Efficacy of incremental loads of cow’s milk as a treatment for lactose malabsorption in Japan

BACKGROUNDLactose intolerance (LI) is commonly seen in East Asian countries. Several studies showed that lactose or milk loading has been used as a treatment for lactose malabsorption (LM) in Western countries, but there have been no reports regarding this type of treatment in Japan. As lactose or milk loading requires ingestion of large amounts of lactose within a short period, this is considered to be too harsh for Japanese people because of their less habitual milk consumption (175 mL per day in average) than Western people. In this study, we demonstrated lactose tolerance acquisition in a suitable way for Japanese.AIMTo examine the efficacy of lactose (cow’s milk) loading treatment in patients with LM.METHODSIndividuals with abdominal symptoms induced by milk or dairy products (LI symptoms) were identified with a questionnaire. A 20 g lactose hydrogen breath test (LHBT) was carried out to confirm LM diagnosis and to evaluate co-existence of small intestinal bacterial overgrowth (SIBO). Respondents diagnosed with LM were selected as study subjects and were treated with incremental loads of cow’s milk, starting from 30 mL and increasing up to 200 mL at 4-7 d intervals. After the treatment, changes in symptoms and LM diagnostic value of 20 g LHBT were investigated. Stool samples pre- and post-treatment were examined for changes in intestinal microbiota using 16S rRNA sequencing. Informed consent was obtained prior to each stage of the study.RESULTSIn 46 subjects with LI symptoms (10-68 years old, mean age 34 years old) identified with the questionnaire, 35 (76.1%) were diagnosed with LM by 20 g LHBT, and 6 had co-existing SIBO. The treatment with incremental cow’s milk was carried out in 32 subjects diagnosed with LM (14-68 years old, median age 38.5 years old). The mean period of the treatment was 41 ± 8.6 d. Improvement of symptoms was observed in 29 (90.6%; 95% confidence interval: 75.0%-98.0 %) subjects. Although 20 g LHBT indicated that 10 (34.5%) subjects had improved diagnostic value of LM, no change was observed in 16 (55.2%) subjects. Analysis of the fecal intestinal microbiota showed a significant increase in Blautia in 7 subjects who became symptom-free after the treatment (P = 0.0313).CONCLUSIONLM was diagnosed in approximately 75% of the subjects who had LI. Incremental loads of cow’s milk is regarded as a useful treatment for LM without affecting everyday life.     

Hydrogen breath test in the diagnosis of lactose malabsorption: accuracy of new versus conventional criteria

Increased hydrogen excretion in the breath after carbohydrate ingestion, an expression of carbohydrate malabsorption, represents the pathophysiologic basis of the hydrogen breath test, a simple, noninvasive, reproducible test for the diagnosis of this condition. Few data are available concerning the breath hydrogen response that most accurately identifies carbohydrate malabsorption. In this article we report our application for the first time in clinical practice of 2 recently described, more accurate criteria for the diagnosis of lactose malabsorption (ie, breath hydrogen excretion value > 6 parts per million (ppm) 6 hours after carbohydrate load and a sum greater than 15 ppm for the breath hydrogen values obtained 5, 6, and 7 hours after carbohydrate load). On 3 separate days, we subjected 84 consecutive patients with functional or organic gastrointestinal disease to measurement of hydrogen excretion in the breath after the administration of lactose to test for lactose malabsorption; after the administration of lactulose as a means of ruling out false-negative results resulting from hydrogen-nonproducer status; and after the administration of a nonabsorbable electrolyte solution as a means of ruling out false-positive results caused by the mixing of intestinal content and release of preformed hydrogen trapped in the feces. According to the conventional criterion, 51% of the subjects proved to be lactose malabsorbers. Positive results were obtained with the use of the 6th-hour criterion in 76% of patients, and positive results were found in 80% when the sum of the excretion at hours 5, 6, and 7 was used as the criterion (P < .05 for both comparisons). Ten of 21 and 11 of 25, respectively, showed intolerance symptoms. It was therefore possible for us to diagnose lactose malabsorption in 24% and 27% of patients, respectively, who tested negative according to the conventional criterion. The conventional criterion must be abandoned and these new criteria adopted.     

