Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are lifelong conditions that often begin in childhood. The implications of IBD are of particular importance in children because of the potential negative effects on growth, development, psychosocial function, and overall wellbeing. The key management strategy is to achieve sustained control of intestinal inflammation and monitor for potential complications of the disease and side effects of therapies. Overall, the evidence on the management of IBD in children is less extensive than in adults, but good quality multicenter studies and various guidelines and society consensus statements are available. This review summarizes the evidence on the pathophysiology, diagnosis, and approaches to management of children and adolescents with IBD.

The epidemic occurrence of VL in the region must convince authorities to adopt more adequate policies of disease control.

BackgroundFolate and choline are essential methyl donor nutrients throughout the life span; however, the adverse effects of combined deficiency on early growth, intestinal epithelial morphology, and the gut microbiome remain only partially understood.ObjectivesWe investigated the effects of dietary folate and choline deficiency on early growth, small intestinal (SI) epithelial architecture, and the gut microbiota of mice. To explore potential mechanisms for adverse effects on gut epithelial morphology, we also evaluated gene expression and DNA methylation in mouse intestinal epithelial organoids (enteroids) maintained in methyl donor–deficient (MDD) conditions.MethodsPregnant dams were administered 1 of 4 diets: 1) control diet (CD−), 2) an isocaloric MDD− diet, or 3) CD+ and 4) MDD+ formulations containing 1% succinylsulfathiazole to inhibit folate-producing gut bacteria. We weaned pups to their dams’ diet at 3 wk of age and monitored body weight and tail length pre- and postweaning. We measured serum folate, SI crypt morphology, and microbiota composition at 7 wk of age.ResultsBoth MDD+ and MDD− diets impaired early ponderal and linear growth, lowered serum folate concentrations, and produced patchy areas of increased crypt depth throughout the SI. Succinylsulfathiazole increased crypt depth independently of diet. MDD or succinylsulfathiazole, alone or in combination, altered the gut microbiome, with decreased Bacteroidales and Clostridiales, increased Lactobacillales and Erysipelotrichaceae taxa, and decreased α-diversity indexes. Enteroids maintained in MDD media displayed dysmorphic crypt domains, altered expression of stem cell and secretory differentiation genes, and decreased DNA methylation of the glycosylation genes Beta-1,4-N-Acetyl-Galactosaminyltransferase-1 (B4galnt1) and Phosphoethanolamine/Phosphocholine-Phosphatase (Phospho1).ConclusionMDD impairs ponderal and linear growth in mice in association with dysmorphic SI crypts and reduced gut microbial diversity. In vitro methyl donor deficiency similarly induced dysmorphic crypts in mouse enteroids in conjunction with altered gene expression and DNA methylation.

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