ESPEN Guideline: Clinical Nutrition in inflammatory bowel disease

Introduction: The ESPEN guideline presents a multidisciplinary focus on clinical nutrition in inflammatory bowel disease (IBD). Methodology: The guideline is based on extensive systematic review of the literature, but relies on expert opinion when objective data were lacking or inconclusive. The conclusions and 64 recommendations have been subject to full peer review and a Delphi process in which uniformly positive responses (agree or strongly agree) were required. Results: IBD is increasingly common and potential dietary factors in its aetiology are briefly reviewed. Malnutrition is highly prevalent in IBD – especially in Crohn's disease. Increased energy and protein requirements are observed in some patients. The management of malnu-trition in IBD is considered within the general context of support for malnourished patients. Treatment of iron deficiency (parenterally if necessary) is strongly recommended. Routine provision of a special diet in IBD is not however supported. Parenteral nutrition is indicated only when enteral nutrition has failed or is impossible. The recommended perioperative man-agement of patients with IBD undergoing surgery accords with general ESPEN guidance for patients having abdominal surgery. Probiotics may be helpful in UC but not Crohn's disease. Primary therapy using nutrition to treat IBD is not supported in ulcerative colitis, but is mod-erately well supported in Crohn's disease, especially in children where the adverse conse-quences of steroid therapy are proportionally greater. However, exclusion diets are generally not recommended and there is little evidence to support any particular formula feed when nutritional regimens are constructed. Conclusions: Available objective data to guide nutritional support and primary nutritional therapy in IBD are presented as 64 recommendations, of which 9 are very strong recom-mendations (grade A), 22 are strong recommendations (grade B) and 12 are based only on sparse evidence (grade 0); 21 recommendations are good practice points (GPP)

How to use: nutritional assessment in neonates

Adequate nutrition and growth during the neonatal period are important, especially for preterm infants, for whom there is evidence of poor nutrient intakes and growth, and this has important implications for their health in later life. Increased nutritional support while on the neonatal intensive care unit has been shown to improve growth, but such support is not universally available. Being able to carry out and interpret a nutritional assessment is therefore an important skill for paediatricians caring for neonates. This article aims to explain how to use nutritional assessment in neonates and provides some tools to make this process as straightforward as possible.</p

Impact of disease activity on resting energy expenditure in children with inflammatory bowel disease

Background and aims: exclusive enteral nutrition is used as primary therapy in Crohn’s disease. Nutrition support is frequently required in children with both Crohn’s disease and Ulcerative Colitis when acutely unwell and during periods of recovery. There is considerable controversy about nutritional needs during phases of active and inactive disease. It is, for example, often assumed that in acute illness a child requires increased nutritional support however the precise relationship between illness severity and energy expenditure is uncertain. This study explores the relationship between disease activity and resting energy expenditure (REE) in children with inflammatory bowel disease.Methods: patients were recruited from the regional paediatric gastroenterology unit at Southampton University Hospitals NHS Trust. Disease activity was assessed using standard scoring systems (Paediatric Crohn’s Disease Activity Index; Simple Colitis Activity Index) and biochemical markers of inflammation (C-Reactive Protein, CRP). Fat free mass was estimated from skinfold thickness and Bioelectrical Impedance Analysis. Resting energy expenditure was measured by indirect calorimetry. A logarithmic correction and a linear regression model were used for analysis of REE corrected for body size.Results: 55 children were studied; 37 (67%) with Crohn’s disease and 18 (33%) with Ulcerative Colitis. Median PCDAI was 10 (range 0–60), 22 (59%) had PCDAI 10 (active disease). Median SCAI was 1.5 (range 0–12). Within disease groups there were strong correlations between REE/KgFFM0.52 and disease activity; PCDAI (r 0.386, p 0.018) in Crohn’s disease and SCAI (r 0.456, p 0.057) in Ulcerative Colitis. In the cohort as a whole there was no increase in REE/KgFFM0.52 with increasing CRP (r 0.129, p 0.361). Using the regression model each mg/l increase in CRP was associated with a reduction in REE of nearly 1.5 kcal/day.Conclusions: we were unable to demonstrate a significant relationship between REE and disease activity in children with inflammatory bowel disease

No relation between disease activity measured by multiple methods and REE in childhood Crohn disease

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 (??=?0.03, P?=?0.7) nor from CRP (??=??0.05, P?=?0.52), ESR (??=??0.07, P?=?0.43), faecal calprotectin (??=??0.07, P?=?0.38), and faecal lactoferrin (??=?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.<br/

Body composition in childhood inflammatory bowel disease

Background &amp; aims: little is known about the impact of disease and treatment on the pattern of growth in children with Inflammatory Bowel Disease (IBD). Significant deficits in height and weight in children with Crohn’s disease have been reported but changes in fat and fat free mass are less well defined. This study aims to describe the height, weight and body composition of a cohort of children with IBD.Methods: height, weight, skinfold thicknesses and bioelectrical impedance analysis was performed. Disease activity was assessed with clinical scoring systems.Results: 55 children, median age 13.7 years (range 6.5–17.7) were studied. Median (25th, 75th percentile) Standard Deviation Score for BMI, Height and Weight were ? 0.3 (? 0.97, 0.65), ? 0.56 (? 1.42, 0.06), ? 0.62 (? 1.43, 0.19). In Crohn’s disease, using multiple regression analysis disease activity measured by PCDAI was significantly inversely related to fat free mass (? ? 0.2, 95% CI ?0.17, ?0.03, p 0.005).Conclusions: children with IBD were both under and overweight. Nutritional deficits were more common in Crohn’s disease. Fat free mass was related to disease activity in children with Crohn’s disease regardless of changes in weight. Weight or BMI may mask deficits in lean tissue in the presence of normal or increased proportions of body fat