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BMC Proceedings

Open Access

The relationship of adiposity to disease severity in a Crohn's patient cohort

  • DJ O’Connor1,
  • G Sexton2 and
  • G McCormack2
BMC Proceedings20159(Suppl 1):A23

Published: 14 January 2015


Body Mass IndexInflammatory Bowel DiseaseChronic Inflammatory Bowel DiseaseChronic Inflammatory BowelSkin Fold Thickness


Crohn’s Disease (CD) is a chronic inflammatory bowel disease characterised by recurrent intestinal inflammation [1]. Adipose tissue has metabolic and immune functions regulated through the expression of hormones and cytokines [2, 3]. Conventionally, adiposity in CD is believed to reflect disease activity, nutritional status and possibly corticosteroids. Emerging data suggests that adipose tissue may play a more complex immunoregulatory role in CD [4].


CD patients attending the gastroenterology department were recruited over a 4 week period were invited to partake in this pilot study. The following data was collected: Extent of disease and previous treatments, current disease activity and biometric measurements of adiposity (Body mass index (BMI), waist hip ratio, mid upper arm circumference, skin fold thickness and percentage body fat using biometric impedance analysis (BIA)).


27 patients were recruited in this pilot study. 16 (59%) had BMI >25 and (classified as overweight or obese), 10 had normal BMI and 1 had BMI <18. 32% had body fat stores above normal, 44% within normal range and 24% had low fat stores as measured with BIA. Numbers were too small in this pilot study to establish a relationship between disease pattern and/or activity, those requiring >1 course of steroids in the previous year and those on anti-TNF therapy were more likely to have normal range BMI than the group as a whole. Self reported abdominal pain and decreased well being was highest in patients with an increased BMI.


Obesity rates in the general population are rising [5]. Our study indicates that obesity does present in the CD population. Adipose tissue may be a source of proinflammatory cytokines thus altering the natural history of CD in these patients [6]. Even if there is no impact on disease progression, our findings have important implications for current CD drug and nutritional management.

Authors’ Affiliations

School of Medicine, National University of Ireland, Galway, Ireland
Midland Regional Hospital at Tullamore, Tullamore, Ireland


  1. Crohn BB, Ginzburg L, Oppenheimer GD: Regional ileitis – A pathological and clinical entity. JAMA. 1932, 99: 1323-1329.View ArticleGoogle Scholar
  2. Kershaw EE, Flier JS: Adipose tissue as an endocrine organ. J Clin Endocrinol Metab. 2004, 89 (6): 2548-View ArticlePubMedGoogle Scholar
  3. Mohammed AV, Pinknev JH, Coppack SW: Adipose tissue as an endocrine and paracrine organ. Int J Obes Relat Metab Disord. 1998, 22 (12): 1145-1158.View ArticleGoogle Scholar
  4. Peyrin-Biroulet L, Chamaillard M, Gonzalez F, Beclin E, Decourcelle C, Antunes L, et al: Mesenteric fat in Crohn’s disease: a pathogenetic hallmark or an innocent bystander. GUT. 2007, 56 (4): 577-583.View ArticlePubMed CentralPubMedGoogle Scholar
  5. Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tobak CJ, Flegal KM: Prevalence of overweight and obesity in the united states 1999-2004. JAMA. 2006, 295 (13): 1549-1555.View ArticlePubMedGoogle Scholar
  6. Curat CA, Miranville A, Sengenès C, Diehl M, Tonus C, Busse R, et al: From blood monocytes to adipose tissue-resident macrophages: induction of diapedesis by human mature adipocytes. Diabetes. 2004, 53 (5): 1285-1292.View ArticlePubMedGoogle Scholar


© O’Connor et al; licensee BioMed Central Ltd. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.