Increased serum amylase and lipase in fructose malabsorbers

BACKGROUND: Fructose malabsorption is frequently seen in the general population and is characterised by the inability to absorb fructose efficiently. Due to fructose malabsorption, fructose reaches the colon where it is broken down by bacteria to short fatty acids, CO(2) and H(2). Bloating, cramps, osmotic diarrhea and other symptoms of irritable bowel syndrome are the consequence. We recently found that fructose malabsorption is associated with low plasma folic acid concentrations and low serum tryptophan and zinc. Because fructose malabsorption apparently is associated not only with malabsorption of other nutrients, but also with abdominal discomfort, it was of interest to examine whether mild pancreatitis may be involved. METHODS: We retrospectively examined our data in 159 otherwise healthy adults (110 females, 49 males) aged 14-84 years (mean 45.6+/-14.4 S.D.) with gastrointestinal complaints for serum amylase and serum lipase concentrations. The patients have been tested earlier for fructose malabsorption and lactose maldigestion by measuring breath H(2) concentrations after an oral dose of 25 g fructose and 50 g lactose, respectively, 1 week apart. RESULTS: Fructose malabsorption (H(2) concentrations > or =20 ppm over baseline values) was detected in 107 of 159 individuals (67.3%). These subjects with fructose malabsorption presented with significantly higher serum amylase concentrations (73.1 U/l+/-25.7 S.D.) compared to individuals with normal fructose absorption (59.6 U/l+17.9 S.D; p=0.0009). Fructose malabsorbers also presented with higher serum lipase concentrations (122.0 U/l+/-100.3 S.D.) compared to normals (89.5 U/l+/-46.5 S.D.; p<0.05). To determine whether this finding is a consequence of any sort of malabsorption syndrome or whether it is specific for fructose malabsorption, all subjects were screened for lactose maldigestion. Lactose maldigestion (H(2) concentrations>20 ppm over baseline after lactose loading) was found in 50 of 159 individuals (31.4%). There were no significant differences in either amylase or lipase concentrations in lactose maldigestors. CONCLUSION: Serum amylase and lipase concentrations are higher in subjects with fructose malabsorption compared to normals. Therefore, fructose malabsorption should be considered as a differential diagnosis in moderately elevated serum amylase.     

Individual sensitivity to lactose in lactose malabsorption.

The clinical significance of lactose malabsorption and the individual sensitivity to lactose were investigated in 20 patients with verified lactose malabsorption. Thirteen patients were relieved of all symptoms while seven improved only on a lactose-free dth lactose-free milk but following provocation with increasing amounts of lactose, the tendency to diarrhea and abdominal discomfort increased considerably. Three patients experienced discomfort after provocation with only 5 gl lactose. On provocation with increasing amounts of lactose the seven patients who had not recovered also developed increased abdominal discomfort but none of them developed increased tendency to diarrhea. It is concluded that, in addition to lactose malabsorption, these patients must suffer from ittitable colon with tendency to constipation.     

Manifestation and occurrence of selective adult-type lactose malabsorption in Finnish teenagers. A follow-up study

In 1969--1970, a simple random sample of 129 Finnish school-aged children was examined to study selective adult-type lactose malabsorption (SLM) in this age category. SLM was found in 8 children. All subjects were reexamined 5 years later. SLM was reconfirmed in these 8 persons and found in 3 additional subjects who had normal lactose absorption in the first examination. The prevalence of SLM was 9.3%, being 8.5% in the age category 12--15 years and 9.9% in that 16--20 years. Low rise of blood glucose in the lactose tolerance test of the first examination, very low milk consumption, milk intolerance, and history of gastrointestinal symptoms were found to be of low predictive value as indicators of SLM. It was also concluded that information about dietetic sources of lactose is important to persons with SLM, but categorical exclusion of lactose from the diet is not necessary, at least in the Finnish population.     

Lactose intolerance: analysis of underlying factors

BACKGROUND: We studied the degree of lactose digestion and orocecal transit time (OCTT) as possible causes for the variability of symptoms of lactose intolerance (LI) in a sample of a population with genetically determined low lactase activity. METHODS: Lactose digestion index (LDI) was measured by the recently developed 13C-lactose/2H-glucose test. The OCTT was determined using the breath hydrogen test. Based on a 6-h symptom score (SSC) after a challenge dose of 25 g of lactose the subjects were divided into a tolerant group (T: n= 15; SSC = 0) and an intolerant group (IT: n= 28; SSC 1-40). The intolerant group was subdivided according to the severity of symptoms: group ITa (n = 17; mild symptoms without diarrhoea) and group ITb (n = 11; with diarrhoea). RESULTS: The LDI was lower in the intolerant group (0.34 +/- 0.14) (mean +/- SD) than in the tolerant group (0.47 +/- 0.14) (P = 0.008). The OCTT of group IT (60, 30-90 min) (median, quartiles) was significantly shorter than that of group T (105, 60-120 min) (P = 0.003) and was positively correlated with the LDI (P = 0.050). In groups ITa and ITb the OCTT (60, 30-90 min; 60, 26-83 min) and LDI (0.30 +/- 0.14; 0.39 +/- 0.14) were similar. CONCLUSIONS: Lactose digestion capacity, which is determined by small intestinal lactase activity as well as by OCTT, affects the occurrence of lactose intolerance. However, the major difference in intolerance symptoms is caused by differences in the colonic processing of maldigested lactose.     

