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At least 433 records · Page 24Linked to original sources
PubMed2000

Lactose-[13C]ureide breath test: a new, noninvasive technique to determine orocecal transit time in children.

BACKGROUND: The lactose-[13C]ureide breath test (LUBT) is a novel, noninvasive test to determine orocecal transit time. Lactose ureide resists the action of brush border enzymes and is metabolized by colonic bacteria. The purpose of the present study was to adapt this breath test for children of various age groups and to determine whether it can be applied in infants, newborns, and preterms to study the development of small intestinal motility. METHODS: In a group of 20 children (3-17 years) in vitro stool analysis and in vivo LUBT results were compared. From each subject a blank stool sample and a sample produced after induction with unlabeled lactose ureide were incubated with 10 mg lactose-[13C]ureide in small, closed bottles. Ten-milliliter CO2 samples were aspirated from the bottles using a needle and a syringe every 30 minutes for 24 hours. All children performed the breath test after induction of 500 mg unlabeled lactose ureide three times the prior day. A liquid test meal (chocolate milk) with 250 mg lactose-[13C]ureide was ingested. Breath samples were collected every 15 minutes for 10 hours. In a second group of 32 children (age range, 0-3 years) consisting of 6 children between 1 and 3 years of age, 6 infants between 6 and 12 months, 13 infants between 0 and 6 months, and 7 preterm infants, only the in vitro stool analysis was performed. Stools were collected for stool incubation, as described. RESULTS: The mean orocecal transit time in the group of 20 children aged 3 to 17 years was 255 minutes (range, 165-390 minutes). Stool incubations demonstrated a clear 13CO2 peak in all infants aged more than 8 months, indicating that their colonic bacterial enzymic activity hydrolyses lactose ureide. However, in all infants aged less than 6 months and in preterm infants, the 13CO2 signal was absent, indicating that those subjects were unable to hydrolyze lactose ureide. CONCLUSION: Infants aged less than 6 months do not host the appropriate bacterial enzymic activity for splitting lactose ureide. The authors conclude that the LUBT can be applied in infants aged more than 8 months, after weaning to solid foods, to determine orocecal transit time.

Adolescent↗
PubMed2001

Irritable bowel syndrome: is the search for lactose intolerance justified?

OBJECTIVES: To determine if confirmation of hypolactasia offers any benefit to the dietary treatment of patients with irritable bowel syndrome (IBS). METHODS: One hundred and twenty-two consecutive IBS patients (37 male, 85 female) were given lactose hydrogen breath tests (LHBT). Those with positive LHBT followed a low lactose diet for 3 weeks. Those improving on the diet were given double-blind, placebo-controlled challenges (DBPCC) with 5 g, 10 g and 15 g of lactose and a placebo, to confirm lactose intolerance. Those who did not respond to the low lactose diet followed either an exclusion or low fibre diet. Symptoms scores were kept prior to the LHBT, 8 h post-LHBT and daily whilst following any dietary change. Patients with negative LHBT returned to clinic and subsequent dietary interventions were recorded. RESULTS: LHBT was positive in 33/122 (27%) IBS patients. Syrr otom scores prior to LHBT were not significantly different between the two groups, but after LHBT the symptoms in the positive group were significantly worse. Twenty-three patients followed a low-lactose diet of which only nine (39%) improved. Six who did not improve followed an exclusion diet, three improved and all were intolerant of milk. Three tried a low fibre diet with two improving. DBPCC were inconclusive. In the negative LHBT group 35 agreed to try a diet and 24 improved (69%). Eight were intolerant of cow's milk. CONCLUSIONS: Use of a low lactose diet was disappointing in IBS patients with lactose malabsorption. Food intolerance was demonstrated in IBS patients with positive or negative LHBT and milk was identified as a problem in both groups. DBPCC were inconclusive. There appears to be little advantage in trying to separate patients who malabsorb lactose from others with IBS.

Adult↗
PubMed1991

Possible mechanisms underlying the slow lactose fermentation phenotype in Shigella spp.

