d-1, alpha 1-antitrypsin clearance was: 58 +/- 13 ml.d-1 (N less than 10 ml.d-1). The mean endogenous steatorrhea was therefore 5 fold larger than normal and creatorrhea 1.8 fold larger than normal. This discrepancy could be due to metabolism of nutrients by colonic bacterial flora. The comparison of patients with and without increased endogenous losses showed significant differences in the mean number of intestinal lesions (1.4 +/- 0.3 versus 0.5 +/- 0.2) and in the presence or absence of ileal involvement (p less than 0.05). A positive correlation was found between steatorrhea and stool weight but not between steatorrhea and creatorrhea or fecal clearance of alpha 1-antitrypsin. This first study of pathological endogenous steatorrhea does not suggest a relationship of this parameter with protein losing enteropathy. The main contribution to increased endogenous losses may be related to increased epithelial cell renewal of the intestine associated with malabsorption. The role of bacterial overgrowth in the gut cannot be ruled out by the present data.
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PMID:[Endogenous steatorrhea during total parenteral nutrition. Study of 22 patients with gastrointestinal diseases]. 642 Feb 23

Fat absorption was studied in 11 Cystic Fibrosis patients and 6 controls by measuring a) fecal fat excretion and b) serum turbidity using a nephelometer between 0 and 2 hours after a butter-fat load. Cystic Fibrosis patients showed a mean +/- SEM fecal fat excretion of 21.6 +/- 5.5%, and controls a mean of 2.7 +/- 0.45%, of the dietary fat. The turbidity change expressed as delta turbidity showed a mean value of 1.37 +/- 0.57 in Cystic Fibrosis patients and 31.8 +/- 5.7 in controls. Fecal fat excretion method showed a good negative correlation with the butter fat method. The butter fat absorption method was also compared with fecal fat excretion in rats with induced malabsorption and control rats. The results obtained were comparable to those in the patients. The method described here is rapid and can be performed with small blood volumes and therefore may be suitable to study fat malabsorption in pediatric patients.
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PMID:A study of fat absorption in cystic fibrosis patients and controls by a rapid micro procedure: a comparison with fecal fat excretion method. 665 87

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

Hydrogen produced by colonic bacteria and excreted in breath is a useful index of carbohydrate malabsorption. Since colonic contents are often acidic in individuals with carbohydrate malabsorption and in normal newborns, we determined the effect of colonic acidification on H2 production. Acidification of colonic contents by dietary means significantly reduced excess breath H2 excretion from 55.4 +/- 11.1 (SEM) to 12.2 +/- 3.1 ml/4 h (P less than 0.05) after administration of 0.3 g/kg of the nonabsorbable sugar lactulose to five normal adult subjects. Similarly, the breath H2 response to lactose was reduced or eliminated in two proven lactose malabsorbers after acidification. The correlation between pH and H2 production from carbohydrate was further investigated in adults and neonates, using an in vitro fecal incubation system. Glucose disappearance and H2 production were pH dependent and highly correlated (r = 0.94) in the pH range 5.5-7.6. Maximal production of H2 from glucose by fecal incubates occurred at pH 7.0-7.45. Inhibition of H2 production from carbohydrate occurred at acid pH. H2 per hour from glucose at pH 6.2 and 5.5 averaged 60.2% and 24.2%, respectively, of that produced at neutral pH. Rapid reversal of pH-induced inhibition by neutralization indicated a metabolic, rather than a bactericidal process. The observations indicate that the breath H2 response to malabsorbed carbohydrate is affected by colonic pH. It appears that the efficiency of bacterial carbohydrate metabolism in the colon is pH dependent.
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PMID:Role of pH in production of hydrogen from carbohydrates by colonic bacterial flora. Studies in vivo and in vitro. 719 87

We assessed ileal functional integrity, as reflected in the capacity to reabsorb the bile acid, cholylglycine, by sequential measurement of postprandial serum levels of this compound. A consistent increase in cholylglycine concentration (mean +/- SEM, peak above fasting baseline = 1.86 +/- 0.14 microM) occurred in eight normal children. Five patients with ileal resection and two with primary bile acid malabsorption had a minimal postprandial increase (0.27 +/- 0.08 microM; P less than 0.005 vs controls) and excess bile acid loss in feces. Similarly, in seven patients with Crohn disease involving the ileum the postprandial increase (0.38 +/- 0.06) was less than controls (P less than 0.001). In eight patients with cystic fibrosis, the administration of pancreatic enzymes normalized the blunted response demonstrated when enzymatic therapy was interrupted suggesting an intact ileal active transport mechanism. Meal-stimulated response of serum cholylglycine concentration is a sensitive indicator of altered ileal integrity and bile acid malabsorption due to ileal resection, inflammation, or dysfunction.
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PMID:Serum bile acid response to a test meal stimulus: a sensitive test of ileal function. 735 62

Honey contains fructose in excess of glucose, which may lead to incomplete fructose absorption associated with abdominal symptoms and/or diarrhea. This hypothesis was investigated in 20 healthy volunteers (13 males, 7 females) with a mean (+/- SD) age of 35.9 +/- 12.1 y. Each subject drank the following aqueous solutions in random order: 20 g lactulose, 100 g honey, 50 g honey, and 35 g each of a glucose and fructose mixture. The breath-hydrogen concentration was measured every 15 min for 6 h. Semiquantitative estimates of carbohydrate malabsorption were assessed with lactose as a nonabsorbable standard. Breath-hydrogen concentrations increased by 52 +/- 6, 30 +/- 4, 20 +/- 3, and 4 +/- 1 ppm (mean +/- SEM) after each of the four test solutions, respectively. The estimated carbohydrate malabsorption was 10.3 +/- 1.8, 5.9 +/- 1.2, and 0.5 +/- 0.2 g after 100 g honey, 50 g honey, and the glucose-fructose mixture, respectively (F[2,57] = 16.05, P < 0.001). Within 10 h after the ingestion of 100 g honey, 50 g honey, and the glucose-fructose mixture, six, three and none of the volunteers, respectively, reported loose stools (chi 2 = 7.1, df = 2, P < 0.03). The results of this study suggest that carbohydrate malabsorption after ordinary doses of honey is frequent in healthy adults and may be associated with abdominal complaints. Honey may have a laxative effect in certain otherwise healthy individuals, probably because of incomplete fructose absorption.
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PMID:Honey may have a laxative effect on normal subjects because of incomplete fructose absorption. 749 82


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