Effects of probiotics administration on lactose intolerance in adulthood: A meta-analysis.

This meta-analysis aimed to investigate the effect of probiotic administration on adults with lactose intolerance. Twelve studies were identified from databases such as PubMed, Cochrane Library, and Web of Knowledge based on the inclusion and exclusion criteria. The effect size was estimated using the standardized mean difference (SMD), and Cochrane's Q test was used to evaluate the statistical heterogeneity of the effect size. Moderator analysis, including meta-ANOVA and meta-regression, were performed to determine the cause of heterogeneity in the effect size using a mixed-effect model. Egger's linear regression test was conducted to evaluate publication bias. The results showed that probiotic administration alleviated the symptoms of lactose intolerance, including abdominal pain, diarrhea, and flatulence. Among them, the area under the curve (AUC) showed the greatest decrease following probiotic administration (SMD, -4.96; 95% confidence interval, -6.92 to -3.00). In the meta-ANOVA test, abdominal pain and total symptoms decreased with monostrain probiotic administration. This combination was also effective for flatulence. The dosage of probiotics or lactose was significantly associated with a reduction in the total symptom score, and the linear regression models between the dosage and SMD were found to be Y = 2.3342 × dosage - 25.0400 (R2 = 79.68%) and Y = 0.2345 × dosage - 7.6618 (R2 = 34.03%), respectively. Publication bias was detected for most items. However, even after effect size correction, the probiotic administration effect for all items remained valid. The administration of probiotics was effective at improving adult lactose intolerance, and it is expected that the results of this study could help improve the nutritional status of adults by increasing their consumption of milk and dairy products in the future.

Adverse food reactions in dogs and cats.

Adverse food reactions (AFR) are a common problem that may cause cutaneous and/or gastrointestinal signs in dogs and cats. They comprise food intolerance, food intoxication, and food allergy. Response to a dietary elimination trial and recurrence of signs during dietary provocation remain the centerpiece of diagnosis and management of dogs and cats with AFR. Response to an elimination trial is frequently observed in dogs and cats with chronic idiopathic enteropathies. However, only a fraction of them relapse after a dietary challenge. These animals may have mild to enteritis and/or colitis and benefit from various additional properties of the elimination diet.

Secondary lactose intolerance in a neonatal goat.

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.

Use of breath hydrogen testing to detect experimentally induced disaccharide malabsorption in healthy adult dogs.

OBJECTIVE: To develop a noninvasive method to detect disaccharide malabsorption in dogs by measuring hydrogen concentration ([H2]) in exhaled breath before and after experimentally induced disaccharide malabsorption. ANIMALS: 8 healthy mixed-breed dogs. PROCEDURE: [H2] was measured every 30 minutes for 8 hours after administration of disaccharide solutions (lactose, 0.5 g/kg of body weight; lactose, 1.0 g/kg; sucrose, 2.0 g/kg; maltose, 1.5 g/kg; and lactose [0.5 g/kg] and sucrose [2.0 g/kg]) to determine reference ranges of [H2] for each solution, which were compared with [H2] in dogs with experimentally induced disaccharide malabsorption. To induce disaccharide malabsorption, dogs were given a mild overdose of lactose (1.5 g/kg) or a disaccharidase inhibitor. In the latter experiment, acarbose (10 mg/kg, PO) was given with the combination of lactose (0.5 g/kg) and sucrose (2 g/kg), and with maltose (1.5 g/kg). RESULTS: Overdosing with lactose resulted in [H2] persistently outside the reference range for lactose in 5 of 8 dogs. Acarbose administration resulted in [H2] persistently outside the reference range in 7 of 8 dogs that received a combination of sucrose and lactose but did not consistently affect [H2] after administration of maltose. CONCLUSIONS: Disaccharide malabsorption resulted in [H2] outside the reference ranges in most of the adult dogs studied, suggesting that the technique may be useful in detecting naturally occurring disaccharidase deficiency.

Association of Clostridium difficile with enterocolitis and lactose intolerance in a foal.

Diagnoses of Clostridium difficile enterocolitis and lactose intolerance were made in a neonatal foal with persistent diarrhea. It was determined that the foal had lactose intolerance on the basis of the results of a lactose tolerance test, and a diagnosis of C difficile enterocolitis was subsequently made. The foal responded to oral administration of metronidazole and lactase. Lactose intolerance is a secondary problem most commonly associated with rotavirus infection, but it can be caused by any condition affecting the small intestine. Because C difficile can affect the small intestine in foals, it was presumably the cause of the lactose intolerance in this foal with persistent diarrhea. Oral administration of lactase was not initially successful in this foal, most likely because of ongoing C difficile enterocolitis. Presumably, metronidazole was an effective treatment for C difficile enterocolitis and administration of lactase allowed for normal digestion of milk until endogenous lactose production returned. Clostridium difficile enterocolitis and lactose intolerance should be considered as differential diagnoses in neonatal foals with diarrhea, especially when the foal is bright and alert.

