BACKGROUND AND AIMS: It is not clear whether alterations in the intestinal microbiota of children with celiac disease (CD) cause the disease or are a result of disease and/or its treatment with a gluten-free diet (GFD). METHODS: We obtained 167 fecal samples from 141 children (20 with newonset CD, 45 treated with a GFD, 57 healthy children, and 19 unaffected siblings of children with CD) in Glasgow, Scotland. Samples were analyzed by 16S ribosomal RNA sequencing, and diet-related metabolites were measured by gas chromatography. We obtained fecal samples from 13 children with new-onset CD after 6 and 12 months on a GFD. Relationships between microbiota with diet composition, gastrointestinal function, and biomarkers of GFD compliance were explored. RESULTS: Microbiota a diversity did not differ among groups. Microbial dysbiosis was not observed in children with new-onset CD. In contrast, 2.8% (Bray-Curtis

BackgroundOur current understanding regarding the aetiology of infantile acute liver failure largely derives from studies conducted by regional liver units. This may introduce selection bias and therefore not provide a true reflection of the wider population.MethodsEvery coagulation screen with a prothrombin time ≥18 s in our centre was examined over one calendar year. All patients less than 1 year of age were included and their electronic records retrospectively reviewed.Results24 patients were identified, from 9989 coagulation screens, that fit the current definition of acute liver failure. Hypoxic birth injury and ischaemic events were the most common aetiologies. Survival was 75%.ConclusionThe ‘catch-all’ methodology employed demonstrated that acute liver failure is more common than previously reported and suggests that current data may exclude large numbers who either have more minor self-resolving disease or conversely have severe disease leading to death prior to transfer.

Background Exclusive enteral nutrition (EEN) is the recommended induction treatment of mild to moderate active pediatric Crohn’s disease (CD). This study compared outcomes of 2 proprietary polymeric formulas. Treatment effectiveness was examined along with practical aspects of formula delivery and differences in estimated treatment costs. Methods Data were retrospectively collected from patients with CD who received a generic oral nutritional supplement (Fortisip) across 2 centers (RCH, Melbourne and RHSC, Edinburgh). This was compared with a prospective cohort (RHC, Glasgow) that used a specialized formula (Modulen IBD). The data collected included patient demographics, remission rates, biochemical markers, administration method, and anthropometrics. The estimated treatment cost was performed by comparing price per kcal between each formula. Results One hundred seventy-one patients were included (106 Fortisip, 65 Modulen IBD, 70 female; median age 13.3 yrs). No difference was demonstrated in remission rate (Fortisip n = 67 of 106 [63%] vs Modulen IBD n = 41 of 64 [64%], P = .89), nonadherence rate (Fortisip n = 7 of 106 [7%] vs Modulen IBD 3 of 64 [5%], P = .57) or method of administration (NGT Fortisip use n = 16 of 106 [12%] vs Modulen IBD 14 of 65 [22%]; P = .31). There was no difference in reduction of biochemical disease markers between the groups (C-reactive protein , P = .13; erythrocyte sedimentation rate, P = .49; fecal calprotectin, P = .94). However, there was a cost-saving of around £500/patient/course if the generic oral nutritional supplement was used. Conclusions The generic oral nutritional supplement and specialized formulas both had similar clinical effectiveness in induction of remission in pediatric CD. However, there is considerable cost-saving when using a generic oral nutritional supplement.