[ANEW CASE OF CONGENITAL INTOLERANCE TO LACTOSE].
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Carbohydrate Metabolism↗
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Lactose malabsorption and intolerance in Italians. Clinical implications.
Lactose malabsorption was assessed by the hydrogen breath test in 40 Italian patients with irritable bowel syndrome and 42 controls without abdominal disturbances. Sixty-five percent of patients were "low milk consumers" (0-250 ml milk per day) compared with 38% of controls (P less than 0.02). Lactose loads of 25 and 50 g caused malabsorption in 82.5 and 87.5% patients and in 55 and 62% controls, respectively (patients vs controls P less than 0.02). Malabsorption was more frequent in the "low milk consumers" group (P less than 0.05). During a four-month lactose-free diet as the only treatment 7.5% of patients became symptom-free (and remained so for a further eight-month diet), 52.5% improved, and 40% showed no change.
Adult↗
Lactose malabsorption and intolerance and peak bone mass.
BACKGROUND & AIMS: Lactose malabsorption per se is not associated with alterations of bone mineral density (BMD) or calcium intake, but when intolerance symptoms are present a lower calcium intake and reduction of BMD values are evident. The purpose of this study was to evaluate whether lactose intolerance interferes with the achievement of an adequate peak bone mass in young adults. METHODS: Of 103 enrolled healthy subjects, 55 proved to be lactose malabsorbers with H(2) breath test after lactose administration, and 29 of them experienced intolerance symptoms (diarrhea, abdominal pain, bloating, flatulence). Lumbar and femoral BMD by dual-energy X-ray absorptiometry was measured, and calcium intake and biochemical indices of bone and mineral metabolism were evaluated. RESULTS: Lumbar and femoral BMD, calcium intake, and mineral metabolism did not differ between malabsorbers and absorbers, although among malabsorbers, intolerant subjects showed significant alterations of all these parameters in comparison with tolerant subjects. A strict correlation was evident between BMD values and both severity of symptoms and calcium intake and between calcium intake and severity of symptoms. CONCLUSIONS: Lactose intolerance prevents the achievement of an adequate peak bone mass and may, therefore, predispose to severe osteoporosis.
Absorptiometry, Photon↗
Evaluation of the pathogenesis of flatulence and abdominal cramps in patients with lactose malabsorption.
Aim of this study was to assess whether the interindividual differences in the development of flatulence and cramps in patients with lactose malabsorption are due to the quantity of malabsorbed lactose or gas accumulation, or if accelerated intestinal transit or increased perception of gas might play a role. Hydrogen breath tests were performed in 43 patients with lactose malabsorption after ingestion of 50 g lactose and, on a separate day, 25 g lactulose. The unabsorbed amount of lactose, small bowel transit time and colonic hydrogen accumulation were assessed in patients who did and did not develop flatulence and cramps after ingestion of lactose. The unabsorbed amount of lactose, small bowel transit time and volume and rate of colonic hydrogen accumulation were the same in patients who did or did not have symptoms after lactose. Patients with flatulence and cramps had a significantly longer time interval between the onset of the increase and peak breath hydrogen concentration (p < 0.05) and a significant correlation between the time of occurrence of peak symptoms and the time of peak breath hydrogen concentration (r = 0.75, p < 0.001). Our data suggest that subjective symptoms of lactose intolerance are not due to the amount of malabsorbed lactose or to the volume or rate of gas accumulation per se, but are related to increased perception of gas.
Adolescent↗
Lactose malabsorption and intolerance in Uruguayan population by breath hydrogen test (H2).
This study of 200 Uruguayans between 0 and 86 years old was designed to determine the prevalence of lactose malabsorption. Lactose intolerance is defined as a clinical syndrome of abdominal pain, diarrhea, flatulence, and bloating after the ingestion of a standard lactose tolerance test dose (2 g of lactose per kilogram of body weight or 50 g/m2 of body surface area, maximum 50 g in a 20% water solution). Lactose malabsorption refers to the state in which dietary lactose remains unhydrolyzed and subsequently unabsorbed from the gastrointestinal tract; symptoms may or may not result from lactose malabsorption. The technique of breath hydrogen (H2) was used after ingestion of 2 g/kg body weight to a maximum of 50 g in a 20% solution. There was no lactose malabsorption in children younger than 5 years old. The prevalence increases progressively after the age of 5, and in adolescence the percentage of malabsorption is similar to that in adults, who show 65% lactose malabsorption, with 25% asymptomatic and 40% intolerant. In 109 white adults, the prevalence of lactose malabsorption is 63%, with 24% asymptomatic and 39% intolerant. In 11 black adults, lactose malabsorption is 82%, with 27% asymptomatic and 55% intolerant. The difference between white and black adults is statistically significant (p less than 0.05). The H2 test is simple, reliable, noninvasive, and appropriate to study large populations.
Adolescent↗
Lactase deficiency in Australian school children.