Effect of lactose on oro-cecal transit in lactose digesters and maldigesters

BACKGROUND: The transit time of the small intestine, in addition to lactase activity, may influence lactose digestion and thus play a role in the occurrence of lactose intolerance. The objectives of this study were to investigate the effect of lactose on the oro-cecal transit time (OCTT) in lactose digesters and maldigesters as well as the possible mechanisms underlying these effects. MATERIALS AND METHODS: Twenty-eight Chinese subjects and 16 Dutch subjects underwent one glucose and one lactose challenge in two single-blinded tests. Twenty of the Chinese subjects without complaints after the challenge then underwent another lactose challenge. A 6-h symptom score (SSC) was recorded, breath-hydrogen concentration was measured and OCTT after consumption of glucose and lactose was determined with the lactose-[13C] ureide breath test. The lactose digestion index (LDI) was determined in both the Dutch and 20 Chinese subjects with the 13C/2H-glucose test. RESULTS: Lactose digesters (n = 13) and maldigesters (n = 20) were classified based on the results of the LDI and the breath-hydrogen test. The OCTT after the lactose and glucose challenges did not differ in the digesters, whereas in the maldigesters the OCTT, after the lactose challenge, was shorter than that after glucose. There was no difference in OCTT after the glucose challenge between the maldigesters and the digesters. However, the OCTT after the lactose challenge in the maldigesters was shorter than that in the digesters. The LDI of the digesters was significantly higher than that of the maldigesters. The OCTT after the lactose challenge was not correlated to the LDI in the maldigesters nor in the digesters. Based on the SSC after the one glucose and two lactose challenges, a tolerant (n = 7) and an intolerant (n = 5) group were classified in the Chinese subjects. The two groups did not differ in their LDI or OCTT after the lactose challenge. The OCTT after the lactose challenge was not correlated to the SSC or the LDI. CONCLUSIONS: Lactose triggers a faster oro-cecal transit in lactose maldigesters, but not in digesters. However, this could not be explained by intestinal distension resulting from the osmotic load posed by maldigested lactose, and thus suggests a direct effect of lactose on intrinsic factors regulating intestinal motility.     

Sensitivity and specificity of the hydrogen breath-analysis test for detecting malabsorption of physiological doses of lactose

We examined the changes in sensitivity and specificity that would occur with alterations in the sample-collection schedule and (or) cutoff criterion for the increase in hydrogen concentration in breath after administration of doses of lactose in the dietary range. In a breath-analysis test to classify individuals as lactose-absorbers or lactose-malabsorbers, 41 subjects drank 360 mL of intact cow's milk, containing 18 g of lactose, and breath samples were collected and analyzed at 30-min intervals for 5 h. An increase in H2 concentration of greater than or equal to 20 microL/L above basal values at any of the 10 intervals was diagnostic of malabsorption. Increases of greater than or equal to 18 or greater than or equal to 15 microL/L were only 85% as specific in classifying the same individuals. Reduction in the number of samples tested per subject uniformly reduced the sensitivity. However, a simplified procedure suitable for field studies (in which four samples--at 0, 2, 3, and 4 h--are collected and analyzed with greater than or equal to 20 microL/L as the cutoff value) gives 80% sensitivity and 100% specificity, as compared with the 11-sample procedure.     

Temperature of a test solution influences abdominal symptoms in lactose tolerance tests

In lactose maldigesters, retarding gastric emptying (food/pharmaceuticals) improves tolerance to lactose. The role of temperature of test solution on the indicators of lactose intolerance was studied. After an overnight fast, 10 lactose maldigesters ingested, in three sessions, 50 g lactose in a randomized cross-over trial. The solutions were at temperatures of 20-21°C (room temperature), 2-3°C (cold) and 55-58°C (hot). Gastrointestinal symptoms and indicators measuring lactose absorption were recorded. Abdominal pain was noticeably increased by the modification of temperature. The cold solution reduced flatulence and abdominal bloating, whereas the hot solution increased bloating and borborygmi. Breath hydrogen excretion tended to be augmented and retarded after cold solution. The temperature of the solution used in a lactose tolerance test affects the gastrointestinal symptoms, but has only minor effects on the other indicators of lactose maldigestion. The constant tendencies observed suggest that a room temperature solution is to be recommended for testing lactose digestion.     

