Sexually dimorphic response of mice to the Western-style diet caused by deficiency of fatty acid binding protein 6 (Fabp6).

Bile acids are natural detergents that aid in the absorption of dietary lipids. Fatty acid binding protein 6 (Fabp6) is a component of the bile acid recovery system that operates in the small intestine. The aim of this study was to determine if Fabp6 deficiency causes dietary fat malabsorption. Wild-type and Fabp6-deficient mice were fed a Western-style diet (WSD) or a reference low-fat diet (LFD) for 10 weeks. The body weight gain, bile acid excretion, fat excretion, energy metabolism, and major gut microbial phyla of the mice were assessed at the end of the controlled diet period. Fabp6-/- mice exhibited enhanced excretion of both bile acids and fat on the WSD but not on the LFD diet. Paradoxically, male Fabp6-/- mice, but not female Fabp6-/- mice, had greater adiposity despite increased fat excretion. Analysis of energy intake and of expenditure by indirect calorimetry revealed sex differences in physical activity level and respiratory quotient, but these did not account for the enhanced adiposity displayed by male Fabp6-/- mice. Analysis of stool DNA showed sex-specific changes in the abundance of major phyla of bacteria in response to Fabp6 deficiency and WSD feeding. The results obtained indicate that the malabsorption of bile acids that occurs in Fabp6-/- mice is associated with dietary fat malabsorption on the high-fat diet but not on the low-fat diet. The WSD induced a sexually dimorphic increase in adiposity displayed by Fabp6-/- mice and sexually distinct pattern of change in gut microbiota composition.

Changes in gut microbial metagenomic pathways associated with clinical outcomes after the elimination of malabsorbed sugars in an IBS cohort.

Specific diets to manage sugar malabsorption are reported to reduce clinical symptoms of irritable bowel syndrome (IBS). However, the effects of diets for malabsorbed sugars on gut microbiota signatures have not been studied, and associations with clinical outcomes in IBS have not been characterized. 22 IBS patients positively tested for either lactose-, fructose-, sorbitol- or combined malabsorptions were subjected to 2-weeks sugar elimination and subsequent 4-weeks re-introduction. 7 IBS patients tested negative for sugar malabsorption were used as controls. Nutrition and clinical symptoms were recorded throughout the study. Fecal samples were serially collected for 16S rRNA amplicon and shotgun-metagenome sequencing. Dietary intervention supervised by nutrition counseling reduced IBS symptoms during the elimination and tolerance phases. Varying clinical response rates were observed between subjects, and used to dichotomize our cohort into visual analogue scale (VAS) responders and non-responders. Alpha -and beta-diversity analyzes revealed only minor differences regarding 16S rRNA-based fecal microbiota compositions between responder and non-responder patients during baseline or tolerance phase. In shotgun-metagenome analyzes, however, we analyzed microbial metabolic pathways and found significant differences in pathways encoding starch degradation and complex amino acid biosynthesis at baseline between IBS controls and malabsorbers, and notably, between diet responder and non-responders. Faecalibacterium prausnitzii, Ruminococcus spp. and Bifidobacterium longum largely informed these metabolic pathways. Our study demonstrates that diet interventions for specific, malabsorbed carbohydrates reshaped the metagenomic composition of the gut microbiota, with a small community of bacterial taxa contributing to these changes rather than a single species.

Animal Models of Undernutrition and Enteropathy as Tools for Assessment of Nutritional Intervention.

: Undernutrition is a major public health problem leading to 1 in 5 of all deaths in children under 5 years. Undernutrition leads to growth stunting and/or wasting and is often associated with environmental enteric dysfunction (EED). EED mechanisms leading to growth failure include intestinal hyperpermeability, villus blunting, malabsorption and gut inflammation. As non-invasive methods for investigating gut function in undernourished children are limited, pre-clinical models are relevant to elucidating the pathophysiological processes involved in undernutrition and EED, and to identifying novel therapeutic strategies. In many published models, undernutrition was induced using protein or micronutrient deficient diets, but these experimental models were not associated with EED. Enteropathy models mainly used gastrointestinal injury triggers. These models are presented in this review. We found only a few studies investigating the combination of undernutrition and enteropathy. This highlights the need for further developments to establish an experimental model reproducing the impact of undernutrition and enteropathy on growth, intestinal hyperpermeability and inflammation, that could be suitable for preclinical evaluation of innovative therapeutic intervention.

