Visceral Adiposity, Genetic Susceptibility, and Risk of Complications Among Individuals with Crohn's Disease.

Introduction: Adipose tissue in mesenteric fat plays a key role in systemic and luminal inflammation. However, little is known about the role of visceral adipose tissue (VAT) and its interaction with genetic predisposition in Crohn's disease (CD) progression.

Methods: Our study population included patients with CD enrolled in Prospective Registry in Inflammatory Bowel Disease Study at Massachusetts General Hospital (PRISM). VAT volume was measured from computed tomography using Aquarius 3D. We used logistic regression models to estimate the multivariable-adjusted odds ratio and 95% CI. We tested for effect modification by genetic predisposition using the log likelihood ratio test.

Results: Among 482 patients with CD with available data on VAT, 174 developed penetrating disease, 132 developed stricturing disease, 147 developed perianal disease, and 252 required surgery. Compared with individuals in the lowest quartile of VAT volume, the multivariable-adjusted odds ratio of surgery among individuals in the highest quartile was 2.02 (95% CI, 1.09-3.76; Ptrend = 0.006). Similarly, the risk of penetrating disease seemed to increase with greater VAT volume (Ptrend = 0.022) but not stricturing or perianal disease (all Ptrend > 0.23). The associations between VAT volume and CD complications were not modified by genetic predisposition (all Pinteraction > 0.12).

Conclusions: Visceral adiposity as measured by VAT volume may be associated with a significant increase in the risk of penetrating disease and surgery in CD. Our data suggest that visceral adiposity as measured by VAT may negatively impact long-term progression of CD regardless of genetic predisposition.