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)

Nine children with sucrase-isomaltase deficiency were assessed up to 10 years after diagnosis. All children continued to have episodes of diarrhoea associated with sucrose ingestion. Sucrose tolerance tests showed that malabsorption of sucrose persists into adolescence. Three older patients were unaware of their condition and were eating normal diets with unrestricted amounts of sucrose. They complained of gastrointestinal symptoms which improved after sucrose restriction.
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PMID:Sucrase-isomaltase deficiency. A follow-up report. 70 8

Sugar alcohols are incompletely digested in the human small intestine. The residual amounts reaching the colon are digested by colonic bacteria or excreted in stools. Clinical tolerance and energy value of sugar alcohols are related to their respective rates of digestion in the small intestine and the colon. Six healthy volunteers were tested in 5 periods during which they ingested 10 g lactulose, and then, in a random order, an iso-osmotic solution of 20 g isomalt, sorbitol, maltitol, and lactitol. The fraction of sugar alcohols absorbed in the small intestine was evaluated by comparing the amounts of hydrogen excreted in breath for 8 h after the ingestion of lactulose and of sugar alcohols. Energy value of sugar alcohols was determined knowing the amounts absorbed in the small intestine and digested in the colon. Tolerance to the sugar alcohols was good in all volunteers, and not different between sugar alcohols. The mean percentage of malabsorption in the small intestine was significantly higher for lactitol (84 +/- 14 percent, m +/- SEM) than for maltitol and isomalt (44 +/- 7 and 40 +/- 7 percent), its energy value (2.3 +/- 0.3 kcal/g) was significantly lower than the energy value of maltitol (3.1 +/- 0.1 kcal/g, P less than 0.05); whereas those of sorbitol and isomalt were close (2.7 +/- 0.2 and 2.8 +/- 0.1 kcal/g, respectively). In spite of these differences, our results suggest that in our experimental conditions, bacterial digestion of the sugar alcohols reaching the colon was complete, and did not affect their clinical tolerance.
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PMID:[Clinical tolerance, intestinal absorption, and energy value of four sugar alcohols taken on an empty stomach]. 178 48

In two randomized, placebo-controlled, double-blind studies, the efficacy, duration of action and tolerability of a single morning dose of 25, 50, and 100 mg miglitol (BAY m 1099), an absorbable inhibitor of intestinal alpha-glucosidases, were assessed after repetitive sucrose or maize-starch loads (50 g of carbohydrates in 400 ml of water each at 08.00, 12.00, and 17.00 h). With sucrose, miglitol reduced the postprandial rise in blood glucose, serum insulin and serum gastric inhibitory polypeptide concentrations at any dosage. This effect was dose-dependent and confined to the first carbohydrate load in the morning, thus indicating the duration of alpha-glucosidase inhibition of less than 4 h. Sucrose malabsorption, indicated by breath hydrogen responses, occurred dose-dependently with 50 and 100 mg, but not with 25 mg of miglitol. Similarly, symptoms of carbohydrate malabsorption were absent with 25 mg of the inhibitor and mild to moderate after 50 and 100 mg of miglitol. With starch as the substrate, BAY m 1099 led to a significant amelioration of glycemic and hormonal rises after the first meal, but not thereafter. A numerical dose dependency was recognized, but this was not significant at the 5% level. Symptoms of carbohydrate malabsorption were absent with 25 mg and negligible with 50 mg BAY m 1099, but occurred almost regularly with the 100-mg dose. Breath hydrogen concentrations increased gradually with the dose of miglitol administered. A single morning dose of 25-100 mg of miglitol thus may be useful for the control of postprandial hyperglycemia after breakfast. Due to the duration of action of less than 4 h, this substance should be given with the three main meals.
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PMID:Inhibition of glycemic and hormonal responses after repetitive sucrose and starch loads by different doses of the alpha-glucosidase inhibitor miglitol (BAY m 1099) in man. 178 28

The objective of this study was to investigate the mechanisms involved in intestinal absorption of fructose. The results indicate that adult rats readily absorbed 0.4 g of fructose, an amount equivalent to 1.4-1.6 g fructose/kg body wt. Acute malabsorption of fructose occurred with doses greater than 0.6 g (2.1-2.4 g/kg body wt). Continued exposure to dietary fructose resulted in a decrease in the evidence of colonic fermentation. Glucose or galactose administered with fructose enhanced the absorption of fructose. The greatest absorption was observed when equal amounts of fructose and glucose were given simultaneously. If glucose was ingested as a polymer (starch or dextrin), the stimulatory effect was dependent on the digestibility of the polymer. Sucrose given with the fructose and glucose diminished the absorption of fructose. Acarbazone, a specific inhibitor of alpha-glucosidases, including sucrase, also inhibited the facilitating effect of glucose and galactose in absorption of fructose. These results give evidence for joint absorption of the two monosaccharides, fructose and glucose.
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PMID:Intestinal absorption of fructose in the rat. 206 11

