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

The degree of which the ability to absorb lactose can be regained after recovery from an acute episode of severe malnutrition is in doubt. Lactase activity was indirectly assessed by means of a standard lactose tolerance test (2 g lactose per kilogram of body weight) in 71 Peruvian Mestizo infants and children (age 5 to 55 months) who had suffered such an episode. All were studied just before discharge after several months of hospital rehabilitation, during which linear growth and weight gain had accelerated and signs of significant malabsorption of other nutrients had disappeared. Only 39% of the total group had a positive test (delta blood glucose greater than 25 mg/dl); there was a decreasing proportion of positive responders with increasing age. No difference in response attributable to type or severity of malnutrition was found. Comparison of the present data with previous data from children in the same community who had never been acutely malnourished suggests that acute malnutrition may hasten the permanent decline of lactase activity normally expected later in life.
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PMID:Effect of an episode of severe malnutrition and age on lactose absorption by recovered infants and children. 10 90

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

Examinations of faeces (pH, Clinitest and Clinistix) are liable to contribute to the diagnosis of lactose malabsorption. To confirm the diagnosis the test is to be repeated while Lactase 500 is added to the child's milk. The enzyme does not split the lactase into the two monosaccharides, thus eliminating the malabsorption. The new drug Lactase 500 was used as a diagnostic parameter and for the treatment of lactose malabsorption in 20 infants. The effect on both groups was confirmed as mentioned by foreign authors. In addition to a very simple diagnostic method, which can be performed in the practitioner's office, there are two methods of treating lactose malabsorption: 1. feeding milk free of lactose, 2. feeding milk with an addition of Lactase 500. As in an earlier publication we assumed that about 10 per cent of the population suffers from secondary malabsorption of lactose, it seems advisable to check with the help of the described to simple methods all children with chronic diarrhoea.
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PMID:[Diagnosis and therapy of lactose malabsorption]. 84 87

Twenty-eight Sioux and 29 Saluteaux Indians from a southern and an isolated northern Manitoban community were screened for lactose malabsorption; 55 were also screened for sucrose tolerance. Sixty percent of the subjects were lactose malabsorbers; the incidence increased with age. Lactase deficiency appeared, on the average, between 8 and 15 years of age. About 45% of the subjects were lactose intolerant. Malabsorbers who did not regularly drink milk had the highest symptom scores. The northern subjects consumed significantly more lactose and sucrose than the southern subjects. Two Sioux children were sucrose malabsorbers. It was hypothesized that the significantly greater sucrose consumption by the Saulteaux subjects were responsible for their markedly higher blood glucose curve following the sucrose tolerance tests. Dietary sucrose increases jejunal sucrase activity and the intestinal transport of glucose and fructose. Three of eight children less than 4 years were lactose malabsorbers; hence, medical personnel treating noninjective diarrhea in Indian children should examine for lactase deficiency. It was recommended that vitamin D fortified milk supplements to Indian school children be continued and that the milk be treated so as to reduce abdominal symptoms in the intolerant individuals.
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PMID:Disaccharide consumption and malabsorption in Canadian Indians. 85 12

Lactase deficiency, manifested clinically by lactose malabsorption, is often the only biochemical evidence of a residual disturbance of jejunal mucosal function after Escherichia coli enteropathy in the infant. Villous morphology is usually normal. A sustained depression of the processes of biochemical differentiation of lactase biosynthesis has been postulated to explain similar states of lactase deficiency, but a possible influence of altered epithelial cell turnover on the mucosal lactase levels has not been investigated. In ten infants with a residual lactose malabsorption, after E. coli infection, jejunal cell renewal activity and disaccharidase activities were studied by analysis of the exfoliated cells collected by lumenal perfusion. Significant increases in DNA and protein exfoliation and in the brush border activities of sucrase and lactase were observed during recovery from the malabsorptive disturbance. DNA and protein efflux increased almost linearly during a 20-day period. Lactase was initially four times more deficient than sucrase activity in the exfoliated cells. Both enzyme activities increased at almost identical rates. Therefore, it took longer for lactase activity to return to normal levels. The lactase/sucrase ratios approached normal at the end of the 20-day period. The changes in the exfoliating levels of the two enzymes, when analysed in relation to the increases in cell renewal activity, suggested a relationship between sucrase and lactase levels and cell age.
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PMID:Intestinal exfoliated cells in infant diarrhoea: changes in cell renewal and disaccharidase activities. 104 54

