Does Oral Enzyme Replacement Therapy Reverse Intestinal Lactose Malabsorption?

The effects of oral enzyme replacement therapy on breath hydrogen excretion and symptoms after milk ingestion were studied in lactase-deficient patients. Sixteen symptomatic patients underwent interval hydrogen breath tests using whole milk as substrate. Each study was repeated with the addition of 250 mg of β-D-galactosidase derived from Aspergillus oryzae (Lactrase) given orally with the milk. Subsequently seven of those 11 patients who did not normalize their hydrogen excretion with 250 mg of Lactrase were available to be restudied with a 500-mg dose. Mean cumulative and peak hydrogen excretions were calculated for the baseline (milk alone), 250 mg, and 500 mg Lactrase groups. Significant (p ≤ 0.05) decreases in cumulative and peak hydrogen excretion were noted between the 500 mg Lactrase versus the baseline group, but not between the 250 mg versus baseline group. Five of the 16 (31%) symptomatic lactase-deficient patients normalized their hydrogen excretion after 250 mg of Lactrase; four of seven (57%) who bad not normalized on 250 mg, normalized their hydrogen excretion with 500 mg of Lactrase. A different pattern was observed in the incidence of symptoms. Five of the nine patients (56%) whose hydrogen excretion normalized with the addition of Lactrase at either dosage became asymptomatic after milk ingestion; in addition, three patients who did not normalize their hydrogen also became asymptomatic. We conclude that oral Lactrase in sufficient dosage temporarily reverses lactose malabsorption in some patients.     

Respiratory methane excretion in children with lactose intolerance

Two evaluate the relationship between colonic methane production and carbohydrate malabsorption, we measured end-expiratory methane levels in 70 normal and 40 lactose-intolerant children. Time-dependent excretion of hydrogen and methane was determined every 30 min for 120 min following a fasting oral lactose challenge (2 g/kg). Mean breath hydrogen levels in normals (lactose-tolerant) equaled 3.7 parts per million (ppm) throughout the study, but increased to >10 ppm by 60 min and remained elevated in lactose-intolerant subjects. Breath methane in normal children averaged 1.6 ppm from 0 to 120 min. In contrast, CH₄ excretion by lactose-intolerant children averaged 5.1 ppm at 90 min; and, by 120 min levels increased significantly compared with control. Breath methane levels in lactose-intolerant subjects following a lactose load continued to increase, however, despite the coingestion of exogenous lactase in amounts calculated to result in complete hydrolysis of the disaccharide. These data demonstrate that lactase-deficient children manifest significant increases in breath methane excretion following lactose ingestion and that enhanced methane production may be a consequence of several factors, including altered fecal pH and increased methanogenic substrates provided by colonic lactose fermentation. Further studies are required to determine the clinical significance of elevated methane production in lactose intolerance.     

Enzyme replacement for lactose malabsorption using a beta-D-galactosidase

We evaluated 10 healthy symptomatic lactose malabsorbers for effect of an oral beta-D-galactosidase derived from Aspergillus oryzae (Lactrase, Kremers Urban Company, Milwaukee, WI, U.S.A.) on symptom and breath hydrogen response to challenge with 50 g lactose. Basally and at 30-min intervals for 8 h after lactose challenge, end-alveolar breath samples were collected and analyzed for hydrogen using gas chromatography. Symptoms were scored at 30 min and hourly for 8 h, rating bloating, cramps, nausea, pain, diarrhea, and flatulence. Four challenges were performed on 4 separate days with at least 3 days between challenges. The first two challenges served as baselines. Just before ingestion of 50 g powdered lactose dissolved in 200 ml water, beta-D-galactosidase capsules were given orally as a 250-mg dose for the third challenge and a 500-mg dose for challenge 4. Hydrogen excretion, quantified by using a trapezoidal method for computing area under the discontinuous curve of breath hydrogen concentration, was decreased in subjects receiving beta-D-galactosidase (base-line I, 346.0 ppm/h; baseline II, 367.2 ppm/h; 250-mg galactosidase 208.2 ppm/h; 500-mg galactosidase, 178.0 ppm/h; p less than or equal to 0.05). Other analyzed parameters of H2 excretion were also decreased. Analysis of symptom response scores showed a dose-related decrease for bloating and flatus (p less than or equal to 0.05) and no statistical difference in the other assessed symptoms. We conclude that beta-D-galactosidase from Aspergillus oryzae, when given just before ingestion of lactose by lactose malabsorbers, can produce a dose-dependent reduction (statistically significant for the 500-mg dose) in breath hydrogen excretion, bloating, and flatus.     