A Southern hybridization analysis revealed that the region homologous to Escherichia coli lacZ was present on the chromosomal DNAs of beta-galactosidase-positive Shigella strains, such as Shigella dysenteriae serovar 1 and Shigella sonnei strains, whereas this region was absent from chromosomal DNAs of beta-galactosidase-negative strains of Shigella flexneri and Shigella boydii. We found that the lacY-A region was deficient in S. dysenteriae serovar 1 and believe that this is the reason for the slow fermentation of lactose by this strain. S. sonnei strains possessed the region which hybridized with E. coli lacY-A despite their slow hydrolysis of lactose. The whole lactose-fermenting region was cloned from S. sonnei and compared with the cloned lac operon of E. coli K-12. Both clones directed the synthesis of beta-galactosidase in an E. coli K-12 strain lacking indigenous beta-galactosidase activity (strain JM109-1), and we observed no difference in the expression of beta-galactosidase activity in S. sonnei and E. coli. However, E. coli JM109-1 harboring the lactose-fermenting genes of S. sonnei exhibited the slow lactose fermentation phenotype like the parental strain. S. sonnei strains had no detectable lactose permease activities. E. coli JM109-1 harboring the lactose-fermenting genes of S. sonnei had a detectable permease activity, possibly because of the multicopy nature of the cloned genes, but this permease activity was much lower than that of strain JM109-1 harboring the lac operon of E. coli K-12. From these results we concluded that slow lactose fermentation by S. sonnei is due to weak lactose permease activity.

Blotting, Southern↗
PubMed1979

Lysis of Escherichia coli mutants by lactose.

Growth of Escherichia coli strain MM6-13 (ptsI suc lacI sup), which as a suppressor of the succinate-negative phenotype, was inhibited by lactose. Cells growing in yeast extract-tryptone-sodium chloride medium (LB broth) were lysed upon the addition of lactose. In Casamino Acids-salts medium, lactose inhibited growth, but due to the high K+ content no lysis occurred. Lysis required high levels of beta-galctosidase and lactose transport activity. MM6, the parental strain of MM6-13, has lower levels of both of these activities and was resistant to lysis under these conditions. When MM6 was grown in LB broth with exogenous cyclic adenosine monophosphate, however, beta-galactosidase and lactose transport activities were greatly increased, and lysis occurred upon the addition of lactose. Resting cells of both MM6 and MM6-13 were lysed by lactose in buffers containing suitable ions. In the presence of MG2+, lysis was enhanced by 5 mM KCl and 100 mM NaCl. Higher slat concentrations (50 mM KCl or 200 mM NaCl) provided partial protection from lysis. In the absence of Mg2+, lysis occurred without KCl. Lactose-dependent lysis occurred in buffers containing anions such as sulafte, chloride, phosphate, or citrate; however, thiocyanate or acetate protected the cells from lysis. These data indicate that both cations and anions, as well as the levels of lactose transport and beta-galactosidase activity, are important in lysis.

Bacteriolysis↗
PubMed2001

Use of nucleotides in weanling rats with diarrhea induced by a lactose overload: effect on the evolution of diarrhea and weight and on the histopathology of intestine, liver and spleen.

Until recently, dietary sources of nucleotides were thought not to be essential for good nutrition. Certain states with higher metabolic demands may require larger amounts that cannot be provided by endogenous production. The objective of the present study was to determine the action of nucleotides on the recovery from lactose-induced diarrhea in weaned rats. Thirty-six weanling Fisher rats were divided into two groups. Group 1 received a standard diet and group 2 received a diet containing lactose in place of starch. On the 10th day, six animals per group were sacrificed for histopathological evaluation. The remaining animals were divided into two other subgroups, each with 6 animals, receiving a control diet, a control diet with nucleotides (0.05% adenosine monophosphate, 0.05% guanosine monophosphate, 0.05% cytidine monophosphate, 0.05% uridine monophosphate and 0.05% inosine monophosphate), a diet with lactose, and a diet with lactose and nucleotides. On the 32nd day of the experiment all animals were sacrificed. Animals with diarrhea weighed less than animals without diarrhea. The introduction of nucleotides did not lead to weight gain. Mean diet consumption was lower in the group that continued to ingest lactose, with the group receiving lactose plus nucleotides showing a lower mean consumption. Animals receiving lactose had inflammatory reaction and deposits of periodic acid-Schiff-positive material in intestinal, hepatic and splenic tissues. The introduction of nucleotides led to an improvement of the intestinal inflammatory reaction. In lactose-induced diarrhea, when the stimulus is maintained--lactose overload--the nucleotides have a limited action on the weight gain and on recovery of intestinal morphology, although they have a protective effect on hepatic injury and improve the inflammatory response.

