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An infant with lactose intolerance is described. A breast-fed infant developed vomiting at 3 weeks, and became dehydrated. Lactosuria, aminoaciduria, and liver damage were preesent. A milk-free diet led to rapid recovery. At 6 months a normal diet was well tolerated.
Lactose intolerance is a common disorder encountered in clinical practice. Evaluation involves obtaining a thorough nutritional history and recognizing associations between diet and gastrointestinal complaints. Lack of suspicion of the problem can lead to expensive and invasive diagnostic procedures, which may further aggravate patients' anxiety and result in iatrogenic complications. Once the diagnosis is confirmed, simple dietary management may resolve symptoms completely.
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The role of lactose malabsorption was studied prospectively in 80 schoolchildren with recurrent abdominal pain. Malabsorption was documented in 40 per cent (16 of 59 whites, 12 of 16 blacks and four of five Hispanic children) on the basis of elevated levels of hydrogen in their breath. Those with lactose malabsorption, however, were not clinically distinguishable on the basis of past milk ingestion (P greater than 0.05), weekly pain frequency (median, five vs. six times), presence of diarrhea (40 vs. 27 per cent) or symptom response to lactose load. In children with malabsorption who completed a six-week diet trial, 70 per cent reported increased frequency of pain (P less than 0.002) when placed on their usual lactose-containing diet. Lactose malabsorption has a substantial role in the symptoms of children with recurrent abdominal pain, and it should be considered before performing invasive procedures or assuming a psychogenic origin.
BACKGROUND: Celiac disease is a common cause of chronic diarrhea and malabsorption syndrome all over the world. Though it was considered uncommon in India in past, it is being described frequently recently. Some patients with celiac disease do not improve despite gluten free diet (GFD). A study described 15 cases of celiac disease unresponsive to GFD in whom small intestinal bacterial overgrowth (SIBO) or lactose intolerance was the cause for unresponsiveness. CASE PRESENTATION: During a three-year period, 12 adult patients with celiac disease were seen in the Luminal Gastroenterology Clinic in a tertiary referral center in northern India. Two of these 12 patients (16.6%), who did not fully respond to GFD initially, are presented here. Unresponsiveness resulted from SIBO in one and lactose intolerance in the other. The former patient responded to antibiotics and the latter to lactose withdrawal in addition to standard GFD. CONCLUSION: In patients with celiac disease partially responsive or unresponsive to GFD, SIBO and lactose intolerance should be suspected; appropriate investigations and treatment for these may result in complete recovery.
The most common cause of apparent ineffectiveness or resistance to treatment with oral levothyroxine (LT(4)) is the result of noncompliance, known as pseudomalabsorption. However, an abnormality in the bioavailability of LT(4) should also be considered in patients requiring large doses of LT(4) to achieve euthyroidism. The incidence of lactose intolerance in Caucasian adult patients is 7%-20%, but the association with resistance to treatment with oral LT(4) is unusual. We report a 55-year-old woman in whom treatment LT(4) for hypothyroidism was found related to a previously undiagnosed oligo-symptomatic lactose intolerance, an unusual association. Although rare, intolerance to lactose should be considered in the differential diagnosis of gastrointestinal diseases that can cause malabsorption of LT(4). The possibility of correcting this disorder with simple dietary measures justifies its consideration.