In a population study on the western coast of Greenland the incidence of sucrose malabsorption was estimated by means of sucrose tolerance tests in 190 persons. Small-intestinal disaccharidase activity was estimated in 19 patients. Sucrose malabsorption was present in 10.5% of the cases studied-a surprisingly high figure and much higher than the incidence reported elsewhere in the world. This incidence is, however, lower than that of lactose malabsorption in Greenland Eskimos (54%). In contrast to lactose malabsorption, sucrose malabsorption is present from birth; this may have important clinical implications since chronic diarrhoea and malnutrition are fairly common during infancy in Greenland.
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PMID:Sucrose malabsorption in Greenland. 501 65

Ten patients were identified at Jackson Memorial hospital/University of Miami Hospitals and Clinics with enteric coccidial infection due to Cryptosporidium spp. or Isospora belli. All had the acquired immunodeficiency syndrome as manifested by Kaposi's sarcoma or multiple opportunistic infections, or both. They presented with profuse diarrhea associated with weakness, anorexia, and weight loss. Routine examinations of stools for eggs and parasites as performed by the hospital laboratory were negative in all patients. Sugar flotation and modified acid fast techniques were used in the Tropical Disease Laboratory to identify oocysts of Cryptosporidium spp. in stools of seven patients. Malabsorption, characterized by a low 5-hour D-xylose and positive fecal fat, was observed in 6/6 of these patients. In three other patients Isospora belli oocysts were identified in stool specimens or via a duodenal string test. Spiramycin was the only drug found to be effective in treating patients with cryptosporidiosis. Patients with Isospora belli responded to a prolonged course of trimethoprim-sulfamethoxazole.
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PMID:Enteric coccidiosis among patients with the acquired immunodeficiency syndrome. 633 48

Sucrose breath hydrogen tests were performed on 7 children with proved sucrase isomaltase deficiency. All children had raised breath hydrogen excretion. The amount of hydrogen produced and symptoms experienced increased with increasing sucrose loads. The sucrose breath hydrogen test appears to be a reliable indicator of sucrose malabsorption in sucrase isomaltase deficiency.
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PMID:Breath hydrogen test and sucrase isomaltase deficiency. 661 73

Sucrose absorption was studied by the Breath Test method (BTH) in 41 infants presenting with acute diarrhea. In 28, studies were performed in children treated orally with a 40% sucrose solution. Malabsorption was demonstrated in 8 cases. In 36 infants, sucrose loading test (1 g/kg) was carried out between the 3rd and the 7th days of the diarrhea: malabsorption was present in 9 cases. Malabsorption was transitory in all children. The frequency of this sucrose malabsorption during acute diarrhea is not sufficient to prevent the therapeutic use of sucrose solution, but differs from the usual lack of sucrose malabsorption in chronic diarrhea, even, as shown here, in children with complete villous atrophy.
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PMID:[Breath test study of sucrose absorption in infants with acute diarrhea ]. 712 38

[14C]Sucrose absorption was studied in 4 healthy controls and 4 patients after jejunoileal bypass using an ileal perfusion technique which made it possible to distinguish 14C-absorption in the small bowel from that occurring in the colon. Healthy controls failed to absorb 2--4% of a 50-g dose of [14C]sucrose in the small bowel; however, virtually none of the [14C] appeared in feces in a dialyzable form with appreciable osmotic activity. In bypass patients, the small bowel failed to absorb 29--84% of the 50-g dose of [14C]sucrose. Approximately two-thirds of the nonabsorbed [14C] was in the form of sucrose and the remainder was nearly all present as monosaccharides. A mean of only 42% of the [14C] Not absorbed in the small bowel appeared in the feces and only about one-third of this fecal [14C] was in a dialyzable form with appreciable osmotic activity. Thus, the colon plays an important role in carbohydrate malabsorption by salvaging carbohydrate and reducing osmotic activity of the nonabsorbed sugar. This conlonic function appears to depend upon bacterial metabolism of the carbohydrate, and individual variations in diarrhea and weight loss associated with carbohydrate malabsorption could reflect individual differences in the bacterial flora of the colon.
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PMID:Colonic conservation of malabsorbed carbohydrate. 735 Dec 83

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


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