Characterization of Proximal Small Intestinal Microbiota in Patients With Suspected Small Intestinal Bacterial Overgrowth: A Cross-Sectional Study.

OBJECTIVES: The composition of the small intestinal microbiota has not yet been characterized thoroughly using culture-independent techniques. We compared small intestinal microbial communities in patients with and without small intestinal bacterial overgrowth (SIBO) using culture-dependent and culture-independent bacterial identification approaches. METHODS: Small bowel aspirate and mucosal samples were collected from patients with suspected SIBO. The aspirates were cultured to diagnose SIBO, defined as ≥10 colony-forming units/mL coliform or ≥10 colony-forming units/mL upper aerodigestive tract bacteria. Bacteria in the aspirates and mucosa were identified using 16S rRNA gene sequencing. We compared small intestinal microbiome composition between groups with and without a culture-based SIBO diagnosis. RESULTS: Analysis of the aspirate and mucosal microbial communities from 36 patients revealed decreased α-diversity but no differences in ß-diversity in patients with SIBO compared with those without SIBO. There were no significant differences in the relative abundance of individual taxa from the aspirates or mucosa after adjustment for false discovery rate between patients with and without SIBO. Subgroup analysis revealed significant differences in mucosal ß-diversity between the coliform and upper aerodigestive tract subgroups. Relative abundances of a mucosal Clostridium spp. (P = 0.05) and an aspirate Granulicatella spp. (P = 0.02) were higher in coliform SIBO vs non-SIBO subgroups. The microbial composition and relative abundance of multiple taxa significantly differed in the mucosal and aspirate specimens. DISCUSSION: Culture-based results of small bowel aspirates do not correspond to aspirate microbiota composition but may be associated with species richness of the mucosal microbiota.

Pathobiome driven gut inflammation in Pakistani children with Environmental Enteric Dysfunction.

Environmental Enteric Dysfunction (EED) is an acquired small intestinal inflammatory condition underlying high rates of stunting in children <5 years of age in low- and middle-income countries. Children with EED are known to have repeated exposures to enteropathogens and environmental toxins that leads to malabsorptive syndrome. We aimed to characterize association of linear growth faltering with enteropathogen burden and subsequent changes in EED biomarkers. In a longitudinal birth cohort (n = 272), monthly anthropometric measurements (Length for Age Z score- LAZ) of asymptomatic children were obtained up to 18 months. Biological samples were collected at 6 and 9 months for the assessment of biomarkers. A customized TaqMan array card was used to target 40 enteropathogens in fecal samples. Linear regression was applied to study the effect of specific enteropathogen infection on change in linear growth (ΔLAZ). Presence of any pathogen in fecal sample correlated with serum flagellin IgA (6 mo, r = 0.19, p = 0.002), fecal Reg 1b (6 mo, r = 0.16, p = 0.01; 9mo, r = 0.16, p = 0.008) and serum Reg 1b (6 mo, r = 0.26, p<0.0001; 9 mo, r = 0.15, p = 0.008). At 6 months, presence of Campylobacter [ß (SE) 7751.2 (2608.5), p = 0.003] and ETEC LT [ß (SE) 7089.2 (3015.04), p = 0.019] was associated with increase in MPO. Giardia was associated with increase in Reg1b [ß (SE) 72.189 (26.394), p = 0.006] and anti-flic IgA[ß (SE) 0.054 (0.021), p = 0.0091]. Multiple enteropathogen infections in early life negatively correlated with ΔLAZ, and simultaneous changes in gut inflammatory and permeability markers. A combination vaccine targeting enteropathogens in early life could help in the prevention of future stunting.

