Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.108 (lactase)
 2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low-lactose milk was produced by incubating cow's milk with yeast lactase. Sixteen lactose tolerant and 15 intolerant volunteers ingested 500 ml of the product twice daily for 1 month. During the testing period all subjects received on three occasions the same volume of unmodified milk in double-blind tests. Symptoms recorded throughout the study and for an additional 15 day base-line observation period were: diarrhea, abdominal pain and distention, flatulence, heartburn, and headache. Low-lactose milk acceptance was excellent. No significant differences were found between tolerants and intolerants during the base-line period and while ingesting low-lactose milk. By contrast, unmodified milk induced severe symptoms only in the intolerants. Availability of low-lactose milk and of its by-products allows consumption of greater volumes of this highly nutritious food by subjects with lactose intolerance with none or less symptoms compared to unmodified milk.
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PMID:Long-term acceptance of low-lactose milk. 11 42

The effect of a single dose or oral lactase on symptoms, breath hydrogen concentration, and glucose absorption in lactose-intolerant subjects challenged with lactose was studied. Volunteers underwent a lactose challenge test; those whose breath hydrogen concentrations increased 20 ppm or more and who met other criteria were admitted as subjects. After fasting, the subjects were given three chewable lactase tablets (total lactase dose, 9900 FCC units) or placebo tablets in a randomized, double-blind, crossover manner. The subjects also consumed 8 oz of whole milk in which 37.5 g of lactose powder was dissolved (total lactose content, 50 g). The washout period between lactose challenges was at least one week. Breath hydrogen and plasma glucose concentrations were measured before and at intervals after the challenges, and the subjects completed symptom-evaluation questionnaires every eight hours for four days. Twenty-four subjects completed the study. The maximum mean breath hydrogen concentration was significantly lower after lactase treatment than after placebo treatment. In 21 subjects, the area under the hydrogen concentration-time curve (AUC) was lower after lactase than after placebo; three subjects had hydrogen AUCs more than 300 ppm.hr lower. There were no significant differences in plasma glucose levels. Subjective ratings of the severity of abdominal cramping, belching, flatulence, and diarrhea were lower during the first eight hours after challenge in lactase-treated subjects; ratings for bloating were lower during the next eight hours. Single doses of a chewable lactase tablet reduced the concentration of expired hydrogen and symptoms of lactose intolerance after a lactose challenge.
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PMID:Effect of a single dose of lactase on symptoms and expired hydrogen after lactose challenge in lactose-intolerant subjects. 153 29

Lactose-intolerant children manifest diminished or nonexistent intestinal lactase activity, resulting in flatulence, abdominal pain, and diarrhea. To assess the hydrolytic capability of lactase-containing tablets taken immediately before oral lactose challenge, we studied 18 children previously identified as being lactose intolerant and having no underlying organic gastrointestinal disease. Subjects had a mean (+/- SEM) age of 11.4 +/- 3.4 years; 72% were male. At time of the study, lactase-containing tablets or placebo tablets were ingested (double-blind) immediately before drinking a solution of lactose. Breath samples were obtained for hydrogen analysis at 30-minute intervals during a 2-hour period, and clinical symptoms were monitored. In lactose-intolerant patients, hydrogen production was significantly greater following placebo (maximum hydrogen excretion, approximately 60 ppm) compared with lactase-containing tablets (maximum hydrogen excretion, 7 ppm). Increased hydrogen production was associated with clinical symptoms including abdominal pain (89% of subjects following placebo ingestion), bloating (83%), diarrhea (61%), and flatulence (44%). These results indicate, therefore, that coingestion of lactose and lactase-containing tablets significantly reduces both breath hydrogen excretion and clinical symptoms associated with lactose intolerance.
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PMID:Beta-galactosidase tablets in the treatment of lactose intolerance in pediatrics. 212 19

Large quantities of yogurt are consumed by some lactase-deficient population groups. We used breath hydrogen measurements to determine whether lactase-deficient subjects absorbed lactose in yogurt better than lactose in milk. Ingestion of 18 g of lactose in yogurt resulted in only about one third as much hydrogen excretion as a similar load of lactose in milk or water, indicating a much better absorption of lactose in yogurt. Ingestion of yogurt also resulted in fewer reports of diarrhea or flatulence than did a similar quantity of lactose ingested in milk or a water solution. The enhanced absorption of lactose in yogurt appeared to result from the intraintestinal digestion of lactose by lactase released from the yogurt organisms. This autodigesting feature makes yogurt a well-tolerated source of milk for lactase-deficient persons and may explain the widespread consumption of yogurt by lactase-deficient population groups.
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PMID:Yogurt--an autodigesting source of lactose. 641 39

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.
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PMID:Lactose malabsorption in Greek adults: correlation of small bowel transit time with the severity of lactose intolerance. 712 6