Genetic test for lactase non-persistence and hydrogen breath test: Is genotype better than phenotype to diagnose lactose malabsorption?

BackgroundAdult-type hypolactasia is a widespread condition throughout the world, causing lactose malabsorption. The lactose breath test is a simple tool for diagnosis but the need for prolonged monitoring of hydrogen excretion has led to a genetic test proposal. The aim of this study was to compare the genetic test with the lactose breath test in order to give some insights into the clinical value of genetic testing.MethodsThirty-two consecutive functional patients underwent lactose breath test and lactase genetic polymorphism analysis (C/T 13910 and G/A 22018). Intolerance symptoms after lactose load were also monitored.ResultsAll patients with positive lactose breath test showed homozygosis for both polymorphisms. Among the nine patients with a negative breath test result, six showed heterozygosis while three showed homozygosis. Intolerance symptoms were present in 16 homozygotic patients but also in one heterozygotic patient. The k value for the agreement between the genetic test and the lactose breath test was 0.74.ConclusionA positive genetic test for lactase non-persistence indicates whether lactase activity decline may represent a clinical problem for the patient, but does not give information on actual patient symptoms. On the contrary, this information is already available by combining the lactose breath test with intolerance symptom evaluation. Lactose absorption phenotype may be not yet evident until young adult age.     

Lactose malabsorption, irritable bowel syndrome and self-reported milk intolerance

BACKGROUND: The relationship between lactose malabsorption, irritable bowel syndrome and development of intestinal symptoms is unclear, especially when the ingested dose of milk is small. Thus, the role of hydrogen breath testing in the diagnostic work-up of patients with nonspecific intestinal symptoms is still debated. AIMS: To establish the relationship between lactose malabsorption, severe self-reported milk intolerance, irritable bowel syndrome and related symptoms. METHODS: The prevalence of lactose malabsorption was prospectively assessed by means of a hydrogen breath test in 839 patients (503 with irritable bowel syndrome, based on the Rome criteria, regularly consuming milk, and 336 subjects who identified themself as milk intolerant, after an oral load of 25 g lactose). The test was considered "positive" when a hydrogen peak exceeding 20 ppm over baseline values was observed in two or more samples. Attempts were also made to establish whether the predominant presenting symptom (diarrhoea, constipation, alternating diarrhoea and constipation, pain and gaseousness) might be helpful in predicting the outcome of the breath test. RESULTS: The prevalence of a positive breath test was comparable in the two groups (337 patients with irritable bowel syndrome (66.9%) vs 240 patients with milk intolerance (71.4%)). The same holds true for the first peak of hydrogen excretion, total hydrogen output and prevalence of symptoms during, and in the four hours after, the test. The predominant presenting symptom was not useful for predicting outcome of the test either in regular milk users or in milk intolerant subjects. CONCLUSIONS: The almost identical results of the lactose breath test of patients with irritable bowel syndrome and subjects with self-reported milk intolerance suggests that the two conditions overlap to such an extent that the clinical approach should be the same. A lactose breath test should always be included in the diagnostic work-up for irritable bowel syndrome, as fermentation of malabsorbed lactose is likely responsible for triggering symptoms. Conversely, lactase deficiency is probably irrelevant in most subjects not affected by irritable bowel syndrome, within a moderate milk consumption.     

Lactose malabsorption

Opinion statement Lactose malabsorption is a syndrome producing constellation of symptoms, including abdominal pain, bloating, flatulence, diarrhea, and sometimes nausea and/or vomiting. Primary causes of lactose malabsorption due to loss of intestinal lactase activity include genetic/racial lactase nonpersistence, congenital lactase deficiency, and developmental lactase deficiency. Secondary lactose malabsorption can be caused by any disorder that injures the small intestinal mucosa, such as viral gastroenteritis, celiac disease, allergic (eosinophilic) gastroenteritis, and radiation enteritis. The diagnosis depends on careful clinical evaluation and is customarily confirmed with a lactose breath hydrogen test. As the symptoms are nonspecific, many adults diagnosed with lactose malabsorption actually have irritable bowel syndrome. Treatment consists of a trial of eliminating lactose-containing dairy foods, with supplementation of alternative calcium and protein sources. Commercial enzyme products containing β-galactosidases can be prescribed to help patients digest dietary lactose. Long-term lactose restriction usually is not necessary and can lead to reduced bone mineral density.     

