Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LACTOSE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources

Lactose ingestion in the adult golden hamster (Mesocricetus auratus).

Adult mammals generally demonstrate a lower preference for the disaccharide sugar lactose than for any other common sugar, and because adults typically have low levels of the intestinal enzyme lactase, lactose ingestion may cause gastrointestinal distress. The lactose intake of adult golden hamsters was examined in three experiments; the main findings were: (a) hamsters allowed to choose between tap water and lactose solutions (maximum concentration = 32% weight/volume) over a 20-day period showed a clear preference for lactose solutions and ingested substantial quantities of lactose (up to 3 g/100 g body weight/day) without noticeable adverse effects; (b) hamsters consuming a single diet with lactose added (maximum concentration = 50%) over a period of days ingested up to 3.42 g/100 g body weight/day of lactose without noticeable adverse effects; (c) both hamsters with prior exposure to lactose solutions and those without such exposure consumed similar amounts of 32% lactose solution over an 8-day period, suggesting that hamsters' lactose intake does not depend on the occurrence of adaptation. It is suggested that the fermentative capacity of the hamster's pregastric pouch may underlie this animal's unusual tolerance for lactose.

Animals↗

Effect of dietary lactose on salt-mediated changes in mineral metabolism and bone composition in the rat.

The effects of salt (sodium chloride) supplementation of rat diets (80 g/kg diet), with or without lactose (150 g/kg), were studied in weanling rats over 14 d. Dietary salt increased water intake and reduced weight gain and food conversion efficiency, but these variables were unaffected by lactose. Salt-supplemented rats exhibited a three- to fivefold increase in urinary calcium excretion and a small increase in urinary magnesium and phosphorus excretion, irrespective of dietary lactose content. In addition, salt supplementation reduced plasma alkaline phosphatase (EC 3.1.3.1) activity. Lactose increased urinary Ca and Mg excretion and plasma Ca and P concentrations. Salt reduced tibia mass but not tibia mass expressed relative to body-weight, but neither variable was affected by lactose. Both tibia Mg content and concentration were reduced by salt but unaffected by lactose, and neither tibia P content nor concentration was affected by salt or lactose. Tibia Ca content was reduced by salt but this was prevented by lactose. Tibia Ca concentration was unaffected by salt or lactose, although there was a reduction (not significant) in tibia Ca concentration in animals fed on the lactose-free diet. These results show that lactose had no independent effect on bone and that reduced accretion of bone mass and mineral content in rats fed on the high-salt diets was due, at least in part, to reduced growth. Failure to offset sodium-induced hypercalciuria by a compensatory increase in net Ca absorption may have contributed to reduced bone Ca accretion. The protective effect of lactose against reduced bone Ca accretion may be due to increased Ca absorption.

Alkaline Phosphatase↗

Ineffectiveness of breath methane excretion as a diagnostic test for lactose malabsorption.

BACKGROUND: In clinical and field conditions, breath gas analysis has been widely used in evaluating carbohydrate digestion. A field study was performed to determine the prevalence of lactose malabsorption in Myanmar children and to evaluate the possibility of using breath methane excretion to indicate lactose malabsorption in a field situation. METHODS: The study population consisted of 118 children aged 1 to 12 years. A hydrogen breath test after a lactose meal (2 g/kg, maximum 50 g) was used as a standard test. RESULTS: Lactose malabsorption was detected in 16.7% of children aged 1 to 2.9 years, with the prevalence increasing with age from 40.5% of those aged 3 to 5.9 years to 88.5% of those aged 6 to 8.9 years and reaching 91.7% in those aged 9 to 11.9 years. Lactose malabsorption was more prevalent when children were weaned before 4 months of age (87.2 vs. 41.1%; p < 0.01). Compared with lactose-tolerant children, those with lactose malabsorption had significantly higher concentrations of breath hydrogen excretion 60 minutes after the lactose test meal. Breath methane excretion was also significantly higher in samples at 120 minutes in children with lactose malabsorption. Breath methane excretion of greater than or equal to 2 parts per million at 180 minutes as a diagnostic test for lactose malabsorption had a sensitivity of 61.5% and a specificity of 84.6%. CONCLUSION: The breath methane test for lactose malabsorption has a lower sensitivity and specificity than the breath hydrogen test and therefore does not replace the lactose breath hydrogen test.