The prevalence of lactase deficiency is high in Mediterranean, Middle Eastern and Asian countries, which suggests that many immigrants and immigrant children from these regions may be unable to produce lactase. Therefore, the aim of this study was to determine the prevalence of lactose malabsorption in primary school-aged children, in two communities with a high proportion of immigrants in metropolitan Sydney. A total of 109 children, aged five to 12 years, were studied by means of the breath hydrogen method. Forty per cent (44/109) showed lactose malabsorption, as defined by a rise in end-expiratory hydrogen levels of 20 ppm or more, two hours after loading with lactose. The prevalence was highest in the subjects of Asian origin (93%; 14/15), followed by Greek subjects (56%; 14/25) and subjects from other Mediterranean and Middle Eastern countries (41%; 15/37). Of the 77 children who were available for follow-up, 57% (44) reported symptoms of lactose intolerance, of whom nearly two-thirds were children who showed lactose malabsorption. The high prevalence of lactase deficiency in children at both schools underlines the need to consider the multiracial identity of Australians in planning educational programmes about nutrition.
Animals↗
Respiratory excretion of hydrogen and methane in Italian subjects after ingestion of lactose and milk.
Lactose malabsorption, by the breath hydrogen test, and lactose intolerance (presence of symptoms) were studied in twenty healthy Italian subjects after intake of 12.5, 25 and 50 g lactose, whole milk and low-lactose milk. A rise in respiratory concentration of hydrogen (greater than 20 ppm) (malabsorption) was found in fifteen subjects after 50 g lactose, in thirteen after 25 g and in seven after 12.5 g. Symptoms generally occurred in subjects presenting a rise in respiratory hydrogen excretion, but such a rise was often observed without symptoms. Thirteen subjects presented symptoms after 50 g lactose, but only three after 25 g and one after 12.5 g. Whole milk (500 ml) gave a lower incidence of lactose malabsorption than 25 g lactose (7/20 versus 13/20, P less than 0.05) and more subjects developed symptoms (7/20 versus 3/20, NS). Low-lactose milk produced no malabsorbers and one intolerant. Breath methane was detected constantly in seven subjects and in three on some of the days of observation. Respiratory methane excretion generally appeared to be unrelated to lactose ingestion.
Adult↗
[Intestinal lactase and milk consumption before and after gastrectomy].
Intestinal lactase assays before and after a Billroth II procedure for chronic duodenal ulcer did not reveal a significant difference. Postoperative lactose intolerance is due to the loss of pyloric function, causing entrance of lactose into the jejunum at a rate exceeding the hydrolytic capacity of the mucosa if the lactase level is low.
Animals↗
[Urinary lactose determination].
The authors suggests a modified method for nonchromatographic measurement of urinary lactose. The minimal detectable lactose volume is 0.5 g/l. Eighty-four children, mostly babies, with lactose intolerance were examined, breast-fed or formula-fed with lactose-containing mixtures. Lactosuria was detected in 27.4% of the examinees. Urinary lactose levels were (mean +/- m) 0.69 +/- 0.02 g/l. No lactosuria was detected by this method in 29 babies without lactose tolerance (control group).
Breast Feeding↗
Cow's milk protein-sensitive enteropathy: number and timing of biopsies for diagnosis.
Intestinal biopsy is an essential procedure in the diagnosis of cow's milk protein-sensitive enteropathy. The number and timing of biopsies, however, is still controversial. Twenty-two infants who were clinically suspected of having cow's milk protein intolerance were put on a milk-free diet, during which they all improved. In the first 14 infants (Group I), milk withdrawal lasted 6-8 weeks; in the following 8 infants (Group II), milk withdrawal lasted 3.5-4 months. At the end of the withdrawal period, each patient was submitted to an oral lactose tolerance test and then to a first jejunal biopsy, followed by a cow's milk challenge, and a second biopsy (1-2 days later). None of the infants showed evidence of lactose intolerance, but they all reacted adversely to milk reintroduction. In Group I, the distribution of mucosae from grade 0 (normal) to III was almost the same before and after challenge (p greater than 0.5); this is considered to be due to the severe mucosal damage still present in prechallenge biopsies. In Group II, however, a significant difference was found in the distribution of mucosae before and after challenge (p less than 0.05), and a deterioration could be observed in each case after challenge. Intraepithelial lymphocyte counts and mitotic index determinations before and after milk reintroduction were of no diagnostic value in either group. It is suggested that the diagnosis of cow's milk protein-sensitive enteropathy may rely on two biopsies, the first after a period of 3.5-4 months on milk-free diet and the second following milk challenge.
Animals↗
Effect of a lactase preparation on lactose content and osmolality of preterm and term infant formulas.