OBJECTIVE: To study the relationships of molecularly defined lactose malabsorption (LM) and self-reported lactose intolerance (LI) to bone mineral density (BMD) and fractures among Finnish postmenopausal women. DESIGN: A cross-sectional study of two cohorts. SETTING: Helsinki University Central Hospital. SUBJECTS: One cohort was population-based and comprised 453 women, aged 62-78 (mean 69) y. Another comprised 52 women, aged 69-85 (mean 75) y, with osteoporotic fractures and 59 control women, aged 69-83 (mean 74) y, without osteoporosis. METHODS: A single nucleotide polymorphism of the lactase (LCT) gene at chromosome 2q21-22 was studied. It shows complete association with intestinal disaccharidase activity, with the genotype CC(-13 910) meaning adult-type hypolactasia (primary LM) and the genotypes CT(-13 910) and TT(-13 910) lactose absorption. BMD of the heel was measured by dual-energy X-ray absorptiometry (DXA). RESULTS: In the population-based cohort, 16.0% of women had self-reported LI but only 15.3% of them had the CC(-13 910) genotype. Calcium intake from dairy products (P = 0.10) and BMD, adjusted for age, weight, height, exercise, smoking, and estrogen use (P = 0.71) were similar for the genotypes. Women with self-reported LI had reduced calcium intake from dairy products (P < 0.0001) but they were more frequent users of calcium supplements than lactose-tolerants (P < 0.0001). Adjusted BMD was similar for lactose intolerant and tolerant women (P = 0.60). Of 104 women with previous fracture in the population-based cohort, 13.5% had the CC(-13 910) genotype, which did not differ from the prevalence of 19.3% among 347 women without fractures (P = 0.29). The frequency of the CC(-13 910) genotype (23.1%) for 52 women with established osteoporosis was similar as for 59 control women (15.3%) (P = 0.19). CONCLUSION: Molecularly defined LM and self-reported LI are not risk factors for osteoporosis, if calcium intake from diet and/or supplements remains sufficient. Our study confirms the poor correlation between self-reported LI and LM established by different techniques.
A non-invasive, interval sampling hydrogen (H2) breath-analysis test for carbohydrate malabsorption was used in a 3 year-old Guatemalan child with severe protein-energy malnutrition (kwashiorkor) and in this relatives: mother half-sister and step-father to examine genetic and nutritional factors in lactose intolerance in young children. Clinical lactose intolerance was present in the patient on admission, and lactose malabsorption, even of 0.88 g per kg of weight, persisted after complete nutritional recobly due to gastric retention of the substrate. Malabsorption of a physiological dose of lactose, 12.5 g, was detected in the mother and step-father while their daughter exhibited normal growth and development and normal lactose absorption at 8 months of age. The H2 breath test proved to be a sensitive, well-tolerated procedure for both adults and young children. Pitfalls, such as delayed gastric emptying, absence of normal bacterial flora, prior use of antibiotics, must be considered in interpreting H2 breath test results in children.
OBJECTIVE: To determine lactose metabolism and lactase activity in Chinese children of different ages, prevalence of lactase deficiency (LD), and lactose intolerance (LI). METHODS: All 1168 healthy subjects between 3 and 13 years were recruited from schools in four large cities in China. They were screened by a 25 g lactose tolerance test. Some subjects were challenged with 50 g milk powder on different days. Both indicators, the expiratory H2 concentration and intolerance symptoms, were analyzed. RESULTS: LD occurred in 38.5% of children in the 3-5 year age group, and 87% of the 7-8 year and 11-13 year old groups. The age of occurrence for LD may be at 7-8 years among Chinese children. The prevalence of LI among Chinese children was 12.2% at age 3-5 years, 33.1% at age 7-8 years, and 30.5% at age 11-13 years, respectively. CONCLUSION: The results demonstrate that LD is very common in Chinese children from these four cities. LD and LI have a dose dependent response: lactose absorption and symptoms are based on lactase activity. The relationship between breast feeding history (or the history of cow milk intake) and lactase activity among Chinese children has not been established.