Temperature of a test solution influences abdominal symptoms in lactose tolerance tests

In lactose maldigesters, retarding gastric emptying (food/pharmaceuticals) improves tolerance to lactose. The role of temperature of test solution on the indicators of lactose intolerance was studied. After an overnight fast, 10 lactose maldigesters ingested, in three sessions, 50 g lactose in a randomized cross-over trial. The solutions were at temperatures of 20-21 degrees C (room temperature), 2-3 degrees C (cold) and 55-58 degrees C (hot). Gastrointestinal symptoms and indicators measuring lactose absorption were recorded. Abdominal pain was noticeably increased by the modification of temperature. The cold solution reduced flatulence and abdominal bloating, whereas the hot solution increased bloating and borborygmi. Breath hydrogen excretion tended to be augmented and retarded after cold solution. The temperature of the solution used in a lactose tolerance test affects the gastrointestinal symptoms, but has only minor effects on the other indicators of lactose maldigestion. The constant tendencies observed suggest that a room temperature solution is to be recommended for testing lactose digestion.     

Intestinal permeability and lactose hydrolysis in human rotaviral gastroenteritis assessed simultaneously by non-invasive differential sugar permeation

Changes in intestinal permeability and lactose hydrolysis have been investigated in three adults and fifteen infants with acute rotaviral gastroenteritis by differential sugar absorption. The method involves chromatographic measurement of urinary lactose, lactulose and L-rhamnose excretion following combined ingestion in an iso-osmolar test solution. All patients had abnormal intestinal permeability indicated by raised urine lactulose/L-rhamnose excretion, ratio of percentages recovered in 5 h, of 0.462 (0.100-1.227) mean and range, compared with 0.027 (0.008-0.052) for healthy controls (P less than 0.001). Ten patients also had urinary lactose/lactulose excretion ratios raised above the normal range (0.014-0.41, mean 0.258) during their acute illness, indicating impaired intestinal lactose hydrolysis. Both indices had become normal 4 weeks after the acute illness, serial investigation of five patients showing that improvement was complete much earlier. Except for the short duration these changes are similar to those associated with villous atrophy in coeliac disease. The test procedure was verified with respect to intestinal lactose hydrolysis by demonstrating a linear relationship between lactose/lactulose excretion and log jejunal mucosal lactase activity by in vitro assay (R2 = 0.95) in a further group of subjects. Differential lactose/lactulose/L-rhamnose absorption provides a non-invasive and sensitive index of small intestinal integrity of value for the interpretation of prolonged or otherwise complicated enteritis and the distinction of primary secondary intestinal lactase deficiency.     

Beneficial effects of oral tilactase on patients with hypolactasia

Background A lactose‐free diet is commonly prescribed to subjects with hypolactasia. We tested the effectiveness of a single ingestion of tilactase (a β‐d ‐galactosidase from Aspergillus oryzae) in adults with hypolactasia, previously assessed by lactose H₂‐breath test. Materials and methods After measurement of orocecal transit time (OCTT, by lactulose H₂‐breath test) and lactose H₂‐breath testing plus placebo, a total of 134 subjects were positive to hypolactasia and underwent lactose H₂‐breath testing plus either low (6750 U) or standard (11 250 U) doses of tilactase. The appearance of gastrointestinal symptoms during the tests was monitored. Results OCTT was longer in malabsorbers (subjects without bloating, abdominal pain and/or diarrhoea, n = 25) than in intolerants (bloating, abdominal pain and/or diarrhoea, n = 109, P < 0·02). Malabsorbers had longer time to H₂ peak (P < 0·03), lower H₂ peak levels (P < 0·002) and smaller integrated H₂ excretion levels (P < 0·005) than intolerants. After tilactase ingestion, integrated H₂ levels were decreased by 75% (low dose) and 87% (standard dose) in malabsorbers, and by 74% (low dose) and 88% (standard dose) in intolerants. In the latter group, total symptom score were decreased by 76% (low dose) and by 88% (standard dose) (P < 0·0001). Conclusion A single oral administration of tilactase is highly effective in decreasing symptoms and hydrogen excretion of hypolactasia assessed by lactose H₂‐breath test. If confirmed by long‐term observations, ingestion of tilactase might be a better option than exclusion diets in intolerant subjects with hypolactasia.     

