Chronic Liver Disease Chronic selleck inhibitor liver disease has long been associated with alcohol consumption and includes alcoholic liver disease, hepatitis C, and nonalcoholic steatohepatitis. Despite this clear association, however, there is a lack of strong clinical measures to describe and predict the progression of chronic liver disease. Dr. James Everhart noted that the course of alcoholic liver disease is several decades in duration and begins as simple steatosis (fatty liver) before progressing to more advanced stages including steatohepatitis, alcoholic cirrhosis, and, eventually, liver failure. Dr. Everhart noted that alcoholic liver disease may be overrepresented in terms of mortality because of the current classification system. Histologically, alcoholic fatty liver and nonalcoholic fatty liver look similar (Scaglioni et al.

2011), and patients with otherwise similar multiple risk factors and histology may be classified as having alcoholic liver disease rather than nonalcoholic steatohepatitis simply because they do or do not drink. According to Dr. Everhart, the current strict separation of alcoholic and nonalcoholic fatty liver disease limits epidemiology, public health, and clinical understanding. In examining the effects of drinking amounts on liver disease, little association has been found between moderate drinking and alcoholic liver disease, and only a minority of very heavy drinkers develops alcoholic liver disease, although the reason is not clear. It is possible that drinking patterns and diet each play a role in risk.

More information also is needed to determine if drinking at times other than during meals could increase risk. Other factors that put people at higher risk for liver disease include being obese, using cannabis, having diabetes, and being female (Hart et al. 2010). Conversely, coffee consumption seems to lower risk and smoking seems to have no effect on the development of chronic liver disease. Genetic susceptibility is another important risk factor for liver disease. For example, a variant in one gene, PNPLA3, originally associated with fatty liver, has been GSK-3 strongly associated with alcoholic liver disease. Again, additional research is needed to determine how these factors influence alcohol��s effects. Dr.