Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.108 (lactase)
 2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Breath hydrogen (H2), collected by end-expiratory sampling, was measured in twenty-five patients with abdominal symptoms or diarrhoea after ingesting 50 g. of lactose. This was compared with established tests of hypolactasia. Fifteen patients with a blood-glucose rise of more than 20 mg. per 100 ml. had less than 4 parts per million (p.p.m.) rise in breath H2 at 2 hours. In contrast, ten patients with blood-glucose rises of less than 20 mg. per 100 ml. had more than a 20 p.p.m. H2 rise (mean 85.8 p.p.m. plus or minus s.d. 44.3) at 2 hours. Similarly, two patients with normal jejunal lactase activity had no significant H2 production, whereas six patients with hypolactasia had more than a 20 p.p.m. rise in H2. Symptoms related to milk or lactose ingestion were found to be unreliable. End-expiratory sampling of breath H2 would seem to be a simple, non-invasive, and accurate method of diagnosing hypolactasia, which is also very acceptable to patients. This should make it a valuable tool both in diagnostic gastroenterology and in epidemiological surveys.
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PMID:Breath hydrogen as a diagnostic method for hypolactasia. 4 74

Thirty-six hospital in-patients in London had breath-hydrogen concentrations measured after 50 g lactose were given orally; in 23 or them serial blood glucose concentrations were also estimated. Eight had tropical malabsorption (TM), 14 were Europeans with no detectable disease (normal group) and 14 who also had no detectable disease, were from ethnic groups known to have a very high incidence of genetically determined adult hypolactasia (hl). In 21 of them breath-hydrogen concentrations were also measured after 33.5 g of lactulose were given orally. There was a good inverse correlation between breath-hydrogen production and blood-glucose rise after lactose. Correlations between the first appearance of hydrogen (T) and the area under the hydrogen curve between 0 and 120 min (A) were inversely significant both for lactose and lactulose. Mean T was earlier and mean A greater for lactose compared with lactulose. Correlation between individual values for A after lactase and after lactulose was significant. Indirect measurements of lactase are of no value in either detecting or assessing the severity of TM; that is largely due to the very high incidence of HL in individuals exposed to that disease.
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PMID:Breath hydrogen concentrations after oral lactose and lactulose in tropical malabsorption and adult hypolactasia. 9 20

To determine the amount of lactose that could be tolerated in a meal, 59 lactase-deficient American Indians, ranging in age from 5 to 62, were given graded doses of lactose. The diagnosis of lactase deficiency had beeen documented previously by showing increased breath hydrogen after an oral lactose load (2 g per kg, maximum 50 g). With this load, 88% of the subjects had symptoms. On 6 consecutive mornings, each subject was given a breakfast that contained graded doses of lactose ranging from 0 to 18 g. The order of the breakfasts was randomized and the contents were double-blinded. Symptoms, which were assessed by a "blinded" observer, were present after 9% of the breakfasts at all dosage levels, including the lactose-free breakfast. Thus, under the conditions of this study, a modest amount of lactose, equivalent to that present in 1 to 1 1/2 glasses of milk, when taken with a meal, is well tolerated by the lactase-deficient American Indian.
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PMID:Tolerance to lactose among lactase-deficient American Indians. 33 50

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

Intestinal lactase activity was assessed indirectly in 156 American Indians by measuring breath hydrogen after an oral lactose load. Lactase deficiency was present in 66% of subjects and correlated highly with the percentage of Indian blood. Lactase deficiency was present by the age of 5 years and was unrelated to sex. Most lactase-deficient subjects (81%), but only a minority (23%) of lactase-sufficient subjects, developed symptoms after the oral lactose load, and among lactase-deficient subjects, symptoms occurred more frequently in adults than in children (P = 0.05). Indeed, by history, 53% of lactase-deficient adults, but only 10% of lactase-deficient children under 18 years of age, were aware of milk intolerance. Despite these differences, milk consumption was only slightly less (19 g) in the lactase-deficient subjects than in those with normal lactase activity (25 g) (P less than 0.05). The results indicate that lactase deficiency is a common autosomal genetic trait in the American Indian that becomes manifest in early childhood. Tolerance to dietary lactose appears to decline in the American Indian as he reaches adulthood, but in this population the decline in tolerance had only minor influence on lactose intake.
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PMID:Lactase deficiency: a common genetic trait of the American Indian. 57 36

We determined the prevalence of lactase deficiency by analysis of respiratory hydrogen (H2) in 30 women with idiopathic postmenopausal osteoporosis and in 31 female control subjects without evidence of metabolic bone disease. Eight subjects with osteoporosis had breath H2 excretion greater than 0.20 ml/minute at 2 h after receiving 50 g of lactose and were considered lactase deficient; only one control subject was lactase deficient (P less than 0.05). Symptoms developed in seven of the nine lactase-deficient persons after receiving 50 g of lactose; in contrast, only three of the 52 lactase-normal subjects had symptoms. Although none of the lactase-deficient subjects was aware of milk intolerance, their intake of both lactose and calcium was significantly lower than that in the lactase-normal group. Lactase deficiency appears to be one of several factors that predispose to the development of osteoporosis, probably through diminished calcium intake and possibly through an effect on calcium absorption.
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PMID:Lactase deficiency: prevalence in osteoporosis. 67 85