Analysis of Variance↗
PubMed2006

Influence of calcium and phosphorus, lactose, and salt-to-moisture ratio on Cheddar cheese quality: manufacture and composition.

Eight Cheddar cheeses with 2 levels of calcium (Ca) and phosphorus (P), residual lactose, and salt-to-moisture ratio (S/M) were manufactured. All cheeses were made using a stirred-curd procedure and were replicated 3 times. Treatments with a high level of Ca and P were produced by setting the milk and drawing the whey at a higher pH (6.6 and 6.3, respectively) compared with the treatments with a low level of Ca and P (pH of 6.2 and 5.7, respectively). The lactose content in the cheeses was varied by adding lactose (2.5% by weight of milk) to the milk for high lactose cheeses, and washing the curd for low lactose cheeses. The difference in S/M was obtained by dividing the curds into halves, weighing each half, and salting at 3.5 and 2.25% of the weight of the curd for high and low S/M, respectively. All cheeses were salted at a pH of 5.4. Modifications in cheese-making protocols produced cheeses with desired differences in Ca and P, residual lactose, and S/M. Average Ca and P in the high Ca and P cheeses was 0.68 and 0.48%, respectively, vs. 0.53 and 0.41% for the low Ca and P cheeses. Average lactose content of the high lactose treatments at d 1 was 1.48% compared with 0.30% for the low lactose treatments. The S/M for the high and low S/M cheeses was 6.68 and 4.77%, respectively. Mean moisture, fat, and protein content of the cheeses ranged from 32.07 to 37.57%, 33.32 to 35.93%, and 24.46 to 26.40%, respectively. The moisture content differed among the treatments, whereas fat and protein content on dry basis was similar.

Animals↗
PubMed1983

Influence of lactose concentration of milk and yogurt on growth rate of rats.

Growth rates of rats fed lyophilized diets of yogurt, milk, 100% lactose-hydrolyzed milk, and 100% lactose-hydrolyzed yogurt were compared. No differences were significant in weight gains between the animals fed lactose-hydrolyzed diets over 3 wk. Further more, rats fed the lactose-hydrolyzed diets had significantly larger weight gains during the 1st wk than those fed unhydrolyzed diets. This may have been from the deleterious effect of lactose, which was in concentrations of 43% in milk and 36% in yogurt. However, by the 2nd wk, rats fed yogurt had growth rates similar to those fed lactose-hydrolyzed diets, and by the 3rd wk, no differences of growth rates were significant. Continued consumption of high concentrations of lactose improved digestion of lactose. Yogurt fermentation produced growth benefit as compared to the milk from which it was made by reducing the lactose content and by supplying microbial lactase activity.

Animals↗
PubMed1992

Effects of dietary lactose on incidence and levels of salmonellae on carcasses of broiler chickens grown to market age.

Two trials were conducted to evaluate the effects of lactose in the diet of broilers grown to market weights on incidence and levels of salmonellae on the carcass. Lactose was substituted for sand in otherwise nutritionally complete diets at levels of 0, 2.5, 5, and 7.5% and fed from day-old to 49 days of age. Birds were reared on used (Trial 1) or new (Trial 2) litter and inoculated via the drinking water on Days 2, 7, and 14 with 10(8) cfu/mL Salmonella typhimurium (ATCC 14028). At 50 days, 12 (Trial 1) or 24 (Trial 2) birds per treatment were processed and prechill carcasses were evaluated for salmonellae incidence and level by the most probable number (MPN) method. Body weight of male broilers was significantly reduced by feeding diets containing up to 7.5% lactose. Feed intake of broilers fed diets containing lactose was significantly reduced and feed utilization improved, suggesting that lactose provided some metabolizable energy. The degree of litter caking was significantly increased, and cecal pH was significantly decreased as dietary lactose increased. Prechill carcases of broilers fed diets with 7.5% lactose had significantly higher levels of salmonellae than did prechill carcasses of broilers fed 0% lactose. The results of the present study suggest that supplementing poultry diets with lactose is not a viable means in itself of reducing or eliminating salmonellae incidence or levels on processed broiler carcasses.