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.     

The 13C/2H-glucose test for determination of small intestinal lactase activity

To diagnose hypolactasia, determination of lactase enzyme activity in small intestinal biopsy material is considered to be the golden standard. Because of its strongly invasive character and the sampling problems, alternative methods have been looked for. We analysed the 13C-glucose response in serum after consumption of 25 g of naturally enriched 13C-lactose. As an internal standard, 0.5 g of 2H-glucose was added and the 2H-glucose response in serum was measured simultaneously. The studies were performed in healthy volunteers with a background of genetically determined lactase nonpersistence (n = 12; low lactase activity) and lactase persistence (n = 27; high lactase activity). The results were compared with those of the lactose hydrogen breath test, the lactose 13CO2 breath test and the previously described 13C-lactose digestion test. After consumption of 13C-lactose and 2H-glucose, the mean ratio 13C-glucose/2H-glucose concentration in serum at 45-75 min was 0.26 +/- 0.09 in the low lactase activity group and 0.93 +/- 0.17 in the high lactase activity group (P < 0.01). Threshold of the ratio between digesters and maldigesters was calculated as 0.46. Accuracy of the new test was superior to all other tests. We conclude that the 13C/2H-glucose test has the potential of determining the small intestinal lactase activity in vivo and of estimating the amount of lactose which is digested in the small intestine.     

Reversible lactose malabsorption and intolerance in Graves' disease

Ten patients with untreated Graves' disease underwent tests to determine lactose absorption, liquid gastric emptying, and oral cecal transit time. To determine the influence of thyroid hormone status on lactose absorption, eight of these same patients had repeat studies when rendered euthyroid. Two of these eight patients also underwent studies while transiently hypothyroid. Motility studies were also evaluated in a group of 11 control subjects. Lactose malabsorption occurred in nine patients with Graves' disease. In seven patients who repeated these studies, lactose malabsorption normalized in three, symptoms induced by lactose improved in two and were unchanged in two. However, these latter two patients appeared to have improved symptoms in the transient hypothyroid state. Liquid gastric emptying was significantly faster in untreated patients than controls and treated self-same patients. Transit time was significantly faster in untreated patients than when they were rendered euthyroid. There may be a relationship between altered lactose absorption states and changes in intestinal motility in patients with Graves' disease.     

Lactose (mal)digestion evaluated by the 13C-lactose digestion test

BACKGROUND: The prevalence of genetically determined lactase nonpersistence is based on the results of the lactose H2 breath test. This test, however, is an indirect test, which might lead to misinterpretation. DESIGN: We determined lactase activity in healthy Chinese and Dutch students using a novel 13C-lactose digestion test. The cut-off value of this test was established in a Chinese population with a homogenous genetic background of lactase nonpersistence and was compared with the results obtained in a Caucasian population. Twenty-five grams of a 13C-lactose solution was consumed by 12 known H2-positive and 5 H2-negative Chinese students and 48 Dutch students and, subsequently, 13C-glucose concentration in plasma and H2 excretion in breath were measured. RESULTS: A similar 13C-glucose response curve was found in all Chinese students. The mean response curve in the Dutch students was more pronounced (P < 0.01). The 1 h (peak) plasma 13C-glucose concentration was the best discriminator between lactose digesting and maldigesting subjects. The cut-off level of 2 mmol L-1 13C-glucose in plasma was defined in the H2-positive Chinese students group. Based on the 13C-glucose response the prevalence of lactose maldigestion in the Dutch subjects was 25%; based on the lactose H2 breath test 17%. CONCLUSIONS: Using the 13C-lactose digestion test the results demonstrate a higher prevalence of lactose maldigestion in a Caucasian population than indicated by the results of the H2 breath test. A moderate increase in the plasma 13C-glucose concentration after consumption of 13C-lactose in the young adult Chinese subjects indicates a residual lactase activity in that age group, even when a positive H2 breath test result is obtained. These results indicate that the 13C-glucose concentration in plasma more accurately reflects the small intestinal lactose digestion capacity than the lactose H2 breath test.     

