Body Composition Trajectories From Infancy to Preschool in Children Born Premature Versus Full-Term.

Objectives: The aim of the study was to longitudinally characterize infancy to preschool body composition trajectories and the association of early fat and fat-free mass gains with preschool age body composition in children born premature versus full-term. Methods: A cohort of appropriate-for-gestational age preterm (n = 20) and term (n = 51) infants were followed at 3 visits: "neonatal" visit 1 at 2 weeks of age for term and near term corrected age for preterm; "infancy" visit 2 at 3 to 4 months (preterm corrected age); "preschool" visit 3 at 4 years. Body composition via air displacement plethysmography and anthropometrics were measured at all visits. Tracking of infancy weight and body composition with preschool measurements was tested using Pearson partial correlation coefficients. Associations between serial body composition measurements were assessed using multiple linear regression. Results: Early differences in body composition between premature (mean gestational age 31.9 weeks, mean birth weight 1843 g) and full-term (mean gestational age 39.8 weeks) infants were not present at preschool age. Visit 1 body composition was not correlated with preschool measurements in the preterm infants. Visit 2 measurements were correlated with preschool measures. Fat-free mass accretion from visit 1 to visit 2 was positively associated with preschool lean mass ([beta] = 0.038, P = 0.049) in preterm children, whereas fat accretion was not associated with preschool body composition. Conclusions: Children born prematurely and full-term have similar body composition at preschool age. For preterms infancy fat-free mass gains, and not adiposity gains, are positively associated with preschool fat-free mass; this may be associated with lower risk of later obesity and adverse metabolic outcomes. (C) 2016 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,

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Diverting Ileostomy for the Treatment of Severe, Refractory, Pediatric Inflammatory Bowel Disease.

Objectives: Diverting ileostomy is used as a temporizing therapy in patients with perianal Crohn disease; however, little data exist regarding its use for colonic disease. The primary aim of the present study was to determine the role of diversion in severe refractory colonic inflammatory bowel disease (IBD) in a pediatric population. Methods: Retrospective study of patients who underwent diverting ileostomy at The Children's Hospital of Philadelphia from 2000 to 2014 for the management of severe, refractory colonic IBD. Clinical variables were compared in the 1 year before ileostomy and 1 year after diversion. Surgical and disease outcomes including changes in diagnosis were reviewed through 2015. Results: Twenty-four patients underwent diverting ileostomy for refractory colonic disease. Initial diagnoses were Crohn disease in 10 (42%), ulcerative colitis in 1 (4%), and IBD-unclassified in 13 patients (54%). Comparing data before and after surgery, there were statistically significant improvements in height and weight velocities, height velocity z score, blood transfusion requirement, hemoglobin, and hospitalization rates. Chronic steroid use decreased from 71% to 22%. At the conclusion of the study, 10 patients had undergone subsequent colectomy, 7 had successful bowel reanastomosis, and 7 remain diverted. Seven patients (29%) had a change in diagnosis. There were 13 surgical complications in 7 subjects, including prolapse reduction, stoma revision, and resection of ischemic bowel. Conclusions: In pediatric patients with refractory colonic IBD, diverting ileostomy can be a successful intervention to induce clinical stability. Importantly, diversion is a steroid-sparing therapy and allows additional time to clarify the diagnosis. (C) 2016 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,

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Clinical Variability Following Partial External Biliary Diversion in Familial Intrahepatic Cholestasis 1 Deficiency.

Objectives: Familial intrahepatic cholestasis 1 (FIC1) **deficiency is caused by a mutation in the ATP8B1 gene. Partial external biliary diversion (PEBD) is pursued to improve pruritus and arrest disease progression. Our aim is to describe clinical variability after PEBD in FIC1 disease. Methods: We performed a single-center, retrospective review of genetically confirmed FIC1 deficient patients who received PEBD. Clinical outcomes after PEBD were cholestasis, pruritus, fat-soluble vitamin supplementation, growth, and markers of disease progression that included splenomegaly and aspartate aminotransferase-to-platelet ratio index. Results: Eight patients with FIC1 disease and PEBD were included. Mean follow-up was 32 months (range 15-65 months). After PEBD, total bilirubin was 0.7 suggesting development of fibrosis 24 months after PEBD. Conclusions: Clinical variability is evident among genetically defined FIC1 deficient patients after PEBD, even among those with identical mutations. Recurrent, self-limited episodes of cholestasis and pruritus are reminiscent of the benign recurrent intrahepatic cholestasis phenotype. Despite diversion of bile from the intestinal lumen, weight gain improved while fat-soluble vitamin requirements persisted. Significant progression of liver disease was not evident during follow-up. (C) 2016 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,

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Isolated Appendiceal Pinworms on Colonoscopy.

