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Lactulose mannitol ratio tests are clinically useful for assessing disorders characterised by changes in gut permeability and for assessing mixing in the intestinal lumen. Variations between currently used test protocols preclude meaningful comparisons between studies. We determined the optimal sampling period and related this to intestinal residence. Half-hourly lactulose and mannitol urinary excretions were determined over 6 hours in 40 healthy female volunteers after administration of either 600 mg aspirin or placebo, in randomised order at weekly intervals. Gastric and small intestinal transit times were assessed by the SmartPill in 6 subjects from the same population. Half-hourly percentage recoveries of lactulose and mannitol were grouped on a basis of compartment transit time. The rate of increase or decrease of each sugar within each group was explored by simple linear regression to assess the optimal period of sampling. The between subject standard errors for each half-hourly lactulose and mannitol excretion were lowest, the correlation of the quantity of each sugar excreted with time was optimal and the difference between the two sugars in this temporal relationship maximal during the period from 2½-4 h after ingestion. Half-hourly lactulose excretions were generally increased after dosage with aspirin whilst those of mannitol were unchanged as was the temporal pattern and period of lowest between subject standard error for both sugars. The results indicate that between subject variation in the percentage excretion of the two sugars would be minimised and the differences in the temporal patterns of excretion would be maximised if the period of collection of urine used in clinical tests of small intestinal permeability were restricted to 2½-4 h post dosage. This period corresponds to a period when the column of digesta column containing the probes is passing from the small to the large intestine.

Hepatic encephalopathy (HE) is a serious neuropsychiatric complication of cirrhosis and/or porto-systemic shunting. The clinical symptoms are widely variable, extending from subtle impairment in mental state to coma. The utility of categorizing the severity of HE accurately and efficiently serves not only to provide practical functional information about the current clinical status of the patient but also gives valuable prognostic information. In the past 20–30 years, there has been rapid progress in understanding the pathophysiological basis of HE; however, the lack of direct correlation between pathogenic factors and the severity of HE make it difficult to select appropriate therapy for HE patients. In this review, we will discuss the classification system and its limitations, the neuropsychometric assessments and their challenges, as well as the present knowledge on the pathophysiological mechanisms. Despite the many prevalent hypotheses around the pathogenesis of the disease, most treatments focus on targeting and lowering the accumulation of ammonia as well as inflammation. However, treatment of minimal HE remains a huge unmet need and a big concerted effort is needed to better define this condition to allow the development of new therapies. We review the currently available therapies and future approaches to treat HE as well as the scientific and clinical data that support their effectiveness.

Although often used as a reference standard in the breath hydrogen test (BHT), lactulose fermentation produces more hydrogen, compared to starch, and may therefore not be ideal. This study compares inulin with lactulose as reference standard in the study of carbohydrate malabsorption. Seventeen patients with malabsorption due to chronic pancreatitis and 15 normal controls were studied. Following overnight fasts, BHTs were performed after ingesting 10 g lactulose, 10 g inulin, and 200 g (16 g highly resistant starch) maize meal. Lactulose fermentation produced significantly more hydrogen than inulin in patients with malabsorption (97 +/- 20 vs 45 +/- 22 ppm x hr; P < 0.05) and controls (43 +/- 18 vs 21 +/- 10 ppm x hr; P < 0.05). Patients produced more hydrogen than controls with both standards (lactulose, 97 +/- 20 vs 43 +/- 18 ppm x hr, P < 0.05; inulin 45 +/- 22 vs 21 +/- 10 ppm x hrs; P < 0.05), suggesting adaptation of the colonic flora. Calculated CHO malabsorption was 2.5 +/- 0.8 vs 5.2 +/- 3.8 g with lactulose and 5.2 +/- 3.1 vs 11.2 +/- 9.6 g with inulin as standards in controls and patients, respectively (P < 0.05). Lactulose produces more breath hydrogen than inulin. Calculation of CHO malabsorption using these standards is therefore not comparable.

The increased availability of noninvasive breath tests, each with limitations, has led to widespread testing for small intestinal bacterial overgrowth (SIBO) in patients with non-specific gastrointestinal complaints. The lactulose breath test (LBT) is based upon an incorrect premise and therefore incorrect interpretations which has resulted in the over-diagnosis of SIBO and the excessive use of antibiotics in clinical practice. Despite limitations, the glucose breath test (GBT) should be exclusively employed when considering SIBO in appropriately chosen patients. This review suggests guidelines for the optimal use and appropriate interpretation of the GBT for suspected SIBO. The LBT should be discarded from future use, and the literature based upon the LBT should be discounted accordingly.

