Search

Predicting response to exclusive enteral nutrition (EEN) in active Crohn’s disease (CD) could lead to therapy personalization and pretreatment optimization.

It remains unclear whether suboptimal response to exclusive enteral nutrition (EEN) in some children with Crohn disease (CD) is explained by poor compliance. The present study measured faecal gluten immunogenic peptides (GIP), a biomarker of gluten intake, in 45 children (3– 17 years) with CD, and explored associations with faecal calprotectin (FC) levels at 33 and 54 days of EEN. FC decreased in patients with undetectable GIP at both 33 and 54 days of EEN (mean decrease, 33 days: -743 mg/kg, 54 days: –1043 mg/kg, P<0.001) but not in patients who had detectable levels. At EEN completion, patients with undetectable GIP had a lower FC by 717 mg/kg compared with patients with a positive GIP result (P= 0.042) and demonstrated a greater decline from baseline FC (–69% vs +5%, P= 0.011). Poorer response to EEN is explained in part by diminished compliance. Faecal GIP might be useful as proxy biomarker of EEN compliance.

In the human gut resides a vast community of microorganisms which perform critical functions for the maintenance of whole body homeostasis. Changes in the composition and function of this community, termed microbiome, are believed to provoke disease onset, including non-communicable diseases. In this review, we debate the current evidence on the role of the gut microbiome in the pathogenesis, outcomes and management of paediatric gut disease. We conclude that even though the gut microbiome is altered in paediatric inflammatory bowel disease, coeliac disease, intestinal failure, necrotising enterocolitis and irritable bowel syndrome, there are currently very few implications for unravelling disease pathogenesis or guiding clinical practice. In the future, the gut microbiome may aid in disease differential diagnosis and prediction of clinical outcomes, and comprise a target for therapeutic interventions.

Diet is a key modifier of risk of inflammatory bowel disease development and potentially a treatment option in patients with established disease. International organisations in gastroenterology and inflammatory bowel disease have published guidelines for the role of diet in disease onset and its management. Here, we discuss the major overarching themes arising from these guidelines and appraise recent literature on the role of diet for inflammatory bowel disease prevention, treatment of active disease and maintenance of remission, considering these themes. Except for exclusive enteral nutrition in active Crohn’s disease, we currently possess very little evidence to make any further dietary recommendations for the management of inflammatory bowel disease. There is also currently uncertainty on the extrapolation of epi­demiological dietary signals on risk of disease development and preclinical experiments in animal models to management, once disease is established. Until high-quality evidence from clinical research becomes available, the only specific recommendations for inflammatory bowel disease we might safely give are those of healthy eating which apply for the general population for overall health and well-being.

The present study aimed to provide evidence on whether children at risk of gastrointestinal inflammation have increased measurements of faecal calprotectin (FC). FC was measured in 232 children; 55 children (n = 11 treatment naïve) with juvenile idiopathic arthritis (JIA), 63 with coeliac disease (CD); 17 with new diagnosis before and after treatment on gluten-free diet and 114 controls. None of the treatment-naive children with JIA had raised FC. Four JIA patients on treatment had a raised FC but in all cases a repeat test was normal. In newly diagnosed patients with CD, the median (interquartile range) FC was higher 36.4 (26–61) than that in controls 25.0 (23–41) mg/kg (P= 0.045) but this significantly decreased 25 (25–25) mg/kg (P= 0.012) after 6 months on gluten-free diet. Random measurements of FC are not raised in children with JIA or CD. A significant elevation of FC in these groups is not explained by their diagnosis and therefore needs further investigation.