The superiority of human milk as compared with milk of other origin for the feeding of newborns, term or preterm, can be analysed in terms of biological development related to digestive, metabolic and excretory functions during foetal and postnatal life. The macro- and micro-anatomical developments of the intestine are complete in the 6th foetal month. The brush border and some of its enzymes (saccharase-isomaltase) exist already from the 6th foetal week, whereas other enzymes (lactase and intracellular transport enzymes) appear much later. The major gastric and pancreatic enzymes, as well as the synthesis of biliary acids, do not reach maturity until after birth. Several metabolic functions, e.g. the synthesis of cystine from methionine, of tyrosine from phenylalanine, and of urea from ammonia, are still limited at the time of birth. The capacity for excretion of sodium, the osmotic urinary load, and hydrogen ions is suboptimal, especially in the prematurely born. All these circumstances imply that human milk, with its protective properties, represents optimal adaptation to the needs of the child in the perinatal period.
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PMID:Breast feeding and biological development. 69 1

To determine the pattern of inheritance of lactase deficiency, we studied 104 American Indian and 2 white subjects in 19 families. Subjects were considered deficient in lactase if breath-hydrogen excretion exceeded 0.20 ml per min above fasting at 2 hr after a lactose load of 2 g per kg of body weight (maximum 50 g). Seventy-one per cent of the males and 75% of the females were lactase deficient. In three families in which both parents were lactase normal, 40% of the children were lactase deficient; and in the three families with one parent lactase normal and the other lactase deficient, 65% of the children were deficient in lactase; and finally, in the seven families with both parents lactase deficient, 93% of the children were lactase deficient. This distribution of lactase deficiency in the families suggests that this trait shows an autosomal-recessive pattern of inheritance.
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PMID:Family studies of lactase deficiency in the American Indian. 90 10

To compare sensitivity, specificity and convenience, four indirect methods of detecting lactase deficiency were tested prospectively in 25 subjects with biopsy-proved lactase deficiency and in 25 with normal lactase activity. After ingestion of 50 g of lactose, containing 1-14Clactose, breath hydrogen was abnormally elevated in all 25 lactase-deficient subjects (greater than 0.30 ml per minute at two hours); breath 14CO2 was below the normal range in 23, and in 19 the plasma glucose increased by less than 20 mg per deciliter. When lactose and ethanol were given together, the rise in plasma galactose remained less than 5 mg per deciliter in 24 of the lactase-deficient subjects. The specificity of the four tests was excellent, with only one false-positive plasma glucose test. Measurement of breath hydrogen is sensitive and specific, and does not require ethanol or isotopes. It is noninvasive, and is not influenced by gastric emptying or metabolic factors. We believe it to be the most suitable test for population screening for lactase deficiency.
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PMID:Prospective comparison of indirect methods for detecting lactase deficiency. 118 2

The quantity of lactose not absorbed by 4 normal and 6 lactase-deficient subjects was determined by three indirect methods which involved: (1) measurement of pulmonary hydrogen (H2) excretion, (2) pulmonary (14)CO2 excretion, and (3) stool (14)C excretion, after ingestion of 12.5 g of 1-(14)C-lactose and 4 g of polyethylene glycol (PEG). Results were compared with absorption determined directly from the (14)C:PEG ratio of multiple terminal ileal aspirates. The fraction of lactose not absorbed determined by ileal aspiration ranged from 0 to 8% in normals and 42 to 75% in mild-intolerant subjects. Whereas all three indirect methods were useful in qualitatively separating normal from deficient subjects, the quantity of lactose absorbed as determined by H2 excretion correlated most closely with ileal measurements (r = 0.94). Pulmonary (14)CO2 excretion for 24 hr after (14)C-lactose ingestion did not distinguish normal (17 +/- 4% (SEM) of ingested (14)C per 24 hr) from lactase-deficient subjects (21.1 +/- 3%). Likewise, stool (14)C:PEG ratios grossly underestimated malabsorption with less than one-quarter of the nonabsorbed (14)C appearing in the stool. This study suggests that individual differences in susceptibility to diarrhea after milk ingestion by lactase-deficient subjects may be due to differences in the quantity of lactose not absorbed and/or differences in the rate of bacterial metabolism of lactose in the colon. Analysis of ileal fluid collected during passage of the lactose meal indicated that about two-thirds of the osmotic load delivered to the colon consists of endogenous electrolytes. Thus the water load delivered to the colon is about 3 times that calculated to be osmotically held by the nonabsorbed sugar.
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PMID:Quantitative measurement of lactose absorption. 126 65


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