CVID enteropathy is characterized by exceeding low mucosal IgA levels and interferon-driven inflammation possibly related to the presence of a pathobiont.

Common variable immunodeficiency (CVID), the most common symptomatic primary antibody deficiency, is accompanied in some patients by a duodenal inflammation and malabsorption syndrome known as CVID enteropathy (E-CVID).The goal of this study was to investigate the immunological abnormalities in CVID patients that lead to enteropathy as well as the contribution of intestinal microbiota to this process.We found that, in contrast to noE-CVID patients (without enteropathy), E-CVID patients have exceedingly low levels of IgA in duodenal tissues. In addition, using transkingdom network analysis of the duodenal microbiome, we identified Acinetobacter baumannii as a candidate pathobiont in E-CVID. Finally, we found that E-CVID patients exhibit a pronounced activation of immune genes and down-regulation of epithelial lipid metabolism genes. We conclude that in the virtual absence of mucosal IgA, pathobionts such as A. baumannii, may induce inflammation that re-directs intestinal molecular pathways from lipid metabolism to immune processes responsible for enteropathy.

The prevalence of small intestinal bacterial overgrowth in non-surgical patients with chronic pancreatitis and pancreatic exocrine insufficiency (PEI).

BACKGROUND: Small intestinal bacterial overgrowth (SIBO) is a condition characterised by symptoms similar to pancreatic exocrine insufficiency (PEI) in chronic pancreatitis patients. SIBO is thought to complicate chronic pancreatitis in up to 92% of cases; however, studies are heterogeneous and protocols non-standardised. SIBO may be determined by measuring lung air-expiration of either hydrogen or methane which are by-products of small bowel bacterial fermentation of intraluminal substrates such as carbohydrates. We evaluated the prevalence of SIBO among a defined cohort of non-surgical chronic pancreatitics with mild to severe PEI compared with matched healthy controls. METHODS: Thirty-five patients and 31 age-, gender- and smoking status-matched healthy controls were evaluated for SIBO by means of a fasting glucose hydrogen breath test (GHBT). The relationship between SIBO and clinical symptoms in chronic pancreatitis was evaluated. RESULTS: SIBO was present in 15% of chronic pancreatitis patients, while no healthy controls tested positive (P = 0.029). SIBO was more prevalent in those taking pancreatic enzyme replacement therapy (PERT) (P = 0.016), with proton pump inhibitor use (PPI) (P = 0.022) and in those with alcohol aetiology (P = 0.023). Patients with concurrent diabetes were more often SIBO-positive and this was statistically significant (P = 0.009). There were no statistically significant differences in reported symptoms between patients with and without SIBO, with the exception of 'weight loss', with patients reporting weight loss more likely to have SIBO (P = 0.047). CONCLUSION: The prevalence of SIBO in this study was almost 15% and consistent with other studies of SIBO in non-surgical chronic pancreatitis patients. These data support the testing of patients with clinically-relevant PEI unresolved by adequate doses of PERT, particularly in those patients with concurrent diabetes. SIBO can be easily diagnosed therefore allowing more specific and more targeted symptom treatment.

Small Intestinal Bacterial Overgrowth: Nutritional Implications, Diagnosis, and Management.

Small intestinal bacterial overgrowth (SIBO), characterized by the presence of excessive bacteria in the small intestine, is typically described as a malabsorptive syndrome occurring in the context of gut stasis syndromes. SIBO is now considered to be a disorder associated with diverse clinical conditions without classic risk factors for SIBO and a cause of several nonspecific gastrointestinal and nongastrointestinal symptoms. Because there is currently no gold standard for diagnosing SIBO, its prevalence and role in the pathogenesis of other diseases remain uncertain; as does optimal treatment of patients with relapsing symptoms.

