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)

One hundred and fifty subjects were studied in a double blind fashion to determine the relationship between lactose malabsorption and milk lactose intolerance. Each participant received 250 ml of a different type of milk on 3 consecutive days. Milk A contained no lactose, milk B had 12.5 g, and milk C contained 37.5 g of lactose. After the experiment was completed each subject was classified with a lactose tolerance test as having "sufficient" or "insufficient" lactase activity. Milk A produced no gastrointestinal symptoms in either sufficient or in insufficient persons. Milk B produced symptoms in 3.8% of sufficient and 37.1% of insufficient individuals, and Milk C induced symptoms in 7.6% of sufficient and 83.5% of insufficient subjects. These differences are very highly significant (P less than 0.0001). It is concluded that lactose-intolerant subjects are indeed milk-intolerant and that the frequency with which symptoms occur in persons with lactose malabsorption increases in direct relation to the lactose content of the milk.
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PMID:Double blind study of milk lactose intolerance. 34 53

Reviewed in this article is evidence bearing on the geographic hypothesis advanced eight years ago to explain the striking ethnic or racial differences in prevalence of primary adult lactose malabsorption that are found around the world. Most evidence is found to support the hypothesis and the likelihood that some human groups came to have low prevalences of such lactose malabsorption because of selective pressures over a long historical period that favored the adult lactose absorber under particular ecological conditions.
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PMID:The geographic hypothesis and lactose malabsorption. A weighing of the evidence. 36 4

Milk intolerance was investigated in 87 healthy elderly individuals with a mean age of 77 years who were given 240 ml of a chocolate dairy drink twice in one week with a light lunch. No significant differences in symptomatic responses distinguished the subjects consuming a lactose-free (LF) drink from those consuming a drink containing 4.5% lactose (LC) under double-blind study conditions. Breath hydrogen analysis during lactose tolerance testing identified 23 malabsorbers, none of whom responded exclusively to the LC drink, although five were symptomatic on both days, and two had symptoms only on the day the LF drink was served. A similar percentage of absorbers (72%) and malabsorbers (70%) were asymptomatic on both days. Factors other than lactose malabsorption appeared to be responsible for the symptoms of intolerance reported, and most may have been psychosomatic in origin.
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PMID:Comparative tolerance of elderly from differing ethnic backgrounds to lactose-containing and lactose-free dairy drinks: a double-blind study. 37 54

The diagnostic value of 1-14C-lactose breath test was compared with the standard lactose tolerance test and lactase assay in jejunal biopsies in 16 control subjects, 14 patients with lactase deficiency (LD) proven by lactase assay and 20 patients with irritable bowel syndrome (IBS). 14CO2 specific activity in the 2-hr breath collection after administration of 1-14C-lactose (5 muCi) provided a satisfactory separation between the control and LD group. Values were 7.0 +/- 2.0% dose administered/mmoles 14CO2 X 10(-3) (mean +/- SD) in the control group versus 2.1 +/- 1.5 in LD (P less than 0.001) versus 4.9 +/- 2.3 in IBS (P less than 0.01). 1-14C-lactose breath test was superior to standard lactose tolerance test in specificity (P less than 0.05) and provided a satisfactory correlation between 14C-lactose absorption and lactase assay (r = 0.77). The prevalence of LD in IBS was 40% by the breath test and 35% by lactase assay, suggesting that lactose malabsorption may play a role in the symptoms in the population of some patients with IBS. It appears that 1-14C-lactose breath test is a sensitive, specific and accurate method for the diagnosis of LD in clinical practice and suitable for large scale epidemiological surveys.
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PMID:Lactase deficiency--a comparative study of diagnostic methods. 41 Feb 88

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 role of lactose malabsorption was studied prospectively in 80 schoolchildren with recurrent abdominal pain. Malabsorption was documented in 40 per cent (16 of 59 whites, 12 of 16 blacks and four of five Hispanic children) on the basis of elevated levels of hydrogen in their breath. Those with lactose malabsorption, however, were not clinically distinguishable on the basis of past milk ingestion (P greater than 0.05), weekly pain frequency (median, five vs. six times), presence of diarrhea (40 vs. 27 per cent) or symptom response to lactose load. In children with malabsorption who completed a six-week diet trial, 70 per cent reported increased frequency of pain (P less than 0.002) when placed on their usual lactose-containing diet. Lactose malabsorption has a substantial role in the symptoms of children with recurrent abdominal pain, and it should be considered before performing invasive procedures or assuming a psychogenic origin.
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PMID:Recurrent abdominal pain of childhood due to lactose intolerance. 44 86