Comparative effects of exogenous lactase (β-galactosidase) preparations onin vivo lactose digestion

Microbial-derived -galactosidase (-gal) enzyme preparations improvein vivo lactose digestion and tolerance through enhanced gastrointestinal digestion of lactose. Three different -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 -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 -gal to assist significantly with lactose digestion. Results from these studies demonstrate the relative equivalency of chewable, caplet, and soft-get -gal products, based on IUs of enzyme fed.Funded by Thompson Medical Co., Inc. and the Minnesota Agricultural Experiment Station.     

乳糖酶缺乏与乳糖不耐受症状的临床特点分析

目的 探讨乳糖酶缺乏及乳糖不耐受症状的临床特点.方法 回顾性分析了84例于广东省人民医院门诊就诊的以腹痛、腹泻、腹胀、肠鸣为主要症状的患者,并接受胃肠镜、腹部CT、抽血及氢呼气试验等检查评估,根据患者的主要诊断,氢呼气试验结果及乳糖不耐受症状进行分组,比较各组的临床指标,包括年龄、性别、体质量指数、血常规、过敏原检测、...     

Lactase deficiency in Singapore-born and Canadian-born Chinese

Seventy-three of 77 adult Singapore-born Chinese (95%) and 48 of 49 Canadian-born adult Chinese (98%) were demonstrated to be lactase deficient using the lactose breath hydrogen test. The similar prevalence of lactase deficiency in the Singapore- and the Canadian-born Chinese despite a larger estimated amount of daily milk ingestion in the Canadian-born Chinese (430 ml vs 157 ml) supports the concept that lactase deficiency, which is transmitted genetically, does not have an adaptable component related to the quantity of lactose ingested. When the lactose breath hydrogen test performed with a dose of 0.5 g/kg of lactose was compared with the test using a standard dose of 50 g of lactose, there was very little loss of sensitivity. In spite of the presence of lactase deficiency, only 32% of the Singapore subjects and 23% of the Canadian subjects had gastrointestinal symptoms when milk was ingested in the daily diet. Peak breath H₂ was higher in females than males, but the difference was more significant in the Canadian cohort.     

Lactose malabsorption in Greek adults: correlation of small bowel transit time with the severity of lactose intolerance.

Using breath hydrogen analysis after 139 mmol (50 g) oral lactose load, we investigated the prevalence of lactose malabsorption in 200 Greek adults and examined the relationship between symptoms and small bowel transit time. One hundred and fifty subjects had increased breath hydrogen concentrations (greater than 20 ppm) after the lactose load. In these individuals peak breath hydrogen concentration was inversely related to small bowel transit time (r = 0.63, 6 = 6.854, p less than 0.001) and the severity of symptoms decreased with increasing small bowel transit time. Lactose malabsorbers with diarrhoea during the lactose tolerance test had a small bowel transit time of 51 +/- 22 minutes (x +/- SD; n = 90) which was significantly shorter than the small bowel transit time of patients with colicky pain, flatulence, and abdominal distension (74 +/- 30, n = 53; p less than 0.001) and both groups had significantly shorter small bowel transit time than that of asymptomatic malabsorbers (115 +/- 21 n:7; p less than 0.001). When the oral lactose load was reduced to 33 mmol (12 g), the small bowel transit time increased five-fold and the overall incidence of diarrhoea and/or symptoms decreased dramatically. These results indicate that the prevalence of lactase deficiency in Greece may be as high as 75% and suggest that symptom production in lactose malabsorbers is brought about by the rapid passage down the small intestine of the malabsorbed lactose.     