Campylobacter jejuni impairs sodium transport and epithelial barrier function via cytokine release in human colon.

Campylobacter jejuni is the most prevalent cause of foodborne bacterial enteritis worldwide. Patients present with diarrhea and immune responses lead to complications like arthritis and irritable bowel syndrome. Although studies exist in animal and cell models, we aimed at a functional and structural characterization of intestinal dysfunction and the involved regulatory mechanisms in human colon. First, in patients' colonic biopsies, sodium malabsorption was identified as an important diarrheal mechanism resulting from hampered epithelial ion transport via impaired epithelial sodium channel (ENaC) ß- and γ-subunit. In addition, barrier dysfunction from disrupted epithelial tight junction proteins (claudin-1, -3, -4, -5, and -8), epithelial apoptosis, and appearance of lesions was detected, which cause leak-flux diarrhea and can perpetuate immune responses. Importantly, these effects in human biopsies either represent direct action of Campylobacter jejuni (ENaC impairment) or are caused by proinflammatory signaling (barrier dysfunction). This was revealed by regulator analysis from RNA-sequencing (cytometric bead array-checked) and confirmed in cell models, which identified interferon-γ, TNFα, IL-13, and IL-1ß. Finally, bioinformatics' predictions yielded additional information on protective influences like vitamin D, which was confirmed in cell models. Thus, these are candidates for intervention strategies against C. jejuni infection and post-infectious sequelae, which result from the permissive barrier defect along the leaky gut.

The clinical value of breath hydrogen testing.

Breath hydrogen testing for assessing the presence of carbohydrate malabsorption is frequently applied to refine dietary restrictions on a low fermentable carbohydrate (FODMAP) diet. Its application has also been extended for the detection of small intestinal bacterial overgrowth. Recently, several caveats of its methodology and interpretation have emerged. A review of the evidence surrounding its application in the management of patients with a functional bowel disorder was performed. Studies were examined to assess limitations of testing methodology, interpretation of results, reproducibility, and how this relates to clinical symptoms. A wide heterogeneity in testing parameters, definition of positive/negative response, and the use of clinically irrelevant doses of test carbohydrate were common methodological limitations. These factors can subsequently impact the sensitivity, specificity, and false positive or negative detection rates. Evidence is also increasing on the poor intra-individual reproducibility in breath responses with repeated testing for fructose and lactulose. On the basis of these limitations, it is not surprising that the diagnosis of small intestinal bacterial overgrowth based on a lactulose breath test yields a wide prevalence rate and is unreliable. Finally, symptom induction during a breath test has been found to correlate poorly with the presence of carbohydrate malabsorption. The evidence suggests that breath hydrogen tests have limited clinical value in guiding clinical decision for the patient with a functional bowel disorder.

Dietary Carbohydrates and Childhood Functional Abdominal Pain.

Childhood functional gastrointestinal disorders (FGIDs) affect a large number of children throughout the world. Carbohydrates (which provide the majority of calories consumed in the Western diet) have been implicated both as culprits for the etiology of symptoms and as potential therapeutic agents (e.g., fiber) in childhood FGIDs. In this review, we detail how carbohydrate malabsorption may cause gastrointestinal symptoms (e.g., bloating) via the physiologic effects of both increased osmotic activity and increased gas production from bacterial fermentation. Several factors may play a role, including: (1) the amount of carbohydrate ingested; (2) whether ingestion is accompanied by a meal or other food; (3) the rate of gastric emptying (how quickly the meal enters the small intestine); (4) small intestinal transit time (the time it takes for a meal to enter the large intestine after first entering the small intestine); (5) whether the meal contains bacteria with enzymes capable of breaking down the carbohydrate; (6) colonic bacterial adaptation to one's diet, and (7) host factors such as the presence or absence of visceral hypersensitivity. By detailing controlled and uncontrolled trials, we describe how there is a general lack of strong evidence supporting restriction of individual carbohydrates (e.g., lactose, fructose) for childhood FGIDs. We review emerging evidence suggesting that a more comprehensive restriction of fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) may be effective. Finally, we review how soluble fiber (a complex carbohydrate) supplementation via randomized controlled intervention trials in childhood functional gastrointestinal disorders has demonstrated efficacy.