Breath Tests↗

Feeding lactose increases ruminal butyrate and plasma beta-hydroxybutyrate in lactating dairy cows.

Ruminal fermentation of lactose increases molar proportions of butyrate, which is metabolized by the ruminal epithelium to beta-hydroxybutyrate (BHBA). To determine the effects of dietary whey, and specifically lactose, on concentrations of ruminal and blood volatile fatty acids (VFA) and blood BHBA, 8 Holstein and 4 Brown Swiss multiparous cows (210 +/- 33 d in milk) were blocked by breed and randomly assigned to one of three 4 x 4 Latin squares. Treatments were control (CON; 7.1% of dietary dry matter [DM] as cornstarch), liquid whey (WHEY; 9.4% of diet DM) containing 70% lactose on a DM basis, low lactose (LOLAC; 7.1% lactose), or high lactose (HILAC; 14.3% lactose). Diets contained 53% forage as corn silage, alfalfa hay, and grass hay (DM basis) and a corn and soybean meal-based concentrate. Average dietary percentage of crude protein and energy density (Mcal/kg net energy for lactation) were 16.8 and 1.47, respectively. Feeding lactose increased DM intake. Milk production and composition were not affected by diet with the exception of decreased urea nitrogen in milk from cows fed lactose. Greater proportions of ruminal propionate were observed in cows fed CON relative to those fed WHEY and LOLAC. Increasing dietary lactose increased proportions of ruminal butyrate and decreased acetate and branched-chain VFA. Concurrent with the increase in ruminal butyrate concentrations, there was an increase in plasma BHBA as lactose in the diet increased. Concentrations of VFA in plasma were not affected by diet with the exception of the branched-chain VFA, which were increased in cows fed LOLAC compared with WHEY. These data indicate lactose fermentation increases proportions of ruminal butyrate and plasma BHBA in lactating dairy cows; however, the observed increase in plasma BHBA is not sufficient to subject cows to ketosis.

3-Hydroxybutyric Acid↗

Lactose intolerance.

Persons with lactose intolerance are unable to digest significant amounts of lactose because of a genetically inadequate amount of the enzyme lactase. Common symptoms include abdominal pain and bloating, excessive flatus, and watery stool following the ingestion of foods containing lactose. Lactase deficiency is present in up to 15 percent of persons of northern European descent, up to 80 percent of blacks and Latinos, and up to 100 percent of American Indians and Asians. A sizable number of adults believe they are lactose intolerant but do not actually have impaired lactose digestion, and some persons with lactase deficiency can tolerate moderate amounts of ingested lactose. A diagnosis of lactose intolerance can usually be made with a careful history supported by dietary manipulation. If necessary, diagnosis can be confirmed by using a breath hydrogen or lactose tolerance test. Treatment consists primarily of avoiding lactose-containing foods. Lactase enzyme supplements may be helpful. The degree of lactose malabsorption varies greatly among patients with lactose intolerance, but most of them can ingest up to 12 oz of milk daily without symptoms. Lactose-intolerant patients must ensure adequate calcium intake.

Calcium, Dietary↗

Prediction of lactose malabsorption in referral patients.

Two hundred forty-two patients referred for various gastrointestinal complaints were evaluated for clinical parameters that would predict findings of lactose malabsorption. Breath hydrogen and blood glucose lactose tests were performed after ingestion of 50 g lactose. Presenting complaints, duration of symptoms, and patient demographics such as age, sex, and ethnic heritage were not different between lactose malabsorbers and absorbers as defined by the breath hydrogen lactose test. Food-related symptoms in general and after specific foods such as milk, ice cream, cheese, and yogurt were also similar between groups. Prior to testing, 30% of malabsorbers (N = 161) and 36% of absorbers (N = 81) reported lactose-related symptoms (P = NS). The blood glucose response to lactose was abnormal in 60% of malabsorbers and 15% of absorbers. This study confirmed our impression that it is difficult to predict lactose absorption status by clinical parameters. The majority of our lactose malabsorber patients were unaware of lactose-associated symptoms. Furthermore, symptom assessment, demographics, food history, and blood glucose testing did not predict abnormal hydrogen responses to lactose.

Adult↗

Chemotherapy-induced lactose intolerance in adults.