Enzyme replacement therapy for primary adult lactase deficiency. Effective reduction of lactose malabsorption and milk intolerance by direct addition of beta-galactosidase to milk at mealtime

The addition of microbial beta-galactosidases directly to milk at mealtime represents a potential "enzyme replacement therapy" for primary lactase deficiency. We used the hydrogen breath test as the index of incomplete carbohydrate absorption to assess the efficacy of two enzymes--one from yeast, Kluyveromyces lactis (LactAid), and the other from the fungus Aspergillus niger (Lactase N)--to assist in the hydrolysis of 18 g of lactose in 360 ml (12 oz) of whole milk when consumed by an adult lactose malabsorber. Graded amounts of Lactase N produced, at best, a 53% relative reduction in breath hydrogen excretion, whereas quantitative elimination of excess hydrogen excretion was produced by 1 and 1.5 g of LactAid. A double-blind, controlled, crossover trial was subsequently performed in 50 healthy, unselected Mexican adults, to whom 360 ml of cow's milk was presented in the three forms in a randomized order: intact milk, prehydrolyzed milk, and milk to which 1 g of LactAid was added immediately before consumption. Among the 25 subjects with incomplete carbohydrate absorption with intact milk, adding enzyme 5-min before consumption produced a 62% reduction in breath hydrogen excretion, and symptoms of intolerance were significantly reduced. The feasibility of effective enzyme replacement therapy with a beta-galactosidase from K. lactis is demonstrated.     

Lactase deficiency and lactose intolerance-related symptoms in adult healthy subjects from western France]

The prevalence of lactase deficiency (LD) and lactose intolerance is not well known in France. Using breath hydrogen and methane analysis after 50 g oral lactose load, we investigated the prevalences of LD, lactose intolerance, and methane producer status in 102 healthy adults born in western France, and we examined the relationships between these parameters and the daily milk consumption. In 10 subjects with LD and lactose intolerance, we studied the reproducibility of the lactose hydrogen breath test results for the diagnosis of LD and lactose intolerance and estimated the quantity of lactose malabsorbed in comparison with the lactulose hydrogen breath test. The prevalence of LD was 23.4 percent and symptoms of lactose intolerance were observed in 50 percent of the 24 subjects with LD. The daily milk consumption was not significantly different in the 24 subjects with LD and in the 78 subjects without LD (281 +/- 197 vs 303 +/- 217 ml/24 h). The prevalence of methane producer status was 42.1 percent. The symptomatic group of lactose malabsorbers (n = 12) was characterized by a shorter lactose mouth to caecum transit time (39 +/- 20 vs 88 +/- 48 min; P less than 0.05), and more marked hydrogen production (6.1 +/- 2.3 vs 3.4 +/- 2.4 10(3) ppm.min; P less than 0.04). In the 10 subjects with LD and lactose intolerance, the hydrogen breath test was reproducible for diagnosis of LD and lactose intolerance, and for hydrogen production. The quantity of lactose malabsorbed was 60 percent. In France, symptoms of lactose intolerance are not severe and do not affect the daily consumption of milk and dairy products.     

Lactose malabsorption and intolerance: What should be the best clinical management?

Lactose malabsorption (LM) is the incomplete hydrolysis of lactose due to lactase deficiency, which may occur as a primary disorder or secondary to other intestinal diseases. Primary adult-type hypolactasia is an autosomal recessive condition resulting from the physiological decline of lactase activity. Different methods have been used to diagnose LM. Lactose breath test represents the most reliable technique. A recent consensus conference has proposed the more physiological dosage of 25 g of lactose and a standardized procedure for breath testing. Recently a new genetic test, based on C/T13910 polymorphism, has been proposed for the diagnosis of adult-type hypolactasia, complementing the role of breath testing. LM represents a wellknown cause of abdominal symptoms although only some lactose malabsorbers are also intolerants. Diagnosing lactose intolerance is not straightforward. Many non-malabsorber subjects diagnose themselves as being lactose intolerant. Blind lactose challenge studies should be recommended to obtain objective results. Besides several studies indicate that subjects with lactose intolerance can ingest up to 15 g of lactose with no or minor symptoms. Therefore a therapeutic strategy consists of a lactose restricted diet avoiding the nutritional disadvantages of reduced calcium and vitamin intake. Various pharmacological options are also available. Unfortunately there is insufficient evidence that these therapies are effective. Further double-blind studies are needed to demonstrate treatment effectiveness in lactose intolerance.     

Differential impact of lactose/lactase phenotype on colonic microflora

BACKGROUND:

The ability to digest lactose divides the world’s population into two phenotypes that may be risk variability markers for several diseases. Prebiotic effects likely favour lactose maldigesters who experience lactose spilling into their colon.

