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

Dietary regimens in gastrointestinal disease can be divided into two categories: First, those of proven value include: (a) Disaccharide elimination for disaccharidase deficiency and exclusion of monosaccharides for sugar malabsorption; (b) gluten-free diet for celiac/sprue; (c) elimination of certain allergens because of food allergies; (d) protein restriction for portal systemic encephalopathy; (e) low-carbohydrate diet for dumping syndrome; (f) low-fiber diet for diarrheal syndromes; and (g) low-fat diet for steatorrhea. Second, controversial diets include a bland diet for acid-peptic disorders, a high-fiber diet for colonic disorders, and a low-fat diet for gallbladder disease. It is important to separate facts from fancy in the dietary management of patients with gastrointestinal disease and base the recommendations for a particular diet on available objective evidence, not on traditional or fashionable trends.
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PMID:Diet therapy in gastrointestinal disease: a commentary. 47 89

In young infants the clinical and investigative features of coeliac disease (CD) may be mimicked by other conditions such as cow's milk intolerance or secondary disaccharidase deficiency. It is therefore especially important to confirm a diagnosis of CD by later gluten challenge in such infants. Sixteen children in whom the diagnosis of CD had been made before the age of 12 months had an oral gluten challenge, after being treated with a gluten-free diet for periods of one month to 5 years. In 15 we showed intestinal xylose malabsorption by the one-hour blood xylose level within 1-28 days of starting ingestion of gluten. One child, with a persistently normal one-hour blood xylose test after gluten challenge for 3 months, had normal absorption and normal jejunal histology after 18 months on a gluten-containing diet; she is considered not to have CD. The one-hour blood xylose test before and after gluten challenge can help to confirm the diagnosis in coeliac patients diagnosed in infancy.
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PMID:Confirming persistence of gluten intolerance in children diagnosed as having coeliac disease in infancy. 114 65

Intestinal disaccharidase activities were determined in 294 jejunal biopsies obtained from 254 children with various disorders of the small bowel, and alkaline phosphatase activity was measured in 251 biopsies. In normal mucosa a broad range of enzyme activity was found corresponding with the data in the literature. A primary disaccharidase deficiency was observed in 5 children with congenital sucrase-isomaltase deficiency and in a 12-year-old Egyptian boy with acquired lactase deficiency. A secondary generalized depression of disaccharidase activity and a diminution of alkaline phosphatase activity existed chiefly in patients who had severe or moderate mucosal damage, also in active coeliac disease and during gluten loading, in protracted diarrhoea of infancy, chronic malabsorption of unknown origin and agammaglobulinemia. During remissions enzyme activities recovered together with mucosal improvement. Low levels of enzyme activities were also seen in some cases of protracted diarrhoea of infancy and chronic malabsorption of unknown origin although only mild mucosal lesions were demonstrated.
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PMID:[Intestinal disaccharidase and alkaline phosphatase activities of jejunal biopsies in small bowel diseases of children (author's transl)]. 127 85

Diarrhea "with" bacterial fermentation is characterized by acidic liquid stools containing high amounts of organic acids. Disaccharide malabsorption is the main cause. The mechanism of diarrhea is osmotic, and colonic fermentations reduce diarrhea. It is unlikely that starch malabsorption induces significant diarrhea, whereas a high-fiber diet is responsible for "physiologic" diarrhea. Colonic fermentations increase diarrhea due to organic colitis and the "motor diarrheas". They may be responsible for some intestinal symptoms in patients with irritable bowel syndrome. This does not imply a "hyperfermentative" process due to a hypothetical disturbance of colonic microbial ecology.
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PMID:[Colonic fermentation: physiological review and role in digestive pathology]. 218 79

The composition of specialized formulas for infants who experience malabsorption or formula intolerance is described in detail. The limited studies of efficacy, as well as a rationale for selecting an appropriate formula for infants with malabsorption or formula intolerance, are discussed. Infants with symptoms of diarrhea or emesis may have intolerance to milk lactose or milk protein. Soy formulas contain no lactose or cow's milk and should be the first choice of an alternative feeding because of cost and convenience. Some infants may be intolerant of soy as well as cow's milk protein. They benefit from formula containing neither cow's milk nor soy protein or from a specially processed milk-based formula containing hydrolyzed casein. A carbohydrate-free formula to which the desired type of carbohydrate is added may be helpful in the diagnosis and treatment of disaccharidase deficiencies and monosaccharide intolerances. Infants with extensive intestinal resections or intractable diarrhea may require specialized infant formulas with qualitative/quantitative modifications of fat, carbohydrate, and protein. Formulas with medium-chain triglycerides may be useful for infants with steatorrhea. "Preterm" formulas or milk from the infant's mother are preferred for preterm infants, since such feedings promote improved fat and carbohydrate absorption and better meet the infant's nutrient requirements.
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PMID:Specialized formulas and feedings for infants with malabsorption or formula intolerance. 351 Nov 29

Sucrase-isomaltase deficiency is an inherited disaccharidase deficiency that leads to malabsorption of sucrose, with resulting diarrhea and abdominal distention and cramps. We investigated the sucrose-splitting effect of viable yeast cells in eight children with congenital sucrase-isomaltase deficiency, by means of the sucrose hydrogen breath test. This test is based on the fact that hydrogen is released from the malabsorbed sucrose by the colonic microflora. We found that 0.3 g of lyophilized Saccharomyces cerevisiae, given after loading with 2 g of sucrose per kilogram of body weight, reduced hydrogen excretion in all patients, on average by 70 percent, in parallel with a complete loss or evident reduction of clinical symptoms. In vitro, lyophilized and fresh S. cerevisiae (fresh baker's yeast) had appreciable sucrase activity, a low isomaltase and maltase activity, and virtually no lactase activity. The sucrase activity was more inhibited by undiluted than by diluted gastric juice. We conclude that patients with congenital sucrase-isomaltase deficiency who intentionally or unintentionally consume sucrose can ameliorate the malabsorption by subsequently ingesting a small amount of viable yeast cells, preferably on a full stomach.
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PMID:Enzyme-substitution therapy with the yeast Saccharomyces cerevisiae in congenital sucrase-isomaltase deficiency. 355 46

