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 CD patients enrolled in Prospective Registry in Inflammatory Bowel Disease Study at Massachusetts General Hospital (PRISM). VAT volume was measured from CT scans using Aquarius 3D. We used logistic regression models to estimate the multivariable-adjusted odds ratio (MV-adjusted OR) and 95% confidence interval (CI). We tested for effect modification by genetic predisposition using the log-likelihood ratio test.
Results
Among 482 CD patients with available data on VAT, 174 developed penetrating disease, 132 developed stricturing disease, 147 developed perianal disease, and 252 required surgery. Compared to individuals in the lowest quartile of VAT volume, the MV-adjusted OR 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 appeared 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 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.