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PubMed2002

Use of the lactose H2 breath test to monitor mucosal healing in coeliac disease.

UNLABELLED: Confirmation of the diagnosis of coeliac disease requires unequivocal evidence of recovery on a gluten-free diet. The lactose H2 breath test is a non-invasive technique for detecting lactose malabsorption, and this may occur in untreated coeliac disease. The utility of this test was investigated in objectively confirming a response to gluten exclusion. The study included 44 children from 0.9 to 14.75 y of age (median 3.2) with coeliac disease. Five children were asymptomatic, being identified through coeliac antibody screening. Breath tests were performed prior to dietary treatment. If positive, they were repeated at 4-wk intervals following gluten exclusion. Overall, 21/44 (48%) children had positive breath tests at presentation. In 18/21 children on a gluten-free diet, this became negative after 4 wk (86%) and in all the children by 8 wk. In two children with positive tests at 4 wk, problems with dietary adherence were identified. A positive test before treatment was not associated with significant differences in individual symptoms, height, weight and body mass index standard deviation scores, serum haemoglobin or albumin. However, no positive results were found in the asymptomatic patients (p = 0.05). Lactose malabsorption was associated with earlier age of presentation (p = 0.008). CONCLUSION: The lactose H2 breath test objectively confirms a response to gluten exclusion. In selected cases it can help confirm a diagnosis of coeliac disease. However, the test tends to be less informative in asymptomatic patients, and in older children.

Adolescent↗
PubMed1999

A metabolic balance study in term infants fed lactose-containing or lactose-free formula.

Lactose-free (L-) formulas are recommended for infants with conditions affecting lactose digestion. Cows' milk protein-based formulas containing other carbohydrate sources are most often used for such infants. This study compared fat absorption and absorption and retention of nitrogen, calcium, phosphorus, and magnesium in term infants fed either a L- or standard lactose-containing (L+) bovine milk protein-based formula. Data from three single-centre, double-blind, randomized, parallel-group metabolic balance studies were combined. After a 4-7-d equilibration period on either L- or L+ formula, a 72-h balance study was performed. Twenty infants received L- and 21 received L+ formula. Besides the L- group having a higher percentage of males (65%) and the L+ group a higher percentage of females (52.4%), other baseline measurements were similar. The majority of nutrient balance data was similar between the two groups. Exceptions were relative nitrogen absorption, calcium intake and calcium retention, magnesium retention, and faecal phosphorus excretion, all of which were significantly higher in the L- group. Vitamin D supplementation did not significantly affect either calcium or phosphorus data. This new L- formula provided similar nutrients and is a suitable alternative to a L+ formula in term infants requiring L- feedings.

Animals↗
PubMed1998

Assignment of the locus for congenital lactase deficiency to 2q21, in the vicinity of but separate from the lactase-phlorizin hydrolase gene.

Congenital lactase deficiency (CLD) is an autosomal recessive, gastrointestinal disorder characterized by watery diarrhea starting during the first 1-10 d of life, in infants fed lactose-containing milks. Since 1966, 42 patients have been diagnosed in Finland. CLD is the most severe form of lactase deficiency, with an almost total lack of lactase-phlorizin hydrolase (LPH) activity on jejunal biopsy. In adult-type hypolactasia, the most common genetic enzyme deficiency in humans, this enzyme activity is reduced to 5%-10%. Although the activity of intestinal LPH has been found to be greatly reduced in both forms, the molecular pathogenesis of lactase deficiencies is unknown. On the basis of the initial candidate-gene approach, we assigned the CLD locus to an 8-cM interval on chromosome 2q21 in 19 Finnish families. At the closest marker locus, a specific allele 2 was present in 92% of disease alleles. On the basis of a genealogical study, the CLD mutation was found to be enriched in sparsely populated eastern and northern Finland, because of a founder effect. The results of both the genealogical study and the haplotype analysis indicate that one major mutation in a novel gene causes CLD in the Finnish population. Consequently, the critical region could be restricted further, to an approximately 350-kb interval, by ancient-haplotype and linkage-disequilibrium analyses. Surprisingly, the LPH gene was shown to lie outside the critical CLD region, excluding it as a causative gene for CLD. The LPH locus was found to reside >2 Mb from the critical CLD region.

Chromosome Mapping↗
PubMed1999

Lactose malabsorption and rate of bone loss in older women.

OBJECTIVES: to study the prevalence of lactose malabsorption with increasing age and to determine whether lactose malabsorbers consume less dietary calcium, have lower bone mineral density or display faster bone loss than lactose absorbers. DESIGN: 80 healthy Caucasian women aged 40-79 years (20 per decade) were studied for 1 year. METHODS: breath hydrogen exhalation was measured for 3 after a 50 g oral lactose challenge. Bone density was assessed in the radius, femoral neck, lumbar spine and total body by dual energy x-ray absorptiometry and dietary calcium intake was estimated by 4-day diet records and food-frequency questionnaires. RESULTS: lactose malabsorption rose with age (15% in those aged 40-59 years versus 50% in those aged 60-79; P < 0.01). Malabsorbers aged 70-79 years consumed significantly less calcium than lactose absorbers of this age (P < 0.05). Baseline total body calcium values were lower in lactose malabsorbers (n=26) than in lactose absorbers (n=54) but age-adjustment eliminated this difference. Bone change (% per year) was correlated with dietary calcium intake at the femoral neck and trochanter (P < 0.05) but was not statistically greater in malabsorbers than in absorbers. CONCLUSIONS: the ability to absorb lactose declines in the 7th decade. This may contribute to decreased dietary intakes of milk products and calcium in elderly women. However, lactose malabsorption without reduction in calcium intake has little effect on bone mineral density or the rate of bone loss.

Adult↗