Use of pulmonary hydrogen (H2) measurements to quantitate carbohydrate absorption: Study of partially gastrectomized patients

A technique was developed to quantitate the absorption of ingested carbohydrate by means of continuous measurements of pulmonary H(2) excretion. This technique is based on the observation that H(2) is produced in the colon when carbohydrate is fermented by colonic bacteria, and this H(2) is then excreted by the lungs. The quantitative relationship of pulmonary H(2) excretion to unabsorbed carbohydrate was studied in nine subjects. After ingestion of 6.5, 13, and 26 g of lactulose (a nonabsorbable disaccharide), H(2) excretion increased linearly, averaging (+/-1 SEM) 13+/-3.5, 23+/-7.2, and 49+/-7 ml per 2 hr. Because of consistent individual differences in H(2) excretion per gram of lactulose, the variability of this linear response was less in a given subject, with the H(2) excretion after 6.5 g and 26 g lactulose dosages averaging 55+/-4.2% and 214+/-16% of that observed after the 13 g dose. It was further demonstrated with fecal homogenates, as well as in rats after direct intracecal instillation of carbohydrate, that there was no significant difference in the rate of H(2) formation from lactulose as compared with the normally ingested sugars. Thus, a subject's H(2) excretion after a 13 g dose of lactulose can be used as a standard to convert H(2) excretion after ingestion of other carbohydrates into grams of carbohydrate not absorbed. Application of this technique to seven partially gastrectomized patients indicated all subjects malabsorbed a portion of a 100 g dose of glucose whereas six of seven completely absorbed a 25 g dose. Malabsorption of physiologic quantities of various carbohydrates was clearly demonstrated in one subject. This technique appears to provide quantitative information on carbohydrate malabsorption not readily obtained by presently available techniques.     

Frequent causes of diarrhea: celiac disease and lactose intolerance

Celiac disease and lactose intolerance are both relatively frequent diseases with symptoms occurring after ingestion of certain food components.In celiac disease wheat gluten and related proteins of other cereals induce an inflammatory disease of the small intestine in predisposed individuals, leading to gastrointestinal and extraintestinal symptoms. Moreover, there is an association with many other diseases and besides classic symptoms (diarrhea, weight loss, malabsorption) atypical courses with less or lacking gastrointestinal symptoms exist. The prevalence is about 1 : 100 (Europe, USA) and higher than supposed earlier. Diagnostic criteria include serologic tests (tissue transglutaminase antibody, endomysial antibody) and characteristic small bowel histology (lymphocytic infiltration, villous atrophy). Therapy is a strict and lifelong gluten-free diet. Rarely, refractory disease or lack of compliance are associated with increased risk of malignancy and worse prognosis.Lactose intolerance is attributed to low intestinal lactase levels, due to reduced genetic expression or mucosal injury and consequent intolerance to dairy products. The frequency is varying in different ethnic groups, occurring in 10-15% of Northern European people. Intensity of clinical symptoms (diarrhea, abdominal pain, bloating) depends on the amount of ingested lactose and individual activity of intestinal lactase. The capacity of lactose malabsorption can be measured using the noninvasive lactose breath hydrogen test. The treatment is based on a reduced dietary lactose intake or in case of secondary form treatment of the underlying disease.     

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.     

Role of pH in production of hydrogen from carbohydrates by colonic bacterial flora. Studies in vivo and in vitro.

Hydrogen produced by colonic bacteria and excreted in breath is a useful index of carbohydrate malabsorption. Since colonic contents are often acidic in individuals with carbohydrate malabsorption and in normal newborns, we determined the effect of colonic acidification on H2 production. Acidification of colonic contents by dietary means significantly reduced excess breath H2 excretion from 55.4 +/- 11.1 (SEM) to 12.2 +/- 3.1 ml/4 h (P less than 0.05) after administration of 0.3 g/kg of the nonabsorbable sugar lactulose to five normal adult subjects. Similarly, the breath H2 response to lactose was reduced or eliminated in two proven lactose malabsorbers after acidification. The correlation between pH and H2 production from carbohydrate was further investigated in adults and neonates, using an in vitro fecal incubation system. Glucose disappearance and H2 production were pH dependent and highly correlated (r = 0.94) in the pH range 5.5-7.6. Maximal production of H2 from glucose by fecal incubates occurred at pH 7.0-7.45. Inhibition of H2 production from carbohydrate occurred at acid pH. H2 per hour from glucose at pH 6.2 and 5.5 averaged 60.2% and 24.2%, respectively, of that produced at neutral pH. Rapid reversal of pH-induced inhibition by neutralization indicated a metabolic, rather than a bactericidal process. The observations indicate that the breath H2 response to malabsorbed carbohydrate is affected by colonic pH. It appears that the efficiency of bacterial carbohydrate metabolism in the colon is pH dependent.