BACKGROUND: Anorexia and weight loss contribute to the morbidity and mortality from cancer. This study was designed to test the hypothesis that chemotherapy produces lactose intolerance which could have an adverse effect on the nutritional status of patients receiving cytotoxic drugs. METHODS: Twenty-seven patients were evaluated for the development of lactose intolerance during chemotherapy. Lactose breath hydrogen testing (LBHT) was used to assess lactose malabsorption objectively. This test is based on the principle that in patients with lactase deficiency, lactose is not hydrolyzed in the small intestine and ultimately is degraded by colonic bacteria. This results in the production of hydrogen gas, which is excreted by the lungs and can be quantified with a breath hydrogen analyzer. RESULTS: Of the 27 patients studied, 8 (30%) had an abnormal postchemotherapy LBHT results, and for the population as a whole, postchemotherapy LBHT values were significantly greater than prechemotherapy values (P = 0.04). However, only three patients (11%) showed clinical symptoms of lactose intolerance during the post-chemotherapy LBHT. Five patients had asymptomatic elevations in breath hydrogen excretion on prechemotherapy testing. One of these patients had a further increase in hydrogen excretion on Day 8 after chemotherapy, which was accompanied by symptoms of lactose intolerance. Twenty-two patients had normal prechemotherapy LBHT results. Two of these patients had abnormal post-chemotherapy LBHT results, which were associated with symptoms of lactose intolerance. CONCLUSION: Although chemotherapy may interfere with lactose metabolism, the development of symptomatic lactose intolerance is uncommon. Dietary restriction of milk products in patients receiving chemotherapy therefore is not warranted unless clinical symptoms of lactose intolerance are observed.

Adult↗

Lactose malabsorption and recurrent abdominal pain in Italian children.

The role of lactose malabsorption (LM) was investigated in 32 children (mean age 8.13 +/- 2.46 years) with recurrent abdominal pain (RAP). LM was detected in 75% of them by a lactose breath hydrogen test (LBHT) after a 2-g/kg (max 50-g) load. Of the 18 malabsorbers who participated in a 3-month lactose-free diet (LFD), 14 were judged "improved" and reported lower pain frequency (p less than 0.001). The malabsorbers who improved versus the not improved had comparable past lactose ingestion but were distinguishable on the basis of their lactose absorption capacity (0.36 vs. 0.81 g/kg; p less than 0.01), as subsequently determined by multiple LBHTs with 25-, 12.5-, and 6-g loads. The ratio between past lactose ingestion and lactose absorption was 1.89 in the improved and 0.55 in the not improved groups (p less than 0.01), retrospectively indicating lactose as a possible cause of the symptoms in the improved group. The reintroduction of lactose in amounts not exceeding the absorption capacity into the diet of each malabsorber who had improved with LFD caused relapse in none of the 14 subjects monitored for 2-6 months. In conclusion, LM seems an important cause of symptoms in Italian children with RAP. Assessment of the lactose absorption threshold of each subject of LBHTs provides a basis for reintroduction of "calibrated" amounts of lactose-containing foods (e.g., milk) into the diet.

Administration, Oral↗

Combined LDI/SAT test to evaluate intestinal lactose digestion and mucosa permeability.

BACKGROUND: Intestinal mucosal damage causes impaired digestive capacity and increased mucosal permeability. Quantification of damage can be used to improve treatment options. Currently, the Lactose Digestion Index (LDI) and the Sugar Absorption Test (SAT) are used for evaluation. The investigation studied whether both tests could be combined to provide a useful multifunctional test and whether measurements in blood (LDI) could be replaced by measurements in urine. MATERIALS AND METHODS: The LDI (25 g 13C-lactose, 0.5 g 2H-glucose), the SAT (5 g lactulose, 1 g L-rhamnose) and the LDI/SAT combination test were performed in seven lactose-digesting and eight lactose-maldigesting adults. Plasma glucose 13C-enrichment was determined by gas-chromatography/combustion/isotope ratio mass-spectrometry (GC/C/IRMS), 2H enrichment determined by gas-chromatography/mass-spectrometry (GC/MS) and urinary sugars by gas-chromatography (GC). RESULTS: The results of the separate LDI test were not different from those of the LDI/SAT in the lactose-digester group (0.82 +/- 0.06 vs. 0.81 +/- 0.09), nor in the lactose-maldigester group (0.36 +/- 0.12 vs. 0.35 +/- 0.06). A significant correlation was found between the 10-h urinary-lactose/lactulose ratio and the LDI (R2 = 0.71, P < 0.01). There were no differences in the lactulose/L-rhamnose ratio between lactose-digesters and lactose-maldigesters using both the SAT and LDI/SAT tests. CONCLUSION: The LDI/SAT test is a reliable method of measuring digestion and permeability simultaneously. The 10-h period urinary lactose/lactulose excretion ratio following lactose consumption reflects lactose digestive capacity.