The maturational decline in lactase activity renders most of the world's adult human population intolerant of excessive consumption of milk and other dairy products. In conditions of primary or secondary lactase deficiency, the lactose sugars in milk pass through the gastrointestinal tract undigested or are partially digested by enzymes produced by intestinal bacterial flora to yield short chain fatty acids, hydrogen, carbon dioxide, and methane. The undigested lactose molecules and products of bacterial digestion can result in symptoms of lactose intolerance, diarrhea, gas bloat, flatulence, and abdominal pain. Diagnosis of lactose intolerance is often made on clinical grounds and response to an empiric trail of dietary lactose avoidance. Biochemical methods for assessing lactose malabsorption in the form of the lactose breath hydrogen test and direct lactase enzyme activity performed on small intestinal tissue biopsy samples may also be utilized. In some adults, however, high levels of lactase activity persist into adulthood. This hereditary persistence of lactase is common primarily in people of northern European descent and is attributed to inheritance of an autosomal-dominant mutation that prevents the maturational decline in lactase expression. Recent reports have identified genetic polymorphisms that are closely associated with lactase persistence and nonpersistence phenotypes. The identification of genetic variants associated with lactase persistence or nonpersistence allows for molecular detection of the genetic predisposition towards adult-onset hypolactasia by DNA sequencing or restriction fragment length polymorphism analysis. The role for such genetic detection in clinical practice seems limited to ruling out adult-onset hypolactasia as a cause of intolerance symptoms but remains to be fully defined. Attention should be paid to appropriate interpretation of genetic detection in order to avoid potentially harmful reduction in dairy intake or misdiagnosis of secondary lactase deficiency.
Lactose malabsorption and lactase deficiency are chronic organic pathologic conditions characterized by abdominal pain and distention, flatulence, and the passage of loose, watery stools. Though malabsorption of the sugar lactose is determinable by breath hydrogen test or jejunal biopsy, intolerance can only be confirmed by challenge with lactose-containing food, the response to which may not be immediate. The difficulty of making a positive diagnosis of these conditions has led to a proportion of lactose-intolerant patients being misdiagnosed with irritable bowel syndrome (IBS), which has a remarkably similar symptom complex and for which there is no current pathophysiologic marker. The incidence of the two disorders is approximately equal, but the actual proportion of patients with IBS incorrectly diagnosed in this way varies as a function of the methodology used. Once correct diagnosis is established, introduction of a lactose-free dietary regime relieves symptoms in most patients. Symptom similarity and the resultant incorrect diagnosis of IBS may explain the refractory nature of some patients labeled as IBS who remain largely unaware of the relationship between food intake and symptoms.
A 2-week-old Toggenburg kid was evaluated for persistent diarrhea and poor body condition. The herd had high morbidity and mortality associated with diarrhea in neonatal kids. Lactose intolerance was diagnosed on the basis of results of a lactose tolerance test and glucose absorption test. Clinically normal herdmates were used as control animals. The kid responded to lactase supplementation. Cryptosporidium organisms were detected in feces of several affected kids during episodes of acute diarrhea. Lactose intolerance was presumed to have developed secondary to intestinal cryptosporidiosis.
The primary acquired lactase deficiency of the adult is known to cause various disturbances in the gastrointestinal tract while extraintestinal symptoms are unusual. Here we report on a histologically proven chronic eczema requiring corticosteroid treatment for several months. It was obviously induced by a concomitant lactose intolerance since the introduction of a lactose-free diet led to a complete disappearance of the eczema and allowed the discontinuation of the corticosteroid treatment. As far as we know, this is the first case report of an eczema caused by a lactose intolerance.
A modified method for estimation of total glycoprotein hexoses in feces, based on their measurements in the blood serum, is presented. Sixty-six nursing children with lactose intolerance, breastfed or formula fed, were examined; formula fed babies were kept on mixtures with high and low lactose content. Glycoprotein hexose parameters were as follows (X +/- m): 13.51 +/- 1.93, 12.05 +/- 2.20, and 3.69 +/- 0.47 g/l feces. In control children without lactose intolerance (n = 33) this value was 3.6 +/- 0.79 g/l. Increased glycoprotein excretion is connected with glycocalix and small intestinal enterocyte alteration.
OBJECTIVE: To assess the effects of the ingestion of milk, yoghurt (10(8) bacteria/ml), heat-treated yoghurt (<15 bacteria/ml) and two products obtained by dilution of yoghurt with heat-treated product (10(6) and 10(5) bacteria/ml) on hydrogen production and symptoms of lactose intolerance in lactose malabsorbers. DESIGN: Double-blind, randomised cross-over design. SETTING: The study was performed in the phase 1 clinical unit of OPTIMED, Nancy, France. SUBJECTS: Twenty-four male lactose malabsorbers were selected for the study. INTERVENTIONS: Hydrogen production and adverse events were followed during 8 h after ingestion of the products. RESULTS: The results clearly demonstrate that ingestion of yoghurt with 10(8) bacteria/ml leads to lower H(2) excretion and complaints than the other products. Results observed with the products containing a reduced population of live flora remain better than those observed with milk. CONCLUSIONS: The importance of a high population of the live flora is underlined.
