Article Text


Inflammatory bowel disease I
PMO-237 Prebotics as primary prevention of Crohn's disease: impact on luminal microbiology and elevated faecal calprotectin is greater in healthy siblings than in patients
  1. C R Hedin1,2,
  2. P Louis3,
  3. F Farquharson3,
  4. S McCartney4,
  5. A J Stagg2,
  6. J O Lindsay2,
  7. K Whelan1
  1. 1Diabetes and Nutritional Sciences Division, King's College London, London, UK
  2. 2Blizard Institute, Queen Mary University of London, London, UK
  3. 3Microbiology Group, Rowett Institute of Nutrition and Health, University of Aberdeen, Aberdeen, UK
  4. 4Department of Gastroenterology, University College Hospitals NHS Foundation Trust, London, UK


Introduction Inflammation in Crohn's disease (CD) is driven by the intestinal microbiota, however, microbial manipulation with prebiotics is ineffective in treating active disease.1 Siblings of patients are at risk of developing CD, and some share aspects of the CD phenotype including raised faecal calprotectin (FC) and dysbiosis. Prebiotics may alter these risk markers.

Methods Patients with inactive CD (n=19, CD activity index <150) and 12 unaffected siblings ingested 15 g/d of fructo-oligosaccharide/inulin (FOS) for 3 weeks. FC (enzyme-linked immunosorbant assay) and faecal microbiota (quantitative PCR targeting 16S ribosomal RNA (rRNA) genes, quantified relative to representative bacterial 16S rRNA genes) were measured at baseline and follow-up. Non-parametric statistical analyses were performed, and values presented as medians.

Results In patients and siblings, Bifidobacteria and Bifidobacterium longum increased post-FOS. In siblings but not patients, Bifidobacterium adolescentis and Roseburia spp. also increased (Abstract PMO-237 table 1). Compared with patients, siblings had a greater median percentage point change in Bifidobacteria (+14.6% vs +0.4%, p=0.028), B adolescentis (+1.1% vs 0.0% p=0.006) and Roseburia spp. (+1.5% vs −0.1% p=0.004). Of those with raised FC at baseline, it decreased post-FOS in only 7/19 patients (37%), compared with 4/5 (80%) siblings (p=0.142). The change in FC was significantly negatively correlated with baseline FC in siblings (r=−0.715, p=0.009) but positively correlated with baseline FC in patients (r=+0.352, p=0.140).

Abstract PMO-237 Table 1

Microbiota at baseline and follow-up

Conclusion In contrast to inflamed CD,1 a prebiotic effect with FOS occurs to a limited extent in non-inflamed CD, and also occurs, more markedly, in at-risk siblings. Furthermore, FC decreased in siblings post-FOS, but did not change significantly (and even tended to rise) in patients with inactive CD. Prebiotics may best be employed in disease prevention rather than treatment.

Competing interests C Hedin: Grant/Research Support from: Clinical Research Fellow funded by Core charity, P Louis: None declared, F Farquharson: None declared, S McCartney: None declared, A Stagg: None declared, J Lindsay: None declared, K Whelan: None declared.

Reference 1. Benjamin JL, Hedin CR et al. Gut 2011;60:923–9.

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.