Environmental enteropathy.

PURPOSE OF REVIEW: Environmental enteropathy has long been recognized as an important intermediary condition leading to chronic malnutrition in children in developing countries. Interest has lately renewed in this topic because of increased focus on improving the quality of lives as opposed to just saving them. Here, we provide an overview of recent scientific literature and our perspective about this disorder. RECENT FINDINGS: Current understanding of the disorder of environmental enteropathy is based on studies conducted decades ago. Results of some new studies on histopathologic characterization of environmental enteropathy are currently awaited. Given the challenges of diagnosing environmental enteropathy using the gold standard test of intestinal biopsy, different biomarkers have been tested as proxies of environmental enteropathy and eventually, chronic malnutrition. Available data fail to point toward a single ideal biomarker, though considerable work is still ongoing. A few interventional studies have also been conducted with improvement in environmental enteropathy as outcome. SUMMARY: The basic histopathology of environmental enteropathy has been defined previously, and more advanced analysis to study the pathophysiology of this disorder is currently being carried out. Many biomarkers, which represent the different mechanisms involved in environmental enteropathy, have been tested as proxies of environmental enteropathy. Although no single biomarker fits the description of an ideal biomarker yet, a few of the more promising biomarkers are being validated in different studies. Finally, the few interventions which have been tried to treat environmental enteropathy, thus far, are summarized.

Common beans and cowpeas as complementary foods to reduce environmental enteric dysfunction and stunting in Malawian children: study protocol for two randomized controlled trials.

BACKGROUND: Interventions to decrease the burden of childhood malnutrition are urgently needed, as millions of children die annually owing to undernutrition and hundreds of millions more are left cognitively and physically stunted. Environmental enteric dysfunction (EED), a pervasive chronic subclinical inflammatory condition among children that develops when complementary foods are introduced, places them at high risk of stunting, malabsorption, and poor oral vaccine efficacy. Improved interventions to reduce the burden of EED and stunting are expected to markedly improve the nutritional status and survival of children throughout resource-limited settings. METHODS/DESIGN: We will conduct, in parallel, two prospective randomized controlled clinical trials to determine whether common beans or cowpeas improve growth, ameliorate EED, and alter the intestinal microbiome during a high-risk period in the lives of rural Malawian children. Study 1 will enroll children at 6 months of age and randomize them to receive common beans, cowpeas, or a standard complementary food for 6 months. Anthropometry will be compared among the three groups; EED will be assessed using a dual-sugar absorption test and by quantifying human intestinal mRNA for inflammatory messages; and the intestinal microbiota will be characterized by deep sequencing of fecal DNA, to enumerate host microbial populations and their metabolic capacity. Study 2 will enroll children 12-23 months old and follow them for 12 months, with similar interventions and assessments as Study 1. DISCUSSION: By amalgamating the power of rigorous clinical trials and advanced biological analysis, we aim to elucidate the potential of two grain legumes to reduce stunting and EED in a high-risk population. Legumes have potential as an affordable and effective complementary food intervention, given their cultural acceptability, nutritional content, and agricultural feasibility in sub-Saharan Africa. TRIAL REGISTRATION: Clinicaltrials.gov NCT02472262 and NCT02472301 .

Hepatic fungal infection in a young beagle with unrecognised hereditary cobalamin deficiency (Imerslund-Gräsbeck syndrome).