The activities of jejunal mucosal peptide hydrolases for glycylglycine, glycyl-L-leucine and L-leucylglycine, were assayed in 37 patients. Eight patients, four of whom had Crohn's disease, were found to have a marked reduction in the activity of glycylglycine dipeptidase and, to a lesser extent, of the other two hydrolases. Although absorption of glycine in the two groups was similar, there was malabsorption of glycylglycine in the patients with reduced dipeptidases as shown by a flat absorption curve. The importance of peptide hydrolases of small-intestinal mucosa in the final digestion of proteins, and the implications of peptidase deficiency in disease states is discussed. It is concluded that significant peptidase deficiency may occur even when the mucosa is otherwise histologically completely normal, similar to some states of disaccharidase deficiency described in recent years.
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PMID:Dipeptidase deficiency and malabsorption of glycylglycine in disease states. 557 98

An oral sucrose tolerance test was performed in a group of 103 children, aged between 3 months and 15 years because of episodic diarrhea and/or abdominal pains. Sucrose malabsorption defined as an abnormal increase in expired hydrogen, was found in only 3 children who suffered from congenital sucrase-isomaltase deficiency. This 1% incidence of sucrose malabsorption was lower than the incidence of lactose malabsorption found in this group (33%). Mean rise in blood glucose during the sucrose test was higher (3.4 +/- 1.4 vs. 2.4 +/- 1.2 mmol/l, p less than 0.0001) and the occurrence of false flat blood glucose curves was lower (3% vs. 12.8%, p less than 0.05) than during the lactose test. These findings are consistent with the higher sucrase activity in the small bowel mucosa compared to lactase. In contrast to the lactose tolerance test, sucrose tolerance test should not be used as a screening procedure for secondary disaccharidase deficiency in children.
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PMID:Diagnostic value of sucrose tolerance test in children evaluated by breath hydrogen measurement. 736 16

To determine the prevalence of short polymers of glucose and starch malabsorption caused by small intestinal glucoamylase deficiency in children with chronic diarrhea, we studied small bowel biopsy specimens from 511 children (aged 1 month to 9 years) with chronic diarrhea evaluated at 54 medical centers. Glucoamylase and disaccharidase (lactase, sucrase, maltase, and palatinase) enzyme assays were performed. Of the 511 children, 15 had glucoamylase deficiency. Six who had significant small intestinal mucosal injury and disaccharidase deficiencies were defined as having secondary glucoamylase deficiency; the other nine patients with normal mucosal morphologic features were defined as having primary glucoamylase deficiency. Secretin tests showed normal pancreatic amylase values for age in all seven children tested. Four of them had abnormal findings on tolerance tests for starch and short polymers of glucose (rise in blood glucose concentration: < 20 mg/dl) and reducing substances in stools, and three of these four had symptoms of intolerance (abdominal distention, flatulence, and diarrhea). All seven patients responded to a starch elimination diet. After reintroduction of a starch diet, diarrhea recurred in four patients; this was alleviated 48 hours after reelimination of starch. We conclude that intestinal glucoamylase deficiency is present in some patients with chronic diarrhea.
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PMID:Small intestinal glucoamylase deficiency and starch malabsorption: a newly recognized alpha-glucosidase deficiency in children. 815 67

Hydrogen breath tests (H2 BT) have been used extensively to investigate intestinal disaccharidase deficiencies. A potentially useful test for assessing intestinal absorptive function, the H2 BT with D-xylose (H2 BT-D-xylose), has received scant attention. We report here the results of our investigation of this test in 45 patients. Fifteen patients had proved malabsorption that was due to nontropical sprue in nine, and to lymphoma, Whipple's disease, or giardiasis in the remainder. Nine patients had small-bowel bacterial overgrowth secondary to either postsurgical sequelae or intestinal dysmotility. Twenty-one patients with irritable bowel syndrome and 21 healthy individuals served as control groups. All participants ingested 25 g of D-xylose, and alveolar breath samples were obtained thereafter at 30 min intervals for 5 hr. Breath H2 was measured by chromatography. Basal H2 production, peak change (delta) and area under the curve (AUC) were calculated. Simultaneously, 5-hr urinary excretion of D-xylose was measured by colorimetry and served as the reference test. In healthy individuals, D-xylose ingestion increased H2 production (delta = 5.8 +/- 1.4 ppm, P < 0.001). Changes were similar in patients with the irritable bowel syndrome. In contrast, the increase was of a much greater magnitude in the malabsorption group (delta = 49.9 +/- 7.2 ppm, P < 0.001 vs healthy controls). AUC analysis yielded comparable results. Test performance analysis showed that, in malabsorption the H2 BT-D-xylose had a sensitivity index of 0.86, which was identical to that of the urinary D-xylose test. Specificity was 1 and 0.95, respectively; and predictability 1 and 0.93, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potential usefulness of hydrogen breath test with D-xylose in clinical management of intestinal malabsorption. 842 44


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