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 aim of the work was to examine the validity of the cultural-historical hypothesis about the origin of lactase deficiency in adults on an example of the populations of the Finno-Ugric group. Examination included 692 healthy subjects aged 20-50 years. It was established that the incidence of lactase deficiency among relevant ethnic groups was identical. The data obtained support the validity of the cultural-historical hypothesis about lactase deficiency (selective lactase malabsorption).
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PMID:[Lactase deficiency in aboriginal inhabitants of the Mordovian and Karelian ASSR]. 253 Mar 93

In a retrospective study, jejunal mucosal disaccharidase and alkaline phosphatase activities have been investigated in 40 controls and patients with proven celiac sprue (n = 26), lactase deficiency (n = 26), osteoporosis or osteomalacia (n = 16), chronic pancreatitis (n = 12), giardiasis (n = 7), or Crohn's disease (n = 7). Apart from a nonselective reduction of mucosal enzyme activities in the sprue syndrome and a selective reduction of lactase activity in the patients with primary lactase deficiency, assays of mucosal disaccharidases revealed only inconstant or slight deviations from the control group and were not of diagnostic significance for any of the above-mentioned disorders. Isolated forms of enzyme deficiencies other than lactase deficiency, such as sucrase-isomaltase or trehalase deficiency were not present among 168 investigations carried out from 1972-1982. It is concluded that assay of small intestinal disaccharidase or alkaline phosphatase activities does not expand the diagnostic impact of morphological examination of small bowel biopsy specimens and modern noninvasive methods for the detection of carbohydrate malabsorption. Thus, the method does not appear a necessary or relevant investigation in routine clinical practice.
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PMID:Is the assay of disaccharidase activity in small bowel mucosal biopsy relevant for clinical gastroenterologists? 274 34

Individuals with sufficient intestinal lactase hydrolyze ingested lactose to galactose and glucose and these monosaccharides are absorbed. Lactose is not digested completely when intestinal lactase activity is low and the disaccharide is malabsorbed. Breath hydrogen excretion after lactose ingestion is used commonly to diagnose lactose malabsorption. However, no direct tests are currently used to assess lactose absorption. We tested a new method of assessing lactose absorption in 26 healthy individuals. Each subject ingested 50 g of lactose. Participants were evaluated for lactose malabsorption using a standard 3-h breath hydrogen test. In addition, the urinary excretions of galactose, lactose, and creatinine were quantitated for 3-5 h after lactose ingestion. On the basis of breath hydrogen analysis after lactose ingestion, 12 individuals were lactose malabsorbers (defined as a rise in the breath hydrogen concentration of greater than 20 parts per million above the baseline value). The 14 subjects who did not malabsorb lactose by breath hydrogen testing (defined as a rise in the breath hydrogen concentration of less than or equal to 20 parts per million above the baseline value), had significantly more galactose in their urine 1, 2, and 3 h after lactose ingestion than lactose malabsorbers. The ratio of excreted lactose to excreted galactose was significantly decreased in lactose absorbers compared with lactose malabsorbers (p less than 0.001). Determination of the ratio of urinary galactose to urinary creatinine separated lactose absorbers from lactose malabsorbers completely (p less than 0.001). We conclude from this study that the determination of urinary galactose, urinary lactose/galactose ratio, and urinary galactose/creatinine ratio may be used to assess lactose digestion and absorption in healthy adults.
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PMID:Assessment of lactose absorption by measurement of urinary galactose. 277 42

The authors present the cases of 4 children who suffered from saccharose-isomaltose malabsorption. The clinical symptoms developed following artificial feeding. The diagnosis was made by the histological examination of small intestine samples and with the simultaneous measurement of disaccharide enzyme activity. The histological picture and activity of lactase enzyme were practically normal. The saccharose H2 breath test gave only in 1 case positive result. The treatment of the children required saccharose-free diet. The tolerance showed no improvement during the treatment.
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PMID:[Current diagnostic method for saccharose-isomaltose malabsorption]. 278 45

The tests with lactose loading followed by the assay of blood sugar were conducted in 500 normal subjects, aged from 18 to 89 years, and 262 patients with gastro-intestinal diseases, aged from 25 to 55 years. When lactose malabsorption was detected, aspiration biopsy of the small intestine mucosa was performed followed by the study of the structure and the level of a number of disaccharidases (lactase, maltase, saccharase). Lactose malabsorption was detected in 72 (14.4%) out of 500 normal subjects (10.6%--aged 18-59, and 20%--aged 60-89 years), among them there were 12.5% of Russians, 13% of Byelorussians and 5.8% of Ukrainians (aged 25-55 years). The secondary lactose malabsorption was recorded in 44% of patients with ulcerative colitis, in 33% of patients with chronic enterocolitis, in 11.5% of patients with gastric ulcer, in 8% of those with duodenal ulcer, in 23.5% of patients with chronic gastritis attended by lowered secretory function, and in 8% of those with enhanced secretory function.
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PMID:[Current problems of lactase deficiency]. 296 77

