OThis lecture focused on the epidemic of obesity and how it influences the practice of hepatology. Obesity is considered a proinflammatory condition. With respect to NASH, well, obesity is a major driving force behind it. An abundance of white adipose tissue generates pro-inflammatory cytokines (or, adipokines), and together with a massive influx of free fatty acids leads to mitochondrial dysfunction and steatohepatitis. BMI has been correlated with fibrosis in NASH.
Obesity also affects hepatitis C virus infection (HCV). Along with alcohol use, HIV and older age at time of infection, BMI is considered a risk factor for more rapid progression of fibrosis. In addition, obesity interferes with efficacy of interferon during treatment, decreasing SVR rates; it does this via upregulation of inhibitory SOCS-3 protein. Fortunately, with the advent of protease inhibitors and better outcomes, the negative risk of BMI is negated.
In other avenues of hepatology: BMI correlates with the prevalence of hepatitis with increasing alcohol use as well as in the setting of binge drinking. BMI also predicts liver decompensation in cirrhotic patients. Obesity increases the relative risk of hepatocellular carcinoma (moreso than any other cancer in men (RR 4.5). It may do this via insulin pathways, and perhaps mTOR pathways.
Obesity also complicates patient’s candidacy for liver transplantation. Some studies also suggest that BMI > 35 is a risk factor for worse outcomes after liver transplantation. This is a major problem, because NASH (obesity) is already the third leading indication for transplantation and the only disease etiology that is increasing over the past decade.
In sum, you must consider obesity in many liver conditions…not just NAFLD.