Jejunal biopsies were obtained from 37 children with cystic fibrosis, 16 with gluten-induced enteropathy, and 18 control subjects for the following studies: (1) disaccharidase activity, (2) L-ALA-L-Phe hydrolase activity, and (3) intestinal uptake of three 14C-labeled amino acids. Values were significantly reduced in the three determinations in patients with gluten-induced enteropathy as compared to control subjects. Lactase and L-ALA-L-Phe hydrolase activities were significantly reduced (p less than 0.01) in CF patients as compared to control subjects. Definite hypolactasia was also observed in 23% of the children with CF. Uptake of lysine was normal in CF patients whereas that of phenylalanine and cycloleucine was reduced as compared to control subjects. This study suggests an intestinal component to the malabsorption of patients with CF.
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PMID:Small bowel mucosal dysfunction in patients with cystic fibrosis. 124 82

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 relationship between primary lactase deficiency, the amount of lactose in the diet, and symptoms of intolerance continues to be debated. Primary adult lactase deficiency is common with a worldwide occurrence of near 70%. Lactase-deficient individuals malabsorb lactose but may or may not show intolerance symptoms. The development of symptoms appears to depend on the dose of lactose ingested, whether it is accompanied by a meal or other food, rate of gastric emptying, and small intestine transit time. Lactose loads of 15 g or greater produce symptoms in the majority of lactase-deficient persons. However, when lactose loads of up to 12 g are fed, symptoms can be minimal or absent. Tolerance to yogurt, acidophilus milk, and other microbe-containing dairy foods has been suggested and is thought to be due to either a low lactose content or in vivo autodigestion by microbial beta-galactosidase. Up to 20 g of lactose in yogurt is tolerated well by lactase-deficient persons. Associated with the consumption of yogurt is a three- to fourfold reduction in lactose malabsorption as compared with similar lactose consumption in milk. Improved lactose digestion appears due to autodigestion by microbial beta-galactosidase. This enzyme may be released from yogurt culture by gastric or bile acid digestion. Feeding yogurt that was pasteurized following fermentation, with only trace amounts of microbial beta-galactosidase activity, results in a threefold increase in lactose malabsorption as compared with feeding yogurt with a viable culture. However, pasteurized yogurt also is tolerated well by lactase-deficient persons, suggesting that tolerance of up to 20 g of lactose in yogurt may be independent of lactose malabsorption. The enhanced lactose absorption and tolerance observed with yogurt feeding are not apparent when unfermented acidophilus milk or cultured milk are fed.
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PMID:Milk intolerance and microbe-containing dairy foods. 355 56

An increased prevalence of osteoporosis has been observed in lactase-deficient subjects. This association has been attributed to an avoidance of calcium-containing dairy products by lactase-deficient subjects and/or an adverse affect of lactose malabsorption on calcium absorption. Because the lactose in yogurt can be digested and absorbed by hypolactasic subjects, we tested the ability of lactase-deficient subjects and controls to absorb calcium from milk and yogurt. Subjects ingested 270 mg of Ca plus 45Ca in 250 g of milk or 147 g of commercial, unflavored yogurt, and blood radioactivity was assessed at intervals over 24 h. Based on the areas under the blood radioactivity curves, lactase-deficient subjects and controls absorbed calcium equally well from yogurt and milk. Lactase-deficient subjects absorbed 45Ca from both sources at least as well as did the controls. While we found no evidence to indicate that calcium in yogurt is better absorbed than calcium in milk, yogurt remains an excellent source of calcium because this fermented product is well tolerated by lactase-deficient subjects.
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PMID:Absorption of calcium from milk and yogurt. 393 56

Lactose malabsorption is not a cause of diarrhea during phototherapy. Jaundiced neonates under phototherapy develop diarrhea or loose stools during the treatment. These phenomena were attributed to an induced lactase deficiency caused by bilirubin breakdown products. We investigated lactose malabsorption in 59 neonates--29 normals and 30 jaundiced under phototherapy. Five-hour hydrogen breath tests were performed. Preprandial and postprandial (at 30, 60, 120, 180, 240, and 300 min) expired air samples were analyzed for hydrogen. Ten controls and five jaundiced neonates had positive hydrogen breath tests. Eighteen controls and 16 neonates under phototherapy had preprandial hydrogen (concentrations above 5 ppm). In our hands, lactase deficiency and lactose malabsorption were not induced by phototherapy. Lactase deficiency is therefore not the cause of diarrhea associated with phototherapy.
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PMID:Lactose malabsorption is not a cause of diarrhea during phototherapy. 398 20


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