Though historically regarded as an inert energy store, adipose tissue is a complex endocrine organ, which is increasingly implicated in the pathogenesis of inflammatory bowel disease (IBD). Accumulating evidence points to visceral adipose tissue and specifically to its mesenteric component, or “creeping fat” as impacting on the disease course through its immunomodulatory properties. On the one hand, mesenteric fat acts as a physical barrier to inflammation and is involved in controlling host immune response to translocation of gut bacteria. On the other hand, however, there exists a strong link between visceral fat and complicated course of the disease with unfavorable therapeutic outcomes. Furthermore, “creeping fat” appears to play different roles in different IBD phenotypes, with the greatest pathogenetic contribution probably to an ileal form of Crohn’s disease. In this review, we summarize and discuss the existing literature on the subject and identify high-priority areas for future research. It may be that a better understanding of the role of mesenteric fat in IBD will determine new therapeutic targets and translate into improved clinical outcomes.

Summary Background Atherosclerotic cardiovascular disease is a key cause of morbidity in non‐alcoholic fatty liver disease (NAFLD) but appropriate means to predict major acute cardiovascular events (MACE) are lacking. Aim To design a bespoke cardiovascular risk score in NAFLD. Methods A retrospective derivation (2008‐2016, 356 patients) and a prospective validation (2016‐ 2017, 111 patients) NAFLD cohort study was performed. Clinical and biochemical data were recorded at enrolment and mean platelet volume (MPV), Qrisk2 and Framingham scores were recorded one year prior to MACE (Cardiovascular death, acute coronary syndrome, stroke and transient ischaemic attack). Results The derivation and validation cohorts were well‐matched, with MACE prevalence 12.6% and 12%, respectively. On univariate analysis, age, diabetes, advanced fibrosis, collagen proportionate area >5%, MPV and liver stiffness were associated with MACE. After multivariate analysis, age, diabetes and MPV remained independently predictive of MACE. The “NAFLD CV‐risk score” was generated using binary logistic regression: 0.06*(Age) + 0.963*(MPV) + 0.26*(DM1) – 16.44; 1Diabetes mellitus: 1: present; 2: absent. (AUROC 0.84). A cut‐off of −3.98 gave a sensitivity 97%, specificity 27%, PPV 16%, and NPV 99%. An MPV alone of >10.05 gave a sensitivity 97%, specificity 59%, PPV 24% and NPV 97% (AUROC 0.83). Validation cohort AUROCs were comparable at 0.77 (NAFLD CV‐risk) and 0.72 (MPV). In the full cohort, the NAFLD CV‐risk score and MPV outperformed both Qrisk2 and Framingham scores. Conclusions The NAFLD CV risk score and MPV accurately predict 1‐year risk of MACE, thereby allowing better identification of patients that require optimisation of their cardiovascular risk profile.

This study shows an association between LSM at the upper extreme and HCC risk. Physicians may find this beneficial as a non-invasive dynamic approach to assessing HCC risk in cirrhosis patients.