Animals↗
PubMed2004

Lactose malabsorption in young Lithuanian children with atopic dermatitis.

AIM: To determine the prevalence of lactose malabsorption in young Lithuanian atopic dermatitis children; to evaluate the relationship between lactose malabsorption and the duration of exclusive breastfeeding, and the relationship between lactose malabsorption and cow's milk intolerance in parents and grandparents. METHODS: 144 children with atopic dermatitis aged 1.5-24 mo (study group) and 32 children without symptoms of allergic diseases aged 1.5-23 mo (control group) were investigated. Lactose and glucose-galactose absorption tests based on serial blood glucose determination, culture of stool, latex agglutination test for rotavirus and microscopic examination of stool for parasites were performed. RESULTS: Lactose malabsorption was determined in 59 (40.9%) and glucose-galactose malabsorption in 17 (11.8%) children with atopic dermatitis. The risk of developing lactose malabsorption was higher in children fed exclusively on breast milk up to 1 mo of age than in children fed exclusively on breast milk for 4 to 6 mo (OR: 2.62; 95% CI: 1.02-6.75). Lactose malabsorption was significantly more frequent in patients whose mothers did not tolerate cow's milk (20/30; 66.7%) than in patients whose mothers were tolerant to it (39/95; 41.1%) (p = 0.02). CONCLUSION: Lactose malabsorption was determined in 40.9% of Lithuanian atopic dermatitis children aged under 2 y. Lactose malabsorption appeared to be associated with the duration of exclusive breastfeeding up to only 1 mo and mothers' milk intolerance.

Child, Preschool↗
PubMedDate not supplied

Effect of dietary lactose on Salmonella colonization of market-age broiler chickens.

The effect of providing lactose in feed and inoculation with volatile fatty acid-producing anaerobic cultures (AC) of cecal flora on Salmonella typhimurium colonization was evaluated in broilers. One-day-old chicks were divided into four groups and provided 1) no lactose, no AC; 2) AC, no lactose; 3) AC and lactose on days 1-10; or 4) AC and lactose on days 1-40. All groups were challenged per os with 10(6) Salmonella on day 3 and with 10(8) Salmonella on day 33. Salmonella growth in the cecal contents was significantly decreased (P less than 0.01) on day 10 in the chicks provided lactose from day 1-10. However, after the removal of lactose from the diet, the chicks were susceptible to Salmonella colonization. The number of Salmonella in the ceca was significantly reduced (P less than 0.05) in the chicks provided lactose throughout the 40-day growing period. Dietary lactose decreased the pH of the cecal contents and was accompanied by marked increases in the concentrations of undissociated bacteriostatic volatile fatty acids in the cecal contents.

Animals↗
PubMed1981

Lactose tolerance in lambs with rotavirus diarrhoea.

It has been suggested that lactose malabsorption is an important factor in producing the diarrhoea of acute rotavirus infection. Accordingly, the lactose tolerance of gnotobiotic newborn lambs, infected with lamb rotavirus, has been investigated by clinical studies and tissue enzyme assays. Although lactase activity is low in affected areas of the small intestine, rotavirus infected lambs are not lactose intolerant as assessed by the measurement of reducing substances in the faeces, or by the clinical effects and blood glucose levels after a 5.8 mmol (2 g)/kg lactose load on the second day post-infection. Lactose intolerance could be demonstrated by using extremely high (29.2 mmol (10 g)/kg) doses of lactose, three or four times the normal dietary lactose intake. These experiments suggest that lactose-containing feeds (such as maternal milk) are not necessarily contraindicated in patients or animals with rotavirus diarrhoea.

Animals↗
PubMed1990

[High lactose content of the Lundh test meal adversely affects the reliability of the ALTAB test].

