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

The pH of the stool and the amount of reducing substances present were observed in 51 normal neonates aged 5 to 8 days. A stool pH of 5 or less was found in 6, 4 of whom were exclusively breast fed. Reducing substances, 0-5% or more, were found in the stools of 16. Stool chromatography in 13 showed lactose, glucose, galactose, or a variable combination of these sugars--that is, a pattern consistent with lactose malabsorption. The stools of 3 infants contained oligosaccharides or maltose only. Chromatography of urine from 60 normal neonates showed detectable sugars in 11 but only 3 had levels above 50 mg/100 ml.
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PMID:Stool and urinary sugars in normal neonates. 0 29

The suitability of the simultaneous azocoupling reaction with 1-naphthyl-beta-D-glucoside and hexazonium-p-rosanilin in the detection of the activity of lactase (or lactase-beta-glucosidase complex) in jejunal biopsies of patients with various forms of the malabsorption syndrome was tested. Results were compared with those obtained with the indigogenic method using 4-Cl-5-Br-3-indolyl-beta-D-fucoside which is the method of choice. Both methods gave identical results as far as the relative intensity of the brush border staining was concerned. The azocoupling method applied in unfixed cold microtome sections can be recommended for the routine diagnostics of the malabsorption syndrome when the indolyl substrate is not available.
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PMID:Suitability of the azocoupling reaction with 1-naphthyl-beta-D-glucoside for the histochemical demonstration of lactase (lactase-beta-glucosidase complex) in human enterobiopsies. 5 35

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

General evidence of malnutrition such as loss in body weight associated with intestinal parasitism has been attributed to decreased food intake, to intestinal malabsorption, and to change in host basal metabolism. To establish the relative importance of these factors in this regard, rats with trichinosis were studied. The weights of infected and uninfected animals were followed after being placed on one of three feeding regimens for 1 week--stock diet ad libitum, intraduodenal nutrition, and intravenous nutrition. Infected rats on a stock diet lost weight whereas those on the other two regimens maintained the same weight pattern as uninfected counterparts. The maintainance of body weight occurred despite alterations at the level of the intestinal brush border as indicated by a depression of intestinal disaccharidase activities (sucrase and lactase) and by reduction of monosaccharide absorption (measured as accumulation of beta-methyl glucoside) in the proximal, heavily infected region of the small intestine. There was no compensatory increase in enzyme activity nor in the absorptive capacity in the distal gut. Results support the conclusion that inadequate oral food intake rather than changes in basal metabolism or intestinal pathophysiology accounts for weight loss during the intestinal phase of infection.
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PMID:Enteral and parenteral feeding to evaluate malabsorption in intestinal parasitism. 11 Jan 62

The effect of a new complex oligosaccharide exhibiting potent inhibitory action on alpha-glucoside hydrolases on intestinal absorption of sucrose in man was tested by constant in vivo perfusion of the jejunum. At concentrations of 4.65 or 15.5 X 10(-6)M the alpha-glucosidehydrolase inhibitor (alpha-GHI) markedly inhibited absorption of glucose from sucrose and absorption of sodium and water. Oral administration of the alpha-GHI resulted as well in depression of solute, sodium, and water absorption. This new compound can serve as an interesting tool to induce carbohydrate malabsorption by inhibition of final digestion and may possibly be of beneficial therapeutic effect in dietary control of diabetes or obesity.
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PMID:Effect of alpha-glucosidehydrolase inhibition and intestinal absorption of sucrose, water, and sodium in man. 38 40

Respiratory hydrogen excretion was measured during tolerance tests with lactose, glucose plus galactose, and skim milk in 52 children, 4 to 15 years of age. Ten children appeared to be lactose-malabsorbers, as reflected by increased respiratory hydrogen excretion after administration of 2 g lactose per kilogram, maximum 50 g. Skim milk, equivalent to 0.5 g lactose per kilogram was administered to all lactose-malabsorbers. Eight children were tolerant and two children were "intolerant" for this physiological amount of lactose when administered as skim milk. Disaccharidase activities of jejunal biopsies were determined in all 10 children with lactose malabsorption. Lactase activity was deficient in nine children and normal in one child. The increase of blood glucose during the lactose tolerance test did reflect lactose malabsorption less accurately than the respiratory hydrogen excretion.
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PMID:Respiratory hydrogen excretion as a parameter for lactose malabsorption in children. 41 7

The influence of malabsorption of lactose, as a result of primary lactase deficiency, on the absorption of the nutrients in milk was tested in four healthy controls and four subjects with lactase deficiency. An ileal perfusion technique was used to quantify arrival in the ileum of nutrients and a nonabsorbable marker (polyethylene glycol, PEG 4000) ingested as a test meal of milk. The meal was 250 ml of whole milk or milk in which the lactose had been hydrolyzed to glucose and galactose. In the fasting state, ileal flow of volume, protein, carbohydrate, and electrolytes was small and not different in controls and lactase-deficient subjects. Ileal flow increased in all subjects after the test meal of milk; more fluid and nutrient was recovered from the ileum in lactase-deficient subjects after whole milk than in control subjects or in lactase deficiency after hydrolyzed milk. Two deficient subjects showed marked malabsorption of lactose (35 and 50%); two did not. Protein, calcium, magnesium, and phosphorus were also recovered from the ileum in greater quantities in lactase deficients after whole milk. However, apart from decreased absorption of lactose, the nutritional consequences of malabsorption in association with primary lactase deficiency in adults are probably minimal.
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PMID:Absorption of nutrients in lactase deficiency. 58 2

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

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

Enprostil, a synthetic E2 prostaglandin, was administered in a dose of 5 micrograms/kg body weight by gastric tube to rats for 14 days following abdominal irradiation with a single dose of 600 cGy from a 137Cs source. Enprostil prevented the body weight loss and the reduced food intake observed in irradiated animals given placebo, and also prevented the irradiation-associated decline in the mucosal weight and surface area of the ileum. Enprostil given to nonirradiated animals reduced the maximal transport rate (Vmax) and the apparent Michaelis constant (Km*) for the ileal uptake of D-glucose, but did not prevent the irradiation-associated decline in the ileal uptake of glucose. Thus, there is a dissociation of the effects of Enprostil on the morphological and the absorptive properties of the intestine. It is concluded that a 2-week course of a daily oral dose of E2 prostaglandin begun shortly after a single exposure to nonlethal abdominal irradiation prevents the radiation-associated reduction in the intestinal mucosal surface area and the animal's body weight, but does not prevent the malabsorption of glucose.
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PMID:Two weeks of oral synthetic E2 prostaglandin (Enprostil) improves the intestinal morphological but not the absorptive response in the rat to abdominal irradiation. 128 67


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