Abdominal body composition in paediatric Crohn's disease

Childhood Crohn's disease is associated with growth failure, weight loss and malnutrition. The aetiology of which is multifactorial; chronic inflammation, therapy induced and reduced calorific intake. These factors contribute to alterations in metabolism and body composition. Visceral adipose tissue is the adipose compartment, most strongly associated with chronic inflammation. Intestinal adipose tissue expansion described as 'creeping fat' is well recognized from surgical specimens as a hallmark of Crohn's disease. Expansion of visceral adipose tissue is associated with cardiometabolic risk factors which have been reported in adults and children with inflammatory bowel disease. I performed a systematic review, to understand gaps in the literature in the context of body composition in children with inflammatory bowel disease. 22 studies were included, reporting on body composition in a total of 1477 children with inflammatory bowel disease . Lean mass deficits were more pronounced in children with Crohn's ; 93.6% of Crohn's and 47.7% of ulcerative colitis. Fat related compartment findings were inconsistent, and no clear conclusions could be drawn. Given that children with Crohn's disease had more pronounced deficits in body composition, and intestinal fat expansion is a hallmark of disease, but there is a paucity of data regarding body fat measures; my main aim was to quantify visceral adipose tissue volumes and liver ectopic fat using magnetic resonance imaging (MRI) and Magnetic Resonance Spectrometry (MRS), in this cohort. My secondary aim was to examine relationship of visceral adipose tissue and ectopic liver fat in children with Crohn's disease, disease specific and, metabolic parameters and plasma adipokines. I tested a null hypothesis in that no difference would be observed in abdominal adipose tissue or ectopic liver fat between children with Crohn's disease and healthy children. A prospective cohort of children (7-17 years) with CD and healthy children, were recruited. Visceral adipose tissue , abdominal subcutaneous adipose tissue, abdominal muscle volumes (expressed in litres), and intrahepatocellular lipid (IHCL), was determined using MRS. Blood was analysed for CRP, ESR, albumin, fasting insulin, fasting glucose, lipid profile, adipokines (adiponectin, leptin, visfatin and resistin). Multiple regression analysis was used to identify factors associated with the dependent variable (compartment volume) significance was set at p<0.05. Spearman's rank coefficient for non-parametric data was determined to examine relationship between adipose tissue volumes and disease and blood parameters, R values were reported as per published cut offs. 33 children were recruited (25 CD; 16 males), and 8 controls (5 males), mean age 14.0 ± 2.3 years and 13.4 ± 2.5 years. No participant with CD was receiving concurrent systemic steroids. CD vs. healthy controls; CD was significantly associated with 0.41 litres [0.15 to 0.55] more visceral adipose tissue and 1.71 litres [1.36 to 2.45] more abdominal subcutaneous adipose tissue; after adjusting for sex, weight z score, height z score, and pubertal status (p<0.05). Abdominal muscle volumes were lower in Crohn's disease. There was no significant difference in intrahepatocellular lipid. In children with CD, disease duration, male sex and CRP were significant positive predictors of visceral adipose tissue volume. abdominal subcutaneous adipose tissue had a positive relationship with plasma leptin. Dyslipidaemia was observed, and visceral adipose tissue was associated with plasma triglyceride levels. Visceral adipose tissue was found to positively influence adiposity in CD, namely intrahepatocellular lipid and abdominal subcutaneous adipose tissue. Children with Crohn's were found to have poor quality diets; low calorie, macronutrient imbalance and high percentage non-milk extrinsic sugars . For the first time in paediatric CD patients, we show an association with abdominal adipose tissue obesity (visceral adipose tissue and abdominal subcutaneous adipose tissue) and a trend towards muscle deficit in the context of normal hepatic lipid. Possible drivers of this obesity phenotype in children with Crohn's disease may be the result of dietary inadequacy, energy imbalance, systemic and local chronic inflammation.