No abstract available

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Nutritional Practices and Growth in Premature Infants after Surgical Necrotizing Enterocolitis.

Objective: To describe the nutritional provisions received by infants with surgical NEC and the associated effects on short-term growth. Study Design: Through the Children's Hospitals Neonatal Database we identified infants born 0.3 between groups for weight and length). Unadjusted and independent associations were identified with HC changes and HP dose ([beta]= 0.1 cm/week, p=0.03) after adjusting for gestational age, the presence of severe bronchopulmonary dysplasia, short bowel syndrome, blood stream infection, severe intraventricular hemorrhage (IVH), or small for gestational age (SGA) and calorie intake. Eventual non-survivors received 18% less protein and 14% fewer calories over the first post-operative month. Conclusions: Post-operative protein doses in infants with surgical NEC appear related to increases in HC. The influence of post-operative nutritional support on risk of adverse outcomes deserves further attention. (C) 2016 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,

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The Association Between Celiac Disease and Eosinophilic Esophagitis: Mayo Experience and Meta-analysis of the Literature.

Background: The association between celiac disease (CD) and eosinophilic esophagitis (EoE) has been the focus of multiple studies with variable results. Both diseases are immune mediated, and dietary triggers play a role in their pathogenesis. Objectives: The aim of the study was to analyze the risk of EoE in children with CD, assess the magnitude of association between CD and EoE in children, and report the characteristics and outcomes of children with both conditions. Methods: We conducted a retrospective study of the Mayo Clinic Electronic medical records between January 1, 1998 and December 31, 2015. Systematic review and meta-analysis of multiple databases was conducted to include studies reporting on the same association. Random-effects model was used to report pooled odds ratio (OR) and 95% confidence interval (CI). Results: In this cohort study, of 10,201 children who underwent at least 1 endoscopy, 595 had EoE, and 546 had CD. The risk of having EoE was not increased in children with CD compared to those without CD (OR, 0.29; 95% CI, 0.154-0.545). Nine of 10 children improved with gluten-free diet, topical glucocorticosteroid, and/or elimination diet. One child lost to follow-up. Meta-analysis of 5 studies showed similar results (OR, 0.525; 95% CI, 0.364-0.797). A total of 45 cases in the literature had both CD and EoE (mean age, 10 years; 64% boys; majority presenting with abdominal pain, vomiting, and diarrhea). Conclusions: Based on our cohort and the observational data, the diagnosis of CD in children is not associated with increased risk of EoE. (C) 2016 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,

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Study of Carnitine/Acylcarnitine and Aminoacid Profile in children and adults with Acute Liver Failure.

Objectives: Fatty acid oxidation defects (FAODs) may underlie or modify the course of acute liver failure (ALF). Overall significance of carnitine/acylcarnitine and aminoacid profile in ALF is similarly undetermined. Thus, this study was undertaken to study the abnormalities in carnitine/acylcarnitine and aminoacid profile in ALF. Patients and Methods: A prospective study was performed including all cases of ALF and detailed evaluation including metabolic testing was done. Results: A total of 55 patients (33 pediatric and 22 adult cases) were included in the study. Three patients (a 1 year 6-month-old child, a 13 year old adolescent and a 21 year old adult) i.e 5.5% of all, were detected to be having underlying metabolic etiology i.e Carnitine Palmitoyl Transferase-1 or CPT-1 deficiency based on abnormal carnitine/acylcarnitine profile. Almost three-fourths of patients (78%) had evidence of serum hyperaminoacidemia. Thirty-one patients (56%) had evidence of abnormal carnitine/acylcarnitine profile with predominant abnormality being low free carnitine (C0). Higher levels of serum tyrosine (p 0.002) and lower levels of serum C0 (p 0.032) in children and higher levels of serum phenyalanine (p 0.047) in adults predicted poor outcome (death/liver transplant) on univariate analysis. Conclusion: FAODs are not uncommon in ALF with a suggested prevalence of around 5.5%. FAODs can cause ALF or modify the natural course of ALF caused by other etiologies. Serum hyperaminoacidemia and low serum free carnitine may predict poor outcome in ALF cases. (C) 2016 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology,

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