A 12-month-old beagle presented for anorexia, pyrexia and vomiting. The dog had been treated intermittently with antibiotics and corticosteroids for inappetence and lethargy since five months of age. Previous laboratory abnormalities included macrocytosis and neutropenia. At presentation, the dog was lethargic, febrile and thin. Laboratory examination findings included anaemia, a left shift, thrombocytopenia, hypoglycaemia and hyperbilirubinaemia. Multiple, small, hypoechoic, round hepatic lesions were observed on abdominal ultrasound. Cytological examination of hepatic fine needle aspirates revealed a fungal infection and associated pyogranulomatous inflammation. The dog's general condition deteriorated despite supportive measures and treatment with fluconazole, and owners opted for euthanasia before hypocobalaminaemia was identified. Subsequent genomic analysis revealed a CUBN:c.786delC mutation in a homozygous state, confirming hereditary cobalamin malabsorption (Imerslund-Gräsbeck syndrome). Similar to human infants, dogs with Imerslund-Gräsbeck syndrome may rarely be presented for infectious diseases, distracting focus from the underlying primary disorder.

Digestive system dysfunction in cystic fibrosis: challenges for nutrition therapy.

Cystic fibrosis can affect food digestion and nutrient absorption. The underlying mutation of the cystic fibrosis trans-membrane regulator gene depletes functional cystic fibrosis trans-membrane regulator on the surface of epithelial cells lining the digestive tract and associated organs, where Cl(-) secretion and subsequently secretion of water and other ions are impaired. This alters pH and dehydrates secretions that precipitate and obstruct the lumen, causing inflammation and the eventual degradation of the pancreas, liver, gallbladder and intestine. Associated conditions include exocrine pancreatic insufficiency, impaired bicarbonate and bile acid secretion and aberrant mucus formation, commonly leading to maldigestion and malabsorption, particularly of fat and fat-soluble vitamins. Pancreatic enzyme replacement therapy is used to address this insufficiency. The susceptibility of pancreatic lipase to acidic and enzymatic inactivation and decreased bile availability often impedes its efficacy. Brush border digestive enzyme activity and intestinal uptake of certain disaccharides and amino acids await clarification. Other complications that may contribute to maldigestion/malabsorption include small intestine bacterial overgrowth, enteric circular muscle dysfunction, abnormal intestinal mucus, and intestinal inflammation. However, there is some evidence that gastric digestive enzymes, colonic microflora, correction of fatty acid abnormalities using dietary n-3 polyunsaturated fatty acid supplementation and emerging intestinal biomarkers can complement nutrition management in cystic fibrosis.

[Non-celiac gluten sensitivity: a critical review of current evidence]. / Sensibilidad al gluten no celiaca: una revisión crítica de la evidencia actual.

Non-celiac gluten sensitivity (NCGS) is an emerging disorder characterized by intestinal and extra-intestinal symptoms related to the ingestion of gluten-containing food in non-celiac patients. Its prevalence has been estimated to be six to ten-times higher than that of celiac disease (CD). A gluten-free diet is the most widely recommended therapy, but the causative agent remains unknown and there are no consensus diagnostic criteria. Recent studies on NCGS have included patients with possibly overlooked minor CD and diarrhea-predominant irritable bowel syndrome without self-reported gluten intolerance, but showing a response to a gluten-free diet. Furthermore, FODMAPs (Fermentable Oligosaccharides, Disaccharides, Monosaccharides And Polyols) have recently been postulated as the culprit component for NCGS in wheat, instead of gluten. This review updates evidence on the pathophysiology of NCGS and the efficacy of different dietary interventions in its treatment, stressing the need for proper screening for CD before a diagnosis of NCGS is made.

[Digestive enzyme functionality in pathology of the gastrointestinal tract with intestinal microbiocenosis disorders].

A change pattern in enzyme release function of digestive glands exerts the organism as a whole. Dysfunctions of hydrolysis and intestinal malabsorption (secondary malabsorption syndrome) are the first step towards nutrition and metabolism processes abnormality and that can play a role in genesis of pathological conditions. Recent researches arouse clinicians interest in determination of biofluid enzyme activity in different physiological and abnormal cases. Intestinal infections are followed by dysbacteriosis and obvious alterations in the hydrolase levels in the blood, urine and motions because of the changes of functional status of the liver, renal and intestinal barriers in relation to increted digestive enzymes. This causes an unfavorable course of recovery with the development of postinfectious digestion disorders as a result of previous acute diarrhea. Future researches are necessary to elaborate appropriate remodeling of developed pathosis with the help of enzymotherapy and probiotic diet.