Adult↗

Lactose intolerance in Thai adults.

Lactose intolerance is common in Thai adults who ingest cow's milk but its incidence has not been clearly defined The authors evaluated 45 volunteers (15 males, 35 females), aged 21-31 yrs old, who drank one 240-ml box of milk daily. A Lactose tolerance test was performed using a breath-hydrogen test (BHT) after oral intake of 25 g of lactose dissolved in 250 ml of water The presence of gastrointestinal symptoms of lactose intolerance, flatulence, abdominal pain and diarrhea, were recorded Twenty-one subjects (47%) were categorized as lactose malabsorbers and intolerant, two subjects (4%) were malabsorbers but tolerant, and 22 of 45 (49%) were absorbers and tolerant. The incidence of lactose malabsorption was, thus, 51%; symptoms of intolerance were found in 21 of the 23 malabsorbers, making the incidence of lactose intolerance 47%. In the lactose malabsorbant and intolerant group, the more breath-hydrogen (H) the more symptoms observed All subjects who had a negative breath-H2 test had no symptoms. The breath-H2 test should be used as a standard method to evaluate lactose absorption and lactose tolerance. The incidence of lactose intolerance has decreased from the past and the symptoms are not so severe that the people limit the consumption of milk since it is a major source of food containing good quality of protein and calcium.

Adult↗

Lactose as a carrier in dry powder formulations: the influence of surface characteristics on drug delivery.

The aim of the study was to investigate the interdependence of carrier particle size, surface treatment of the carrier, and inclusion of fines on the drug delivery from dry power inhaler formulations. Two size fractions (< 63 and 63-90 microm) of alpha-lactose monohydrate were subjected to treatment with 95% (v/v) ethanol to introduce small asperities or cavities onto the otherwise smooth surface without substantially changing the particle shape. After blending with albuterol sulfate [ALB; volume median diameter (VMD), 1.9 microm; geometric standard deviation (GSD), 1.5], the solvent-treated lactose produced a fine particle fraction (FPF; < 6.18 microm) and dispersibility of the drug that was significantly (ANOVA p < 0.01) lower than that which resulted from formulations containing untreated lactose of a similar size fraction, after aerosolization at 60 L min(-1) via a Rotahaler. The two size fractions of the treated lactose resulted in similar deposition profiles of ALB. The effects of such surface asperities or cavities of lactose were offset by introducing a small amount (5% w/w) of smaller-sized lactose (5-10 microm) to the powder formulations. The fine lactose increased the FPF and dispersibility of ALB to such a level that all lactose batches, regardless of particle size or whether solvent treated, produced a similar fraction of aerosolized ALB. The inclusion of recrystallized needle lactose (5-15 microm) was superior to micronized lactose in improving the aerosolization of ALB. The findings of this study indicate that the presence and characteristics of the finer fraction of lactose carrier particles dominate over the particle size and surface smoothness of the carrier particles in determining dispersion and deaggregation of drugs from dry powder formulations for inhalation.

Chemistry, Pharmaceutical↗

Surface roughness contribution to the adhesion force distribution of salmeterol xinafoate on lactose carriers by atomic force microscopy.