We describe a 64-year-old woman with a malignant intestinal T-cell lymphoma who presented four years later with disabling osteomalacia and secondary hyperparathyroidism due to malabsorption. Only two years later, when the patient had developed fatty stools, flatulence and weight loss, diagnosis of gluten-sensitive enteropathy (GSE) was confirmed by small-intestine biopsy. This case report illustrates that in adults GSE can be oligosymptomatic for long periods. In cases of osteomalacia or rare intestinal T-cell lymphoma a detailed history of bowel movements, inspection of stools, quantification of fat excretion in stools and laboratory tests for malabsorption are recommended. Positive antibodies against gliadin, endomysium and reticulin may support the diagnosis of GSE. However, intestinal biopsy is necessary to verify the presence of GSE. In view of the unspecific histological changes, a follow-up biopsy is recommended in oligosymptomatic cases. Serial measurements of antibodies allow supervision of compliance for a diet strictly free of gluten. In addition, lactose containing milk products need to be restricted initially because of secondary lactase deficiency.
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PMID:[Gluten-sensitive enteropathy with intestinal T-cell lymphoma: an unusual cause of in disabling osteomalacia]. 748 45

The prevalence of lactose maldigestion is lowest in Scandinavia and Northwest Europe (3-8%) and close to 100% in most of Southeast Asia. In Europe the frequency increases in the southern and eastern directions, reaching 70% in southern Italy and Turkey. There is also a high prevalence of lactose maldigestion in the people of Africa with the exception of cattle-raising nomads. Lactose maldigestion causes uncharacteristic abdominal symptoms such as bloating, borborygmus, colic, flatulence, and diarrhea. The degree of discomfort depends on the amount of lactose consumed, but also on an individual sensitivity to lactose. The symptoms of irritable bowel syndrome (IBS) and lactose maldigestion are similar. Consequently, most investigations indicate an increased frequency of lactose maldigestion in patients suffering from IBS. Recurrent abdominal pain (RAP) in children corresponds to IBS in adults. Lactose maldigestion is a frequent cause of RAP in regions with a high prevalence of lactose maldigestion in early childhood. Diffuse small-intestinal damage in celiac disease or kwashiorkor leads to a proportional decrease of all disaccharidase activities, with the most pronounced being decrease of lactase. The consumption of milk may then cause abdominal discomfort and increased diarrhea. Several investigations have indicated an increased frequency of lactose maldigestion in patients with osteoporosis. A connection between lactose maldigestion and decreased absorption of calcium has not been proven, however. The increased tendency toward osteoporosis is more likely caused by a lower calcium intake because of milk intolerance. Milk and dairy products with reduced lactose content are better tolerated by patients with lactose maldigestion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The clinical significance of disaccharide maldigestion. 811 58

To determine the prevalence of short polymers of glucose and starch malabsorption caused by small intestinal glucoamylase deficiency in children with chronic diarrhea, we studied small bowel biopsy specimens from 511 children (aged 1 month to 9 years) with chronic diarrhea evaluated at 54 medical centers. Glucoamylase and disaccharidase (lactase, sucrase, maltase, and palatinase) enzyme assays were performed. Of the 511 children, 15 had glucoamylase deficiency. Six who had significant small intestinal mucosal injury and disaccharidase deficiencies were defined as having secondary glucoamylase deficiency; the other nine patients with normal mucosal morphologic features were defined as having primary glucoamylase deficiency. Secretin tests showed normal pancreatic amylase values for age in all seven children tested. Four of them had abnormal findings on tolerance tests for starch and short polymers of glucose (rise in blood glucose concentration: < 20 mg/dl) and reducing substances in stools, and three of these four had symptoms of intolerance (abdominal distention, flatulence, and diarrhea). All seven patients responded to a starch elimination diet. After reintroduction of a starch diet, diarrhea recurred in four patients; this was alleviated 48 hours after reelimination of starch. We conclude that intestinal glucoamylase deficiency is present in some patients with chronic diarrhea.
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PMID:Small intestinal glucoamylase deficiency and starch malabsorption: a newly recognized alpha-glucosidase deficiency in children. 815 67

We reported previously that consumption of one cup of milk (240 mL) per day produced negligible symptoms in lactase-nonpersistent (LNP) individuals self-described as being severely lactose intolerant. We hypothesized that such LNP individuals could also tolerate two cups of milk per day if taken in two widely divided doses with food, and that psychologic factors play a role in perceptions of lactose intolerance. The Minnesota Multiphasic Personality Inventory 2 (MMPI-2) was administered to 19 LNP subjects self-described as markedly lactose intolerant (S-LNP), 13 LNP subjects who denied lactose intolerance (A-LNP), and 10 lactase-persistent individuals who believed they were lactose intolerant (S-LP). Symptoms were recorded when LNP subjects ingested 240 mL regular or lactose-hydrolyzed milk twice daily for 7 d in a double-blind crossover study. The results showed that neither LNP group had a significant increase in symptoms (P < 0.05) during the regular compared with the lactose-hydrolyzed milk periods. However, S-LNP subjects reported significantly greater gaseous symptoms than did the A-LNP subjects during both treatment periods. The MMPI-2 showed a high score on the "lie" validity scale for S-LNP subjects. We conclude that LNP subjects tolerate two cups of milk per day without appreciable symptoms. S-LNP subjects have underlying flatulence that is misattributed to lactose intolerance. MMPI-2 results were of questionable validity because of the high rate of dissimulation by LNP subjects.
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PMID:Tolerance to the daily ingestion of two cups of milk by individuals claiming lactose intolerance. 912 83

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.
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PMID:Lactose intolerance: problems in diagnosis and treatment. 1019 5


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