UNLABELLED: The exocrine pancreatic function was examined in 20 patient without any detectable gastrointestinal disorder. We used 1 g 4(N-acetyl-L-thyrosil) aminobenzoic acid (ALTAB) an Lundh's test meal containing 25 g lactose, and the test was repeated with 3 g lactase (Galantase). The urine was collected for 6 hours to check PABA excretion in urine. Lactose intolerance was diagnosed in 10 patients on the basis of an increase of H2 in the breath at least 15 ppm after Lundh's test meal and/or diarrhoea after test in two hours if this diarrhoea could be prevented by giving Galantase orally. We measured PABA excretion in patients with and without lactose intolerance after Lundh's test meal: 17.8% (SD = 6.7) and 47% (SD = 13) respectively (p less than 0.001), and after Lundh's test meal with Galantase: 34.3% (SD = 12.7) and 43.6% (SD = 10.9) respectively. The increase after Galantase in the group with lactose intolerance was significant (p less than 0.01). CONCLUSIONS: 1. Lactose content of Lundh's test meal causes a considerable lactose load in patients with lactose intolerance. 2. Oral lactase enzyme usually normalises the result of ALTAB test. 3. It is necessary to detect lactose intolerance before use of Lundh's test meal.

4-Aminobenzoic Acid↗
PubMed1978

Double blind study of milk lactose intolerance.

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.

Adolescent↗
PubMed1983

The mechanism of inducer exclusion. Direct interaction between purified III of the phosphoenolpyruvate:sugar phosphotransferase system and the lactose carrier of Escherichia coli.

A hypothesis for the regulation of some sugar transport systems by the bacterial phosphoenolpyruvate:sugar transport system postulates an interaction between III of this system and the carrier whose activity is regulated. We have studied this interaction in more detail, employing one of these transport systems, the lactose carrier of Escherichia coli. Purified III of the phosphotransferase system interacted directly with the lactose carrier. The binding of III to lactose carrier required the presence of the non-phosphorylated form of III and substrates of the carrier and exhibited a stoichiometry of 1.2+/- 0.2 mol III/mol lactose carrier. The K(d) of lactose carrier for III was 10 +/- 5 microM. III is apparently unable to interact with a mutant lactose carrier which still binds but does not transport galactosides. The binding of III to the lactose carrier results in a 3.5-fold increase in the apparent affinity of galactosides for the carrier. Significantly, the binding of III to the lactose carrier results in an inhibition of galactoside translocation both in membrane vesicles and liposomes reconstituted with the purified lactose carrier. This inhibition may thus be the basis for the well-documented phenomenon of inducer exclusion.

Journal Article↗
PubMed1986

Microbial ecophysiology of whey biomethanation: intermediary metabolism of lactose degradation in continuous culture.

The intermediary carbon and electron flow routes for lactose degradation during whey biomethanation were studied in continuous culture. The chemostat was operated under lactose-limited conditions with a 100-h retention time. The carbon balance observed for lactose degradation was 4.65 mmol of CH(4), 4.36 mmol of CO(2) and 1.15 mmol of cellular carbon per mmol of lactose consumed, with other intermediary metabolites (i.e., acetate, lactate, etc.) accounting for less than 2% of the lactose consumed. The carbon and electron recoveries for this biomethanation were 87 and 90%, respectively. C tracer studies demonstrated that lactose biomethanation occurred in three distinct but simultaneous phases. Lactose was metabolized primarily into lactate, ethanol, acetate, formate, and carbon dioxide. During this hydrolytic phase, 82% of the lactose was transformed into lactate. These metabolites were transformed into acetate and H(2)-CO(2) in a second, acetogenic, phase. Finally, the direct methane precursors were transformed during the methanogenic phase, with acetate accounting for 81% of the methane formed. A general scheme is proposed for the exact carbon and electron flow route during lactose biomethanation, which predicts the prevalent microbial populations in this ecosystem.

Journal Article↗
PubMed1993

Comparative effects of exogenous lactase (beta-galactosidase) preparations on in vivo lactose digestion.