Urinary gluten immunogenic peptides (u-GIPs) have been proposed as a complementary marker to classical intestinal permeability tests based on lactulose, mannitol, and the lactulose:mannitol ratio (LMR). However, the effects of gluten dose, urine collection interval, and sampling strategy on their performance remain insufficiently defined. This study evaluated these variables to support protocol standardization. Data from four standardized protocols including 46 healthy adults exposed to 0, 2, 4, or 10 g of gluten were analyzed. All participants ingested fixed doses of lactulose and mannitol. Urine was collected cumulatively (0–6 h and 0–15 h) or by individual voids. u-GIP levels were measured by lateral-flow immunoassay, and lactulose and mannitol by ion chromatography. u-GIP excretion showed a clear dose dependence. Lactulose excretion increased transiently only at the 10 g dose during the 0–6 h interval, while mannitol excretion and LMR were unaffected. The u-GIP excretion index showed linear proportionality at the 2 g and 4 g doses but exhibited saturation kinetics at the 10 g dose. The 4 g dose showed the lowest interindividual variability. Sampling strategies yielded equivalent results. A 4 g gluten challenge combined with a 6 h urine collection demonstrated effectiveness in healthy volunteers and may be suitable for clinical application. Further research involving larger cohorts of both healthy individuals and patients with intestinal hyperpermeability is required to validate this method.

Abstract Background Soft-coated wheaten terriers (SCWTs) have a predisposition to the development of protein-losing enteropathy (PLE). Early recognition of disease may improve morbidity and mortality in these and other at-risk dogs. Preclinical inflammatory bowel disease (IBD), characterized by increased intestinal permeability, immune dysregulation and inflammation, and changes to the gut microbial composition, or biochemical evidence of disease many years before development of clinical signs, has been proposed for people at risk for IBD. Hypothesis/Objectives Determine if changes in fecal metabolites and intestinal permeability could be identified in SCWTs before development of clinical signs. We hypothesized that, in contrast to healthy non-SCWT dogs, healthy SCWT would have changes similar to those of dogs with PLE. Animals Twelve healthy SCWTs, 10 healthy non-SCWTs, and 8 PLE dogs. Methods Prospective study. Fecal calprotectin, targeted metabolites and unconjugated bile acids, intestinal permeability testing, and video capsule endoscopy were evaluated. Single-factor analysis of variance (ANOVA) was performed to evaluate fecal metabolites and bile acids for group differences. A repeated-measures mixed model ANOVA was performed for blood lactulose:galactose area under the curve (AUC). Results Significant differences among groups were found for several fecal fatty acids and sterols. Healthy non-SCWT dogs, but not healthy SCWTs, were found to have significantly lower AUCs than PLE dogs (P = .04). Conclusions Healthy SCWT dogs had changes in several biomarkers used to identify preclinical IBD in humans.

Abstract Background Hepatic supportive diet (HSD), lactulose, and antimicrobials are medical treatments for dogs with congenital extrahepatic portosystemic shunts (cEHPSS). The relative contribution of these treatment components is currently unknown. Objectives To determine which treatment combinations are most efficacious in pre-surgical control of clinical signs of cEHPSS in dogs. Animals Thirty-six dogs with untreated cEHPSS. Methods Three-arm randomized clinical trial. At inclusion (T0), dogs were divided into 3 groups: HSD (n = 12), HSD + lactulose (n = 12), or HSD + metronidazole (n = 12) and received the randomized treatment for 4 weeks (T1) followed by combined treatment of HSD + lactulose + metronidazole for 2 weeks or until cEHPSS attenuation (T2). Clinical score as well as fasting ammonia (FA) and C-reactive protein (CRP) concentrations were compared among groups and time points. Results Thirty-four dogs were evaluated. Thirty-four dogs reached T1 and 29 dogs T2. At T1, clinical scores decreased in the HSD + lactulose (n = 11; P = .001), but not in the HSD (n = 8; P = .96) and HSD + metronidazole (n = 10; P = .06) groups. Adding metronidazole to HSD + lactulose (n = 11) did not result in further clinical score improvement (T2; P = 1.000). Moderate and weak correlation between clinical score and FA and clinical score and CRP was present (ρ = .35, P < .001; ρ = .27, P = .01, respectively) with FA decreasing over time on medical treatment (P = .001). Conclusions and Clinical Importance Combined HSD + lactulose seems sufficient for pre-surgical cEHPSS stabilization unlike sole HSD or HSD + metronidazole. Medical treatment of cEHPSS clinical signs decreases FA.

