No Relation Between Disease Activity Measured by Multiple Methods and REE in Childhood Crohn Disease

Wiskin, Anthony E.; Wootton, Stephen A.; Cornelius, Victoria R.; Afzal, Nadeem A.; Elia, Marinos; Beattie, R. Mark

Journal of Pediatric Gastroenterology & Nutrition:
doi: 10.1097/MPG.0b013e318236b19a
Original Articles: Gastroenterology

Background and Aims: Increased resting energy expenditure (REE) unmatched by dietary intake is implicated as a cause of poor nutrition in childhood inflammatory conditions. Adequate description of disease activity and correction of REE data for body composition are important to reach reliable conclusions about changes in REE associated with disease. The present study aimed to determine the effect of disease activity measured by clinical status, systemic and stool inflammatory markers on REE in children with Crohn disease using appropriate correction for confounding factors.

Methods: Sixty children with Crohn disease were recruited from the regional paediatric gastroenterology unit and studied on 1 occasion. REE was measured by indirect calorimetry. Fat-free mass (FFM) was estimated by skinfold thickness. Disease activity was measured using systemic (C-reactive protein [CRP], erythrocyte sedimentation rate [ESR]) and faecal markers of inflammation (lactoferrin, calprotectin) and clinical scores (Paediatric Crohn Disease Activity Index).

Results: Using a multiple regression model, there was no significant change in REE from active or inactive disease (β = 0.03, P = 0.7) nor from CRP (β = −0.05, P = 0.52), ESR (β = −0.07, P = 0.43), faecal calprotectin (β = −0.07, P = 0.38), and faecal lactoferrin (β = 0.01, P = 0.88). REE/kg FFM0.5 was not associated with the Paediatric Crohn Disease Activity Index (r = 0.1, P = 0.44), CRP (r = −0.3, P = 0.84) or ESR (r = 0.12, P = 0.4), faecal calprotectin (r = 0.04, P = 0.97), or faecal lactoferrin (r = 0.02, P = 0.87).

Conclusions: REE corrected for physiologically relevant confounders is not associated with degree of disease activity using clinical tools or systemic and local inflammatory markers, and therefore is an unlikely mechanism for poor nutritional state.

Author Information

NIHR Biomedical Research Unit (Nutrition, Diet & Lifestyle) Institute of Human Nutrition University of Southampton, Southampton, UK.

Address correspondence and reprint requests to Dr Robert M. Beattie, Paediatric Medical Unit, Southampton General Hospital, Tremona Road, Southampton, S016 6YD, UK (e-mail:

Received 26 June, 2011

Accepted 29 August, 2011

The National Institute for Health Research (NIHR) through the Biomedical Research Unit in Southampton funded this research and provides salary for A.E.W. and V.R.C. Bühlmann Laboratories and Techlab subsidised faecal calprotectin and lactoferrin kits, respectively.

Poster presented at the British Society of Gastroenterology meeting, Birmingham, UK, March 14–17, 2011.

The authors report no conflicts of interest.

Copyright 2012 by ESPGHAN and NASPGHAN