OBJECTIVE:

To evaluate the effects of fixed-dose lactose solutions on fecal bifidobacteria and lactobacilli in digesters and maldigesters, and to determine whether the concept of a difference in ability to digest lactose is supported.

METHODS:

A four-week study was performed in 23 lactose mal-digesters and 18 digesters. Following two weeks of dairy food withdrawal, subjects ingested 25 g of lactose twice a day for two weeks. Stool bifidobacteria and lactobacilli counts pre- and postintervention were measured as the primary outcome. For secondary outcomes, total anaerobes, Enterobacteriaceae, beta-galactosidase and N-acetyl-beta-D-glucosaminidase activity in stool, as well as breath hydrogen and symptoms following lactose challenge tests, were measured.

RESULTS:

Lactose maldigesters had a mean change difference (0.72 log₁₀ colony forming units/g stool; P=0.04) in bifidobacteria counts compared with lactose digesters. Lactobacilli counts were increased, but not significantly. Nevertheless, reduced breath hydrogen after lactose ingestion correlated with lactobacilli (r=−0.5; P<0.001). Reduced total breath hydrogen and symptom scores together, with a rise in fecal enzymes after intervention, were appropriate, but not significant.

CONCLUSIONS:

Despite failure to achieve full colonic adaptation, the present study provided evidence for a differential impact of lactose on microflora depending on genetic lactase status. A prebiotic effect was evident in lactose maldigesters but not in lactose digesters. This may play a role in modifying the mechanisms of certain disease risks related to dairy food consumption between the two phenotypes.     

Lactase deficiency: a common genetic trait of the American Indian

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.     

Assessment of lactose absorption by measurement of urinary galactose

Individuals with sufficient intestinal lactase hydrolyze ingested lactose to galactose and glucose and these monosaccharides are absorbed. Lactose is not digested completely when intestinal lactase activity is low and the disaccharide is malabsorbed. Breath hydrogen excretion after lactose ingestion is used commonly to diagnose lactose malabsorption. However, no direct tests are currently used to assess lactose absorption. We tested a new method of assessing lactose absorption in 26 healthy individuals. Each subject ingested 50 g of lactose. Participants were evaluated for lactose malabsorption using a standard 3-h breath hydrogen test. In addition, the urinary excretions of galactose, lactose, and creatinine were quantitated for 3-5 h after lactose ingestion. On the basis of breath hydrogen analysis after lactose ingestion, 12 individuals were lactose malabsorbers (defined as a rise in the breath hydrogen concentration of greater than 20 parts per million above the baseline value). The 14 subjects who did not malabsorb lactose by breath hydrogen testing (defined as a rise in the breath hydrogen concentration of less than or equal to 20 parts per million above the baseline value), had significantly more galactose in their urine 1, 2, and 3 h after lactose ingestion than lactose malabsorbers. The ratio of excreted lactose to excreted galactose was significantly decreased in lactose absorbers compared with lactose malabsorbers (p less than 0.001). Determination of the ratio of urinary galactose to urinary creatinine separated lactose absorbers from lactose malabsorbers completely (p less than 0.001). We conclude from this study that the determination of urinary galactose, urinary lactose/galactose ratio, and urinary galactose/creatinine ratio may be used to assess lactose digestion and absorption in healthy adults.     

Deadaption and readaptation with lactose, but no cross-adaptation to lactulose: a case of occult colonic bacterial adaptation.

The standard 3 h breath hydrogen (3hBH2) test distinguishes lactose maldigesters from lactose digesters. However, multiple factors impact on BH2 and care is needed to exclude a priori variables. When these factors are controlled, a negative BH2 test implies lactase persistent status or lactase nonpersistent status with colonic adaptation. A case of a Sicilian man who tested negative (lactase persistent status confirmed) on an initial 50 g lactose challenge is described. It was observed that he consumed 28.1 g lactose/day before testing. He subsequently underwent five additional challenge tests in the course of the next 10 months. In four tests the dose intake of lactose was varied upon instruction, and in the fifth test a 30 g lactulose challenge was carried out. It was demonstrated that on radically decreasing lactose intake, a full lactase nonpersistent status was unmasked. Output of 3hBH2 varied inversely with daily lactose intake. Finally, at a time when he was readapted to lactose, there was no discernible adaptation to lactulose challenge. It was concluded that 'occult' colonically adapted subjects may contribute to negative BH2 tests. There is a relationship between variation in lactose intake and the results of BH2 testing. Finally, there was no cross-adaptation to lactulose challenge when lactose was used as the adapting sugar.     