PurposeAlthough acute prolonged strenuous exercise has been shown to increase markers of gastrointestinal permeability and damage, little is known regarding the efficacy of nutritional supplement interventions on the attenuation of exercise-induced gastrointestinal syndrome. This study addressed the effects of oral amino acid supplementation on markers of gastrointestinal permeability and damage in response to exercise.MethodsSixteen active men aged 22.7 ± 2.6 years (mean ± standard deviation) completed placebo or cystine and glutamine supplementation trials in random order. Participants received either a placebo or cystine and glutamine supplements, three times a day for 5 days, separated by a 2-week washout period. On day 6, participants took their designated supplements 30 min before running at a speed corresponding to 75% of maximal oxygen uptake for 1 h, followed by a 4-h rest period. Blood samples were collected pre-exercise, immediately post-exercise, 30 min post-exercise, and 1, 2 and 4 h post-exercise on day 6. The plasma lactulose to mannitol ratio (L:M) and plasma intestinal fatty acid-binding protein (I-FABP) were used as markers of gastrointestinal permeability and damage, respectively.ResultsPlasma L:M (linear mixed model, coefficient ± standard error: − 0.011 ± 0.004, P = 0.0090) and changes (i.e., from pre-exercise) in plasma I-FABP (linear mixed model, − 195.3 ± 65.7 coefficient ± standard error (pg/mL), P = 0.0035) were lower in the cystine and glutamine supplementation trial than in the placebo trial.ConclusionOral cystine and glutamine supplementation attenuated the markers of gastrointestinal permeability and damage after 1 h of strenuous running in young men.Trial registration numberUMIN000026008.Date of registration13 December 2018.

Background and Objectives: This analysis described rifaximin utilization in Italian patients with hepatic encephalopathy (HE). Although rifaximin is effective in preventing HE relapses, therapeutic management and prescriptive attitudes might be improved. Materials and Methods: Between Oct-2020 and Sep-2021, approximately 12.7 million citizens, patients hospitalized for HE, were identified through the ICD-9-CM code 572.2. Among those discharged alive, utilization of rifaximin 550 mg vs. rifaximin 200 mg for two months post-admission was compared. Results: Of 634 patients hospitalized for HE, 447 (70.5%) were discharged alive. In the two following months, 276 (61.7%) received rifaximin, of whom 117 (26.2%) received rifaximin 550 mg (two daily tablets) and 159 (35.6%) received rifaximin 200 mg (six daily tablets); among 171 patients without rifaximin, 56 (32.7%) received lactulose/lactitol. One year after rifaximin initiation, patients on rifaximin 550 mg (vs. 200 mg) were more frequently persistent (i.e., did not interrupt therapy) (78.6% vs. 46.9%, p < 0.001), showed a lower switching proportion (21.4% vs. 40.7%, p < 0.050), and had a mean monthly dose closer to the recommendations of 36,000 mg/month (~33,000 mg/month vs. 11,629 mg/month, respectively). Conclusions: This analysis suggests suboptimal rifaximin utilization for HE management. Although rifaximin 550 mg is the only formulation with specific indication and reimbursability to prevent HE relapses in Italy, rifaximin 200 mg is more largely used. The need to improve rifaximin prescribing choices is supported by higher persistence, lower switching rates, and average doses aligned to recommendations in patients treated with rifaximin 550 mg.

A child’s diet contains nutrients and other substances that influence intestinal health. The present study aimed to evaluate the relations between complementary feeding, intestinal barrier function and environmental enteropathy (EE) in infants. Data from 233 children were obtained from the Brazilian site of the Etiology, Risk Factors, and Interactions of Enteric Infections and Malnutrition and the Consequences for Child Health and Development Project cohort study. Habitual dietary intake from complementary feeding was estimated using seven 24-h dietary recalls, from 9 to 15 months of age. Intestinal barrier function was assessed using the lactulose–mannitol test (L–M), and EE was determined as a composite measure using faecal biomarkers concentrations – α-1-antitrypsin, myeloperoxidase (MPO) and neopterin (NEO) at 15 months of age. The nutrient adequacies explored the associations between dietary intake and the intestinal biomarkers. Children showed adequate nutrient intakes (with the exception of fibre), impaired intestinal barrier function and intestinal inflammation. There was a negative correlation between energy adequacy and L–M ( ρ = −0·19, P < 0·05) and between folate adequacy and NEO concentrations ( ρ = −0·21, P < 0·01). In addition, there was a positive correlation between thiamine adequacy and MPO concentration ( ρ = 0·22, P < 0·01) and between Ca adequacy and NEO concentration ( ρ = 0·23; P < 0·01). Multiple linear regression models showed that energy intakes were inversely associated with intestinal barrier function ( β = −0·19, P = 0·02), and fibre intake was inversely associated with the EE scores ( β = −0·20, P = 0·04). Findings suggest that dietary intake from complementary feeding is associated with decreased intestinal barrier function and EE in children.