Microbial-derived beta-galactosidase (beta-gal) enzyme preparations improve in vivo lactose digestion and tolerance through enhanced gastrointestinal digestion of lactose. Three different beta-gal preparations, Lactogest (soft gel capsule), Lactaid (caplet), and DairyEase (chewable tablet) and placebo were fed to lactose maldigesters with either 20 g or 50 g of lactose to compare the efficacy of these products and to further establish a dose-response relationship for use. All enzyme preparations dramatically reduced both the peak and total breath hydrogen production when fed with milk containing 20 g of lactose. Four capsules of Lactogest, two caplets of Lactaid, or two tablets of DairyEase (each treatment containing approx 6000 IU) reduced total hydrogen production significantly (P < 0.05) below that observed with two capsules of Lactogest (containing approx 3000 IU) in a stoichiometric manner. Symptoms were significantly (P < 0.05) less severe with all the beta-gal products. In contrast, with 50 g of lactose in water, peak and total hydrogen production was modestly, but not significantly reduced by the enzyme treatment. Furthermore, symptom scores for bloating, cramping, nausea, pain, diarrhea, and flatus were not different between treatments and the control. The 50-g lactose dose appeared to overwhelm the ability of either 3000 or 6000 IU of beta-gal to assist significantly with lactose digestion. Results from these studies demonstrate the relative equivalency of chewable, caplet, and soft-gel beta-gal products, based on IUs of enzyme fed.

Administration, Oral↗
PubMed1994

Dietary lactose as a possible risk factor for ischaemic heart disease: review of epidemiology.

International data show stronger correlations of mortality from ischaemic heart disease with per capita supply of dairy products excluding fat than with dairy fat, and of estimated lactose than with dairy fat or margarine and other processed fats (positively) and vegetable oils and fats, fat of fish or wine (negatively). Butter and cheese, which have a low content of lactose, show moderate and zero correlations, respectively. Populations with low or intermediate prevalence of adult lactose absorbers have a lower supply of dairy products excluding butter (and therefore of lactose), and a lower mortality from ischaemic heart disease, than populations with a high prevalence of absorbers. Specific national and ethnic data suggest that a diet low or relatively low in lactose, in populations with low or relatively low prevalence of lactose absorbers, is more consistently associated with protection against ischaemic heart disease than are high intakes of unsaturated fatty acids, wine, alcohol or dietary fibre. In seven countries with a high consumption of dairy products (six at least with a high prevalence of lactose absorbers), trends in ischaemic heart disease mortality appear to have reflected changes in the supply of milk (and therefore of lactose), but not consistently of butter or inversely of unsaturated fatty acids. The findings reviewed in this paper call for further investigation of the subject, epidemiologically and biochemically.

Animals↗
PubMed2003

Effect of predominant methanogenic flora on the outcome of lactose breath test in irritable bowel syndrome patients.

BACKGROUND: The relationship between hydrogen and methane production is a possible confounding factor in the interpretation of H(2) breath tests (HBT), but is usually disregarded for the interpretation of HBT and, in most instances, only H(2) excretion is measured. The present study was designed to evaluate the effect of predominant fasting methane CH(4) or H(2) production on the outcome of lactose HBT, in a large, homogeneous series of adult patients with irritable bowel syndrome (IBS). PATIENTS AND METHODS: A lactose HBT was performed in 237 IBS patients with predominant fasting methane production (CH(4)>H(2)), recording the outcome of the test, amount of gas excreted and occurrence of clinical symptoms. Data were compared to those of 237 age- and sex-matched IBS patients with low fasting CH(4) excretion. RESULTS: The test was positive in 124 predominant CH(4) producers (52.3%) (PMP), as compared to 201 (84.8%) low methane producers (LMP) (P<0.0001). Peak hydrogen concentration and area under the curve of H(2) were significantly (P<0.001) lower, and the occurrence of symptoms during the test less frequent, in PMP vs LMP patients. During the test, CH(4) excretion doubled in 57/113 (50.4%) patients with negative HBT, and in 49/124 (39.5%) with positive HBT. CONCLUSIONS: Patients with predominant fasting methane production excrete less H(2) than LMP, after an oral load of lactose. The lower prevalence of severe lactose intolerance in PMP, as well as lower incidence of symptoms during the test, is, indeed, related to lower and slower H(2) excretion. The assumption that H(2) excretion is an effective means of quantifying the amount of malabsorbed carbohydrates is questionable in PMP. Methane-producing patients likely have a higher 'false negative' rate as compared to LMP after an oral load of lactose. Nonetheless, as symptoms are related to the amount of gas produced in the colon, HBT identifies patients with 'lactose intolerance', irrespective of the presence of lactose malabsorption, and helps in predicting the effect of lactose-restricted diet.

Adolescent↗