Lactase-phlorizin hydrolase (LPH), a membrane-bound glycoprotein present in the luminal surface of enterocytes in the intestine is responsible for lactose intolerance, a phenomenon prevalent in humans worldwide. In the rodent intestine, the post-natal development of the LPH follows a specific pattern, such that the enzyme levels are high in the peri-natal period, but declines considerably upon maturation. The observed maturational decline in the LPH activity is very similar to adult-type hypolactasia observed in humans. Majority of the studies have been carried out using animal models or cell lines and a number of hypotheses have been put forward to explain the maturational decline of lactase activity such as: (a) decreased amount of lactase protein, (b) defect in post-translational modification of precursor lactase to the mature enzyme, and (c) synthesis of an inactive, high molecular weight lactase with altered glycosylation, however, the precise underlying mechanism of adult-type hypolactasia remains undefined. The present review describes the recent developments in understanding the regulation of lactase expression and the possible mechanism of adult-type hypolactasia, as a cause of lactose intolerance.
BACKGROUND/AIMS: Acquired lactase deficiency is a common cause of gastrointestinal symptoms but its etiology remains unclear. Celiac disease could lead to lactase deficiency and is much more common than previously suspected. Several studies have highlighted the prevalence of lactose intolerance in celiac disease, but studies assessing the prevalence of celiac disease in lactose intolerance are lacking. We evaluated the prevalence of celiac disease in patients with a positive H2-lactose breath test compared to a control group. METHODS: This retrospective study included 54 patients (15 males/39 females; mean age 37.8 +/- 7 years) from southern Italy, referred to the Gastroenterology Unit for bloating and diarrhea after the introduction of milk or dietary lactose. They had a positive H2-lactose breath test and a negative H2-glucose breath test. 50 blood donors were drawn from a similar population, matched for sex and age, and enrolled as a control group. All patients were screened for possible celiac disease by measuring the serum level of IgA antibodies to endomysium, anti-transglutaminase and total IgA. Patients positive for at least one of these markers were submitted to upper gastrointestinal endoscopy. RESULTS: None of the patients had a IgA deficiency. 24% of the patients showed positivity of celiac disease antibodies compared to 2% in the control group (p < 0.001). Histologic samples of these patients showed villous atrophy (53.8% Marsh type IIIa, 38.4% Marsh IIIb, and 7.6% with Marsh type IIIc) confirming the celiac disease, while in the control subjects duodenal biopsies were normal. CONCLUSIONS: A high prevalence of celiac disease was observed in patients with a positive H2-lactose breath test compared to healthy controls. In these subjects lactase deficiency seems to be the only manifestation of celiac disease. We suggest serologic screening for celiac disease in all patients with a positive H2-lactose breath test before beginning a milk-exclusion diet.
BACKGROUND: Twenty-five patients of irritable bowel syndrome (IBS) and 25 normal healthy individuals serving as controls, were studied for lactose intolerance. METHODS: Hydrogen breath test was used as an investigation after giving 50 g of oral lactose. Clinically, the patients were classified into 3 types of IBS. RESULTS: Eleven (44%) out of 25 patients belonged to diarrhoeal type of IBS, 7 (28%) of 25 patients to spastic and rest 7 (28%) of 25 patients had features of both types of symptoms. Lactose hydrogen breath test was abnormal in 9 cases (82%) of 11 diarrhoeal type of IBS which was significantly higher (p < 0.02) than controls. However, the difference of abnormal hydrogen breath test between spastic type of IBS and patients with features of both types was not significant as compared to controls. CONCLUSIONS: These results suggest that patients with diarrhoeal type of IBS have a higher incidence of lactose intolerance as compared to spastic type as well as patients with features of both types.