Adhesion force distributions of silica spheres (5 and 20 microm) and salmeterol xinafoate (4 microm) particles with inhalation grade lactose surfaces and spin coated lactose films were determined by atomic force microscopy (AFM) to investigate the influence of surface roughness on the force distributions. The roughness of lactose particles and films was determined by both AFM and confocal microscopy (CM); the lactose particles showed RMS R(q) values between 0.93 and 2.2 microm. The adhesion force distributions for silica and SX probes were significantly different for the different lactose carriers and broad, e.g., the adhesion force distribution between a 5 microm silica sphere and lactose particles ranged from 5 to 105 nN. This contrasted with distributions on smooth spin coated lactose films (RMS R(q) of 0.28 nm) which were not significantly different and were narrow, e.g., the adhesion force distribution between a 5 microm silica sphere and spin coated lactose films was between 42 and 68 nN. In addition, no significant difference in adhesion force distribution occurred with silica probe size on the lactose carrier surface. The use of X-ray photoelectron spectroscopic analysis confirmed that the lactose surfaces were free of impurities that might contribute to variation in adhesion. Although the almost atomically flat films showed some adhesion variability, the surface roughness of the lactose particles was a major contributing factor to the broad distributions seen in this study.

Adhesiveness↗

Prevalence of primary adult lactose malabsorption in Hungary.

Lactose absorption capacity was estimated in 820 apparently healthy, well nourished, Hungarian adults and adolescents (560 females, 260 males, aged 16-54 years) using a field version of the lactose tolerance test with breath hydrogen determination. The test identified 497 lactose absorbers with low, and 323 lactose malabsorbers with high hydrogen excretion 120-150 min after an oral load of 50 g lactose. The prevalence of lactose malabsorption in the general Hungarian sample (n = 535) was 37%. In subgroups from the western and eastern Hungarian plains, frequency of lactose malabsorption reached almost 30%. It tended to be higher in Upper Hungary (ca. 40%) and in subjects stemming from former Hungarian areas in the Carpathian bend. Lactose malabsorption in a Hungarian ethnic subgroup, the Matyo (n = 172), did not differ significantly from that in the general population. Among Romai ("Gypsies", n = 113), the prevalence of lactose malabsorption was significantly higher (56%). Awareness of milk intolerance was significantly more frequent, and severe symptoms of lactose intolerance during the test occurred almost exclusively in lactose malabsorbers.

Adolescent↗

Lactose maldigestion and recurrent abdominal pain in children.

Our objectives were to evaluate children with recurrent abdominal pain for lactose maldigestion and to assess factors which might predict lactose absorption status. One hundred thirty-seven children were referred for specialty evaluation of recurrent abdominal pain of at least three months' duration. Study subjects were evaluated by history and physical examination, dietary interviews, hematologic and biochemical laboratory testing, stool parasite examination, and radiologic or endoscopic structural examinations, as indicated. Lactose hydrogen breath testing was performed after challenge with 1 g/kg lactose 10% aqueous solution). There were 53 males and 84 females, whose ages ranged from 6 to 18 years (9.64 +/- 2.9; mean +/- SD) Lactose maldigestion was detected in 33/137 patients (24%). The prevalence of abdominal pain, bloating, gas, flatulence, diarrhea, and constipation was similar in children with or without lactose maldigestion. The perception of symptoms related to the ingestion of dairy products was similar in both groups. No other clinical parameter predicted lactose maldigestion. However, children with lactose maldigestion had overall clinical improvement with a lactose-restricted diet. Clinical evaluation alone cannot adequately predict the presence of lactose maldigestion in children. Formal evaluation for lactose maldigestion using breath hydrogen testing methods should be considered in children with recurrent abdominal pain.

Abdominal Pain↗

Treatment of lactose intolerance with exogenous beta-D-galactosidase in pellet form.

The effectiveness of a new beta-D-galactosidase pellet formulation in the treatment of lactose intolerance was studied. The encapsuled beta-D-galactosidase (lactase) pellets were first tested in vitro for their enzymatic activity within an environment simulating gastric conditions and subsequently within an environment simulating duodenal conditions. Effectiveness was measured by the % of glucose formed by hydrolysis of lactose. The pellets were found to retain their enzymatic activity in gastric pH conditions (mean 69 +/- 1 mg/dl glucose) and were found to hydrolyse lactose in human duodenal fluid (106.35 +/- 1 mg/dl). Finally the effectiveness of the new lactase formulation on glucose absorption was studied in 8 lactose intolerant subjects in a randomized, double blind, crossover trial. After fasting, the subjects were given one capsule containing 100 u/ml beta-galactosidase (i.e. 10 pellets of 10 u/ml each) or one capsule containing placebo pellets, followed by 100 g lactose dissolved in water. The washout period between lactose challenges was one week. Plasma glucose concentrations were measured before and at intervals after the challenges and the subjects completed symptom questionnaires every eight hours for 24 hours. Results showed a statistically significant increase in plasma glucose levels 30, 60, 90 and 120 min after lactose ingestion (repeated measures analysis of variance, p<0.01). Subjective ratings of the severity of abdominal cramping, belching, flatulence, vomiting and diarrhoea were significantly decreased following ingestion of the lactase pellets and lactose (no incidence of diarrhoea) compared with after ingestion of placebo and lactose. The results of the study were considered to be very promising as the beta-D-galactosidase formulation (which was produced at very low cost and with great ease) resisted inactivation in the stomach, effectively transformed lactose to glucose in vivo and reduced symptoms of lactose intolerance.