The results of previous investigations of lactase deficiency and lactose malabsorption are reviewed. It showed that lactase activity and its decline in animals and humans is controlled genetically, but also that its phenotypic expression as lactose malabsorption is influenced by nongenetic factors: adaptation, biological (circadian) rhythmicity, hormones, gastrointestinal functions, and nutritional components can alter the response to lactose intake.
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PMID:Lactase deficiency and lactose malabsorption. A review. 308 62

Lactase-deficient subjects more effectively digest lactose in yogurt than lactose in other dairy products, apparently due to yogurt microbial beta-galactosidase (beta-gal) which is active in the GI tract. We evaluated the effects of buffering capacity of yogurt, gastric pH, and microbial cell disruption on beta-gal activity and lactose digestion. Three times more acid was required to acidify yogurt than to acidify milk. Yogurt beta-gal was stable at pH 4.0 but inactivated at lower pH. When yogurt was sonicated to disrupt microbial cell structure, only 20% activity remained after incubation at pH 4.0 for 60 min. In vivo gastric pH remained greater than 2.7 for 3 h after ingestion of yogurt. Acidified milk alone or with disrupted yogurt microorganisms caused twice as much lactose malabsorption as did acidified milk containing intact yogurt microorganisms. The results provide a possible explanation for the survival of beta-gal activity from yogurt in the GI tract.
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PMID:Lactose digestion by yogurt beta-galactosidase: influence of pH and microbial cell integrity. 310 80

The object of this study was to compare the indirect diagnostic methods on the basis of urinary galactose determination in the diagnosis of lactose malabsorption with the actual lactase activities. One hundred and seven patients were studied. The specificity and sensitivity of the strip test were 97%. With 30% actual prevalence the positive predictive value was 94%, and the negative predictive value was 99%. In common prevalences of hypolactasia the strip test was reliable.
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PMID:Strip test is reliable in common prevalences of hypolactasia. 311 Sep 39

The effects of oral enzyme replacement therapy on breath hydrogen excretion and symptoms after milk ingestion were studied in lactase-deficient patients. Sixteen symptomatic patients underwent interval hydrogen breath tests using whole milk as substrate. Each study was repeated with the addition of 250 mg of beta-D-galactosidase derived from Aspergillus oryzae (Lactrase) given orally with the milk. Subsequently seven of those 11 patients who did not normalize their hydrogen excretion with 250 mg of Lactrase were available to be restudied with a 500-mg dose. Mean cumulative and peak hydrogen excretions were calculated for the baseline (milk alone), 250 mg, and 500 mg Lactrase groups. Significant (p less than or equal to 0.05) decreases in cumulative and peak hydrogen excretion were noted between the 500 mg Lactrase versus the baseline group, but not between the 250 mg versus baseline group. Five of the 16 (31%) symptomatic lactase-deficient patients normalized their hydrogen excretion after 250 mg of Lactrase; four of seven (57%) who had not normalized on 250 mg, normalized their hydrogen excretion with 500 mg of Lactrase. A different pattern was observed in the incidence of symptoms. Five of the nine patients (56%) whose hydrogen excretion normalized with the addition of Lactrase at either dosage became asymptomatic after milk ingestion; in addition, three patients who did not normalize their hydrogen also became asymptomatic. We conclude that oral Lactrase in sufficient dosage temporarily reverses lactose malabsorption in some patients.
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PMID:Does oral enzyme replacement therapy reverse intestinal lactose malabsorption? 311 Dec 43

A total of 852 healthy Chinese children from 1 month to 14 years of age were investigated for lactose malabsorption using the breath hydrogen test. A lactose load of 2 g/kg was administered to 528 children and 1 g/kg to another 324 children. The incidence of lactose malabsorption was significantly different among various age groups and between the two different lactose dosages. While the incidence of malabsorption increased strikingly from the age of 3 to the age of 5 years, the age effect remained constant after the age of 6 years. The lactose load of 2 g/kg induced a higher incidence of malabsorption in study subjects than 1 g/kg did, and the dose effect increased for those aged below 5 years and decreased above 5 years. Small-intestinal lactase was also studied in 34 children aged from 2 months to 15 years. The lactase activity was highest in children 2 years old or younger, gradually decreasing with increasing age. In conclusion, lactase activity in Chinese children decreases gradually after 3 years of age, a finding that correlates well with the results of the breath hydrogen test.
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PMID:Lactose malabsorption and small-intestinal lactase in normal Chinese children. 312 31


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