Diagnosis and management of food allergy and intolerance in dogs and cats.

This paper reviews food allergy and intolerance in dogs and cats. Adverse reactions to ingested food components can affect many systems and can produce signs involving the skin, gastrointestinal tract, respiratory tract and central nervous system, and these clinical signs are reviewed. Most basic food ingredients have the potential to induce an allergic response, although most reactions are caused by proteins. In particular, dogs and cats can become sensitive to cow's milk, beef, fish or cereal. Food allergy and intolerance is rare in dogs and cats, although the incidence in practice is difficult to establish. Clinical signs are quite variable, depending on the individual response, although the major clinical sign is pruritus. Diagnosis can be difficult, as there is no single test available to help the clinician to confirm or refute the presence of food sensitivity. Diagnosis is based on dietary investigation in the form of elimination diets and test meals. Elimination diets for dogs include lamb, chicken, rabbit, horse meat and fish as sources of protein, with rice or potatoes. Successful elimination diets for cats include lamb, chicken, rabbit or venison, with rice. Improvement in clinical signs while on the elimination diet is suggestive of food allergy. The diagnosis should be confirmed by feeding the original diet, with the development of clinical signs within 7 to 14 days of feeding.

Determination of lactose and xylose malabsorption in preruminant diarrheic calves.

In preliminary studies feeding the poorly absorbed carbohydrate sorbitol at 2.3 g/kg body weight as an indication of maximal fermentative capacity failed to produce the expected large increase in breath hydrogen excretion but did produce a transient diarrhea in five out of six control calves. Twelve healthy control and eighteen diarrheic calves were fed lactose or D-xylose on consecutive days at 1.15 g/kg body weight and a concentration of 46 g/L. Breath and blood samples were collected at 1 h intervals from 0 to 7 h. After administration of lactose, there was a significant increase in breath hydrogen excretion in diarrheic versus control calves. The increase in plasma glucose concentrations was delayed in diarrheic calves but the area under the absorption curve was similar in control and diarrheic calves. After administration of D-xylose, breath hydrogen excretion did not increase significantly but plasma D-xylose concentrations were significantly reduced in diarrheic calves. The pathogens commonly isolated from the feces were Cryptosporidium species, rotavirus and coronavirus. The number of pathogens and the severity of the calves' acid-base deficit were not related to the severity of carbohydrate malabsorption. Decreased absorption of lactose and D-xylose may be the result of intestinal villous atrophy caused by viral or parasite infection. It was concluded that carbohydrate malabsorption rather than a specific lactose maldigestion is a significant problem in diarrheic calves. Diarrheic calves appear to digest and absorb lactose when fed in small amounts.

Lactose intolerance in a calf.

Lactose intolerance was identified as the cause of bovine neonatal diarrhea. Glucose and xylose oral absorptions were normal whereas lactose absorption was reduced relative to normal calves. Lactase deficiency is common in people but rarely reported in animals. The treatment of whole milk with lactase alleviated the diarrhea.

Oral lactose tolerance test in foals: technique and normal values.

Oral lactose tolerance tests were evaluated in 25 healthy foals (principals) assigned to 4 groups of approximately 1 week, 4 weeks, 8 weeks, and 12 weeks of age. Lactose monohydrate (1 g/kg of body weight [in a 20% water solution]) was administered via nasogastric tube after a 4-hour fast. Plasma glucose concentrations were monitored before dosing (0 minutes) and sequentially for 300 minutes. Six control foals were given a volume of water equivalent to the volume of lactose monohydrate administered to principal foals. After oral lactose loading, mean plasma glucose concentrations of all principal foals increased from 99.76 mg/dl at 0 minutes to 176.80 mg/dl by 90 minutes. Peak increases in plasma glucose concentrations were attained by 8% of the foals (2 foals) at 30 minutes, 76% (19 foals) at 60 minutes, and 16% (4 foals) at 90 minutes. The mean plasma glucose concentration increase of principal foals, regardless of age or time of peaking, was 77.04 mg/dl. There was no significant (P greater than 0.05) difference in fasting plasma glucose concentrations (0 minutes) among the 4 groups of principal foals or between principal and control foals; however, there was a significant (P less than 0.05) difference in peak glucose concentrations between 1-week-old and 12-week-old principal foals, with the older foals having the higher concentrations. Mean plasma glucose concentrations of control foals decreased from 79.67 mg/dl at 0 minutes to 55.17 mg/dl by 180 minutes. The mean peak decrease in plasma glucose concentrations of control foals, regardless of time of peaking, was 24.50 mg/dl.(ABSTRACT TRUNCATED AT 250 WORDS)

Neurovisceral and skeletal GM1-gangliosidosis in dogs with beta-galactosidase deficiency.