Risk factors for small bowel bacterial overgrowth and diagnostic yield of duodenal aspirates in children with intestinal failure: a retrospective review.

BACKGROUND: Children with intestinal failure (IF) are at risk for small bowel bacterial overgrowth (SBBO) because of anatomical and other factors. We sought to identify risk factors for SBBO confirmed by quantitative duodenal culture. METHODS: A single-center retrospective record review of children who had undergone endoscopic evaluation for SBBO (defined as bacterial growth in duodenal fluid of >10(5) colony-forming unit per mL) was performed. RESULTS: We reviewed 57 children with median (25th-75th percentile) age 5.0 (2.0-9.2) years. Diagnoses included motility disorders (28%), necrotizing enterocolitis (16%), atresias (16%), gastroschisis (14%), and Hirschsprung disease (10.5%). Forty patients (70%) had confirmed SBBO. Univariate analysis showed no significant differences between patients with and without SBBO for the following variables: age, sex, diagnosis, presence of ileocecal valve, and antacid use. Patients receiving parenteral nutrition (PN) were more likely to have SBBO (70% vs 35%, P = .02). Multiple logistic regression analysis confirmed that PN administration was independently associated with SBBO (adjusted odds ratio, 5.1; adjusted 95% confidence interval, 1.4-18.3; P = .01). SBBO was not related to subsequent risk of catheter-related bloodstream infection (CRBSI). CONCLUSION: SBBO is strongly and independently associated with PN use. Larger prospective cohorts and more systematic sampling techniques are needed to better determine the relationship between SBBO and gastrointestinal function.

Is small-bowel bacterial overgrowth an underdiagnosed disorder in children with gastrointestinal symptoms?

Small-bowel bacterial overgrowth (SBBO) has been implicated in chronic abdominal pain and irritable bowel syndrome in children. This was a retrospective study that aimed to assess the occurrence of SBBO by the lactulose breath hydrogen test in children referred primarily for investigation of carbohydrate malabsorption (n = 287). There were profiles indicative of SBBO in 16% (39/250) of hydrogen-producing children. This indicated that SBBO may be more common in children with gastrointestinal symptoms and apparent carbohydrate malabsorption than previously recognised.

Postinfective bile acid malabsorption: is this a long-term condition?

BACKGROUND: Postinfective bile acid malabsorption comprises a group of patients with a history of an episode of acute gastroenteritis triggering chronic diarrhoea. We identified these patients retrospectively from our medical records and assessed their long-term clinical course. MATERIALS AND METHODS: We examined the records of 135 patients with 75 selenium-homocholic acid taurine results less than 10% (1 week retention). RESULTS: Twenty-five patients (13 female, 12 male) had a diagnosis of postinfective bile acid malabsorption established after extensive investigations. Cholestyramine was used to treat diarrhoea with a mean frequency of diarrhoea decreasing from 7.8 to 1.9 (P=0.001). The mean cholestyramine dose decreased from 8.2 to 5.4 g/day (P=0.005). Eighteen of 25 (72%) patients had a successful resolution of their diarrhoea by cholestyramine and have continued it to date. The median duration of outpatient follow-up was 1.58 years (range: 1-5 years). A further prospective telephone enquiry of these 18 patients revealed that 15 of 18 patients continued to take cholestyramine (median: 6 years, range: 1-15 years). There were no hospital admissions related to diarrhoea and there was no mortality in this group of patients. CONCLUSION: The long-term outlook of this group of patients is excellent. We have shown the chronic nature of this condition as evidenced by the continued requirement of cholestyramine.