One hundred five Iranian subjects, ranging in age from 4 months to 25 years, were tested for lactose absorption and tolerance. After ingesting a lactose dose, on the basis of low blood glucose response, 68% of the subjects were malabsorbers. Prevalence of lactose malabsorption increased with age, i.e., 31% of the children less than 3 years of age malabsorbed lactose, whereas 86% of adults did so. Clinical manifestations of lactose intolerance were shown by 39% of all subjects; of those who were lactose malabsorbers, only 57% manifested clinical symptoms. Among the lactose malabsorbers, the lowest prevalence of clinical symptoms occurred among the children less than 3 years of age and the highest in adults.
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PMID:Lactose intolerance in Iran. 47 84

A study was conducted among 234 Bangladeshi children to determine LM (lactose malabsorption) and its relation with age, history of diarrhea, nutrition, and breastfeeding. LM was determined by using BHT (breath hydrogen test) which showed similar results to a modified lactose tolerance test conducted in hospitals. BHT results indicated that 80% of the children over 36 months had LM while all infants less than 6 months absorbed lactose completely. With recent incidences of diarrhea and acute malnutrition the rates of LM increased. In addition, children who were still breastfeeding had a lower rate of LM than weaned children perhaps since breastfed children suffer less from gastroenteritis and diarrhea or because some component of breast milk protects against LM. The United Nation's Protein Advisory Group encourages milk consumption but other reports cite increased mortality rates and slower recovery when malnourished children were supplied lactose-containing milk. It is suggested that milk be distributed in low doses in areas where there are high LM rates.
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PMID:Lactose malabsorption in Bangladeshi village children: relation with age, history of recent diarrhea, nutritional status, and breast feeding. 47 86

The breath hydrogen test (BHT) was adapted for use in young infants and children. The diagnostic criterion of sugar malabsorption in the BHT was determined by oral administration of 0.5 g/kg of unabsorbable sugar (lactulose) to 21 healthy infants and children. A maximum increase in breath hydrogen less than 0.05 ml/min per m2 was observed in all subjects. A good correlation between results by the BHT and by the ordinary lactose tolerance test was obtained after oral administration of 2 g/kg lactose to 21 healthy infants and children, 2 congenital lactase-deficient infants, and 7 adults. Using this test, 80 healthy Japanese infants and children (aged between one month and 15 years) and 18 adults were examined for lactose malabsorption after a dose of 1 g/kg lactose. All infants and children under 2-years old absorbed lactose completely. The incidence of lactose malabsorption was 30% in 3-year, 36% in 4-year, 58% in 5-year, and 86% in 6-year-old children, 85% in schoolchildren, and 89% in adults. Thus the incidence of lactase deficiency gradually increases with age from 3 years, and about 90% of all normal Japanese adults are lactase-deficient.
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PMID:Breath hydrogen test for detecting lactose malabsorption in infants and children. Prevalence of lactose malabsorption in Japanese children and adults. 47 26

A 10-year-old boy with severe familial lactose intolerance in infancy (vomiting, failure to thrive, lactosuria (5.25 g/l), sucrosuria (12 g/l), and aminoaciduria. Intestinal disaccharidases (including lactase and sucrase) normal at age 6 and 20 weeks. Oral lactose tolerance test at this age resulted in lactosuria (4.6 g/l); sucrose tolerance test, in sucrosuria (18.5 g/l). In contrast, intraduodenal lactose tolerance test gave only low lactose excretion in urine (0.28 g/l). He improved rapidly and had no lactosuria on intraduodenal feeding with citric acid milk. The lactosuria diminished as age increased, but was still higher at age 6 years than that of controls. He tolerated normal disaccharide containing food after 1.5 years of age. At 5.5 to 6 years, he had symptoms of lactose malabsorption, and an isolated lactase deficiency was proved. At 10 years, he still tolerates only limited amounts of milk. The defect in severe familial infantile lactose intolerance seems to be localized in the gastric mucosa. Acquired lactase deficiency can appear later in childhood in this syndrome.
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PMID:A boy with severe infantile gastrogen lactose intolerance and acquired lactase deficiency. 52 43


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