Lactose intolerance due to lactase deficiency often follows acute gastroenteritis. In such situations, a lactose-free formula may be indicated for preterm infants. Therefore, the effect of addition of lactase on the lactose content and osmolality of preterm and term infant formulas was studied. Lactose content of formulas at room temperature was decreased by approximately 50% 1 hour after addition of lactase. Concentration of lactose was reduced by 70% or more after 2 hours in all formulas. Because of the higher initial lactose concentration in term formulas, it took 24 hours to reach the same absolute lactose concentration (10 g/kg formula) found in preterm formulas after 2 hours. There was a moderate increase in osmolality in preterm formulas. The increase was greater in term formulas because of the greater initial concentration of lactose. The addition of lactase appears to be a suitable method for reduction of lactose content of preterm and term formulas, although the increase in osmolality of term formulas may preclude their clinical use.
Diarrhea↗
[Significance of lactose breath test in the newborn].
Lactose breath test have been performed in healthy newborns, in whom breath hydrogen excretion was preliminarily demonstrated by lactulose breath test. 27.5% of newborns showed positive lactose breath test, with no differences related to sex and gestational age, while a higher percentage of positive test has been found in < 2500 g and formula-fed neonates compared, respectively, to > or = 2500 g and breast-fed ones. In healthy newborns, without any clinical signs of lactose intolerance, it is possible to demonstrate hydrogen in expired air; this is not equivalent of lactose malabsorption, but, instead, depends on the phenomenon of colonic fermentation that allows energy and nutrient absorption.
Breath Tests↗
The use of a soy isolate based formula in the treatment of infantile diarrhoea.
Lactose intolerance interferes with the recovery phase in patients with severe diarrhoea. A controlled comparison of a lactose-free soy isolate formula (Isomil) and a standard cow's milk-based formula in 112 infants with severe diarrhoea showed a significant advantage for the lactose-free formula. All the infants were dehydrated on admission and required initial intravenous therapy. The response rate in the two groups was, respectively, 93% and 75%.
Clinical Trials as Topic↗
[Uses of microbial beta-galactosidases to reduce lactose content in milk and dairy products].
The commercial sources of microbial beta-galactosidases (lactases) include the yeasts species Kluyveromyces marxianus, Kluyveromyces lactis and Candida kefyr which are used to hydrolyse lactose in milk due to their optimum pH. On the other hand, lactases obtained from the moulds Aspergillus niger and Aspergillus oryzae have an acid optimum pH and therefore are used to hydrolyse lactose in whey to obtain whey syrups to be used as raw materials in the food industry. The lactose intolerance problem has led to many studies concerning lactose hydrolysis by means of these microbial enzymes to obtain milk suitable for people with lactose maldigestion and special diets for ill persons, elderly population and intolerant babies due to secondary deficiency of lactose. Most industries obtain hydrolyzed lactose milk with free enzyme; however, there are some developments of immobilized lactase catalysts which are being used mainly in whey.
Animals↗
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.
Adult↗
Lowering the milk lactose content in vivo: potential interests, strategies and physiological consequences.
Lactose is the major sugar present in milk and an important osmotic regulator of lactation. It is digested by intestinal lactase, an enzyme expressed in new-borns. Its activity declines following weaning. As a result, adult mammals are normally lactose-intolerant and more than 75% of the human adult population suffers from lactase deficiency. A reduction in milk lactose content could be beneficial for nutritional but also agricultural and industrial purposes (less volume to transport, better milk coagulation, less effluent production). Several attempts to create transgenic mice producing milk with modified carbohydrate compositions have recently been described. Depending on whether these modifications resulted from an alteration of lactose synthesis or from lactose hydrolysis, striking physiological differences are observed.
Animals↗
Lactase insufficiency in Chinese children detected by oral milk and lactose challenge.
A study to determine the incidence of late-onset lactose intolerance was undertaken in 68 normal Chinese children in Singapore using measurements of breath hydrogen concentrations, following a lactose or milk challenge, as indicator of lactose malabsorption. Evidence of lactose malabsorption was detected in 26% of children given a lactose challenge, and in 21% of those given a milk challenge. It is concluded that late-onset lactase insufficiency is common in Chinese children in Singapore.
Animals↗
Darwin's illness revealed.
After returning from the Beagle in 1836, Charles Darwin suffered for over 40 years from long bouts of vomiting, gut pain, headaches, severe tiredness, skin problems, and depression. Twenty doctors failed to treat him. Many books and papers have explained Darwin's mystery illness as organic or psychosomatic, including arsenic poisoning, Chagas' disease, multiple allergy, hypochondria, or bereavement syndrome. None stand up to full scrutiny. His medical history shows he had an organic problem, exacerbated by depression. Here we show that all Darwin's symptoms match systemic lactose intolerance. Vomiting and gut problems showed up two to three hours after a meal, the time it takes for lactose to reach the large intestine. His family history shows a major inherited component, as with genetically predisposed hypolactasia. Darwin only got better when, by chance, he stopped taking milk and cream. Darwin's illness highlights something else he missed--the importance of lactose in mammalian and human evolution.
Famous Persons↗