Beta-galactosidase-deficient siblings in two litters of English springer spaniel puppies showed a progressive neurological impairment, dwarfism, orbital hypertelorism, and dysostosis multiplex. An excess of GM1-ganglioside was found in the brain. Three abnormal oligosaccharides were present in samples of urine, brain, liver, and cartilage. Light microscopy of selected tissue specimens revealed cytoplasmic vacuoles in neurons, circulating blood cells, macrophages, and chondrocytes. Ultrastructural studies demonstrated that these membrane-bound vacuoles were of two types--one containing lamellated membranes and the other, finely granular material. These clinical and pathological findings are similar to those observed in human patients affected by the infantile form of GM1-gangliosidosis.

Differential effects of chemical and physical restraint on carbohydrate tolerance testing in nonhuman primates.

Ketamine hydrochloride, used during glucose or lactose tolerance tests to aid restraint of rhesus and stumptail macaques unconditioned to handling, prevented the establishment of definitive baseline plasma glucose tolerance curves from which meaningful interpretations could be derived. Repetition of the tests after the animals were restraint-chair conditioned provided clear baseline control data. It is suggested that ketamine might invalidate those carbohydrate tolerance tests which are based on the absorption of glucose from the gastrointestinal tract.

Lactose intolerance in the stumptail macaque (Macaca arctoides): case report.

A female stumptail macaque had signs of intermittant diarrhea and chronic weight loss over a 2-year period during which she was fed a commercial laboratory maintenance diet. Intolerance of this individual to lactose, a ubiquitous constituent of most commercial primate diets, was diagnosed on the basis of lactose tolerance tests and favorable clinical response to dietary carbohydrate substitution with glucose. Oral administration of varying doses of glucose to this animal consistently produced elevations in plasma glucose concentrations exceeding 20 mg/dl, while orally-administered doses of lactose did not cause significant elevations in blood glucose concentrations.

Lactose malabsorption in two sibling rhesus monkeys (Macaca mulatta).

Observation of two sibling rhesus monkeys, Macaca mulatta, indicated that they were intolerant to lactose. While on a lactose formula the monkeys had severe diarrhea and weight loss but were otherwise healthy. When a lactose-free formula was instituted, the diarrhea abated and there was a steady weight gain.

Carbohydrate digestion and absorption in the equine small intestine.

Dietary carbohydrates, which constitute a most important source of equine nutrition, are digested and absorbed by a series of complex processes principally in the small intestine, beginning with intraluminal starch hydrolysis by the action of pancreatic amylase. The continuous secretion of a copious volume of pancreatic juice, low in enzyme activity, presumably releases sufficient oligosaccharides for further hydrolysis at the intestinal cell surface by brush border enzymes. Active carrier mediated mechanisms then transport the final hexose products across the intestinal cell for uptake in the hepatic portal system. Brush border disaccharidase activities in the equine small intestine are of the same order of magnitude, and have a similar distribution pattern, to those reported in omnivorous and carnivorous species. The disaccharidase development patterns are characteristic and reflect the ability of the horse to digest the major nutrient sources adequately at various stages of life. The efficiency of the mucosal disaccharidases and the monosaccharide transport systems in the equine small intestine have been established by a series of oral disaccharide and monosaccharide tolerance tests. Horses older than three years of age are unable to hydrolyse lactose, but young and adult horses are fully capable of rapidly hydrolysing sucrose and maltose loads. Several tests have clinical application for assessing small intestinal dysfunction in the investigation of diarrhoea and malabsorption. The deficient digestion or absorption of carbohydrate, whether primary or secondary, can almost always be localized to a defect in the enzymic or transport capacity of the small intestinal surface cell. The continued ingestion of lactose could be detrimental in severely diarrhoeic foals.

Carbohydrate digestion and absorption studies in the horse.

The ability of the horse to digest and absorb soluble carbohydrates was assessed using a series of oral disaccharide tolerance tests followed in the same animals by tolerance tests with the constituent monosaccharides. In horses older than three years, lactose did not produce an increase in the plasma glucose levels but induced the passing of soft faeces, indicating that adult horses are lactose intolerant. Horses of all ages could absorb the glucose: galactose mixture without any change in the faeces. The tolerance is due to a failure to hydrolyse lactose and does not involve the monosaccharide transport systems. These findings correspond to the known development pattern of brush border lactase activity in the equine small intestine. Both sucrose and maltose were rapidly hydrolysed, the resulting tolerance curves closely approximating to those for the constituent monosaccharides. Galactose was absorbed at a similar rate to glucose, although a dose of 1g/kg was necessary to produce galactosaemia. An oral lactose tolerance test (1 g/kg as a 20 per cent solution) could be of clinical value to determine small intestinal mucosal damage in diarrhoeic foals when the continued ingestion of lactose might be detrimental.