Adult↗

Surgical removal of the pregastric pouch reduces voluntary lactose consumption in golden hamsters.

Unlike other adult mammals, golden hamsters voluntarily consume substantial amounts of the disaccharide sugar lactose. It was hypothesized that the hamster's readiness to consume lactose depends upon its possession of a pregastric pouch in which ingested lactose is broken down into its constituent monosaccharides, thus preventing the aversive gastrointestinal symptoms that monogastric animals experience following lactose ingestion. Adult golden hamsters underwent either surgical removal of the pregastric pouch or sham surgery. Following recovery from surgery, hamsters were given continuous free access for 14 days to tap water, Purina Rodent Chow, a 24% sugar solution (either lactose or sucrose), and a Purina chow-based diet containing 30% added sugar (for each hamster, the same sugar that was provided in solution). Surgical removal of the pregastric pouch caused a 40% reduction in total lactose consumption: this reduction resulted from equivalent decreases in consumption of the lactose solution and the lactose-containing diet. Pouch removal had no effect on total sucrose consumption, and sham surgery had no effect on either lactose or sucrose consumption. These results support the conclusion that the adult hamster's unusually high level of voluntary lactose consumption depends upon its possession of a pregastric pouch, which plays an important role in lactose digestion.

Animals↗

Lactose-induced cell death of beta-galactosidase mutants in Kluyveromyces lactis.

The Kluyveromyces lactis lac4 mutants, lacking the beta-galactosidase gene, cannot assimilate lactose, but grow normally on many other carbon sources. However, when these carbon sources and lactose were simultaneously present in the growth media, the mutants were unable to grow. The effect of lactose was cytotoxic since the addition of lactose to an exponentially-growing culture resulted in 90% loss of viability of the lac4 cells. An osmotic stabilizing agent prevented cells killing, supporting the hypothesis that the lactose toxicity could be mainly due to intracellular osmotic pressure. Deletion of the lactose permease gene, LAC12, abolished the inhibitory effect of lactose and allowed the cell to assimilate other carbon substrates. The lac4 strains gave rise, with unusually high frequency, to spontaneous mutants tolerant to lactose (lar1 mutation: lactose resistant). These mutants were unable to take up lactose. Indeed, lar1 mutation turned out to be allelic to LAC12. The high mutability of the LAC12 locus may be an advantage for survival of K. lactis whose main habitat is lactose-containing niches.

Alleles↗

[Lactose malabsorption in ulcerative colitis. A case-control study].

BACKGROUND: The role of lactose malabsorption in ulcerative colitis is controversial. The aim of this study was to compare the prevalence of lactose malabsorption in a group of ulcerative colitis patients and a control group and to modify lactose consumption in view of the results. METHODS: Lactose malabsorption was studied using the hydrogen breath test in 52 patients with ulcerative colitis and 34 controls after ingestion of 25 g of lactose. A questionnaire on ingestion of milk products was also administered. RESULTS: Of the 52 patients with ulcerative colitis, 13 (25%) presented lactose malabsorption compared with 11 of the 34 (32%) controls (p = 0.45). Twenty-four patients (46%) had been advised to completely eliminate lactose from their diets. Twenty-seven of the 39 patients without malabsorption had reduced or eliminated lactose consumption after being diagnosed with ulcerative colitis. CONCLUSIONS: No significant differences in the prevalence of lactose malabsorption was found between patients with ulcerative colitis and controls. We believe that systematic elimination of lactose from the diets of these patients is erroneous. In our environment, we recommend the hydrogen breath test only in patients with symptoms of lactose intolerance.

Adolescent↗