Lactose intolerance in active Crohn's disease: clinical value of duodenal lactase analysis.

BACKGROUND: Patients with active Crohn's disease (CD) often report having abdominal symptoms after ingestion of milk products, but the pathomechanism for lactose malabsorption seems to be complex. GOALS: To investigate the prevalence of clinical milk intolerance and to objectify symptoms with hydrogen (H 2 ) breath testing, analysis of lactase protein, and enzyme activity in the duodenal mucosa in patients with CD and in healthy controls. STUDY: In 49 patients with CD and 24 controls, H 2 breath testing was performed. All individuals underwent endoscopy of the upper gastrointestinal tract, in which multiple pinch samples were taken from the distal duodenum. Lactase activity was measured using the method of Dahlquist. The lactase protein expression was analyzed by gel electrophoresis using the monoclonal antibody mlac 10 and by immunochemistry using the monoclonal antibody mlac 4. RESULTS: Prevalence of milk intolerance in healthy controls was 16.6% versus 46.9% in patients with CD, with a high frequency (83.3%) in patients with active disease (CD activity index >150). Milk intolerance was correlated to the duration of inflammatory bowel disease ( p = 0.023) but not to the location or previous bowel resection. Hydrogen breath testing had a moderate sensitivity in detecting lactose maldigestion (70.4%) and a high specificity (95.6%). Duodenal lactase levels were also correlated to disease activity, whereas correlations to clinical symptoms remained poor. Patients with milk intolerance had a significantly reduced bone density at the lumbar spine (z-score, -1.33 +/- 0.92 vs. -0.19 +/- 0.95 [mean +/- SD]; p = 0.002) CONCLUSIONS: Milk intolerance is a frequent problem in active CD, which can be objectified accurately by H 2 lactose breath testing. Decreased lactase levels in the duodenal mucosa may be found during an acute flare but are not the predominant cause of milk intolerance in CD.     

Efficacy of Addition of Exogenous Lactase to Milk in Adult Lactase Deficiency

The efficacy of lactase by Kluyveromyces lactis in hydrolyzing milk lactose and reducing milk intolerance symptoms was tested in 52 proved lactose malabsorbers. The enzyme was added to milk administered to the patients, and H2 breath excretion (as an index of carbohydrate malabsorption), was determined by gas chromatograph technique, and milk intolerance symptoms were recorded. H2 mean excretion was 78.3 +/- 5.49 ppm after administration of intact whole milk 500 ml (test A), 43.5 +/- 4.99 ppm when lactase 2000 U was added to milk 500 ml immediately before administration (test B); 36.7 +/- 5.01 ppm when milk 500 ml was incubated for 12 h with lactase 1000 U (test C), and 29.7 +/- 4.35 ppm when the incubation was prolonged for 24 h (test D). Symptoms score was: test A = 5.85 +/- 0.56, test B = 3.71 +/- 0.45, test C = 2.77 +/- 0.63, test D = 1.7 +/- 0.68. A correlation index of r = 0.44 (p less than 0.01) was obtained between reduction in H2 mean excretion and reduction in symptoms score of a single individual. The addition of this lactase to milk seems to be effective in correcting lactose malabsorption, thus representing a convenient approach in milk intolerance.     

Inverse Dose Effect of Pretest Dietary Lactose Intake on Breath Hydrogen Results and Symptoms in Lactase Nonpersistent Subjects

The aim of this study was to determine a relationship between pretest intake of lactose and outcome of lactose breath hydrogen test. Patients presented at a testing laboratory participated in the study. A 3-hour breath hydrogen, 50-g lactose challenge was carried out. Results were tabulated and patients completed a 3-day recall diet questionnaire. Daily lactose intake was independently calculated and was associated with breath hydrogen and total symptom score. Statistical analysis used Spearman's correlation, Mann-Whitney U-test and χ² or Fisher exact test. Of 118 patients, 50% were lactose maldigesters. In these patients, measured breath hydrogen and symptom scores were significantly higher in the lowest intake group (< 5 g/d) than in the highest intake group (> 20 g/d) (P < .05). In the presumed lactose digesters, 59% experienced some symptoms during testing for unclear reasons. Pretest dietary intake of lactose inversely affects results of breath hydrogen.