Treatment of active Crohn’s disease with an ordinary food-based diet that replicates exclusive enteral nutrition

Svolos, V. et al. (2019) Treatment of active Crohn’s disease with an ordinary food-based diet that replicates exclusive enteral nutrition. Gastroenterology, 156(5), 1354-1367.e6. (doi: 10.1053/j.gastro.2018.12.002) (PMID:30550821)

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Background & Aims: Exclusive enteral nutrition (EEN) is the only established dietary treatment for Crohn’s disease (CD), but its acceptability is limited. There is a need for novel dietary treatments for CD. Methods: We evaluated the effects of an individualized, food-based diet (CD-TREAT), with similar composition to EEN, on the gut microbiome, inflammation and clinical response in a rat model, healthy adults, and children with relapsing CD. Twenty-five healthy adults randomly received EEN or CD-TREAT for 7 days, followed by a 14-day washout period, followed by the alternate diet. Fecal microbiome and metabolome were assessed before and after each diet. HLA-B7 and HLA-B27 transgenic rats with gut inflammation received EEN, CD-TREAT, or standard chow for 4 weeks. Fecal, luminal and tissue microbiome, fecal metabolites and gut inflammation were assessed. Five children received CD-TREAT with clinical activity and fecal calprotectin evaluated after 8-week treatment. Results: Among healthy adults, CD-TREAT was easier to comply with and more acceptable than EEN. CD-TREAT induced similar effects to EEN (EEN vs CD-TREAT) on fecal microbiome composition, metabolome, mean total sulfide (increase 133.0±80.5 vs 54.3±47.0 nmol/g), pH (increase 1.3±0.5 vs 0.9±0.6), the short-chain fatty acids (μmol/g) acetate (decrease 27.4±22.6 vs 21.6±20.4), propionate (decrease 5.7±7.8 vs 5.2±7.9), and butyrate (decrease 7.0±7.4 vs 10.2±8.5). In the rat model, CD-TREAT and EEN produced similar changes in bacterial load (decrease 0.3±0.3 log10 16S rRNA gene copies/g), short-chain fatty acids, microbiome, and ileitis severity (mean histopathology score reductions 1.25 for EEN (P=.015) and 1.0 for CD-TREAT (P=.044) vs chow). Among the children receiving CD-TREAT, 4 (80%) had a clinical response and 3 (60%) entered remission, with significant concurrent reductions in fecal calprotectin (mean decrease 918±555 mg/kg, (P=.002)). Conclusion: CD-TREAT replicates EEN changes in the microbiome, reduces gut inflammation, is well-tolerated and is potentially effective in patients with active CD.

Item Type:Articles
Glasgow Author(s) Enlighten ID:Hansen, Dr Richard and Russell, Dr Richard and Gaya, Mr Daniel and Bolognini, Dr Daniele and Ansalone, Dr Cecilia and Svolos, Dr Vaios and Papadopoulou, Ms Rodanthi and Edwards, Professor Christine and Nichols, Mr Ben and Milling, Professor Simon and Gerasimidis, Professor Konstantinos and Salmond, Dr Jonathan and Ijaz, Dr Umer
Authors: Svolos, V., Hansen, R., Nichols, B., Quince, C., Ijaz, U.Z., Papadopoulou, R.T., Edwards, C.A., Watson, D., Alghamdi, A., Brejnrod, A., Ansalone, C., Duncan, H., Gervais, L., Tayler, R., Salmond, J., Bolognini, D., Klopfleisch, R., Gaya, D.R., Milling, S., Russell, R.K., and Gerasimidis, K.
College/School:College of Medical Veterinary and Life Sciences > School of Infection & Immunity
College of Medical Veterinary and Life Sciences > School of Medicine, Dentistry & Nursing
College of Science and Engineering > School of Engineering > Infrastructure and Environment
Research Centre:College of Medical Veterinary and Life Sciences > School of Infection & Immunity > Centre for Immunobiology
Journal Name:Gastroenterology
ISSN (Online):1528-0012
Published Online:11 December 2018
Copyright Holders:Copyright © 2018 AGA Institute
First Published:First published in Gastroenterology 156(5): 1354-1367.e6
Publisher Policy:Reproduced under a Creative Commons License

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Project CodeAward NoProject NamePrincipal InvestigatorFunder's NameFunder RefLead Dept
652771Understanding microbial community through in situ environmental 'omic data synthesisUmer Zeeshan IjazNatural Environment Research Council (NERC)NE/L011956/1ENG - ENGINEERING INFRASTRUCTURE & ENVIR
715631Defining mechanisms that control T cell migrationSimon MillingMedical Research Council (MRC)MR/N023625/1III -IMMUNOLOGY