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 FFM 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.
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 FFM 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.
Authors: Ioannis D Kostakis; Kyriaki G Cholidou; Aristeidis G Vaiopoulos; Ioannis S Vlachos; Despina Perrea; George Vaos Journal: Dig Dis Sci Date: 2012-08-17 Impact factor: 3.199