036; OR = 2.34; 95% CI = 1.0–5.1). Conclusion:  These results suggest that SLCO1B1 Exon4 C > A polymorphism confers increased risk for gallstone

MEK inhibitor disease in North Indian population. “
“We read with great interest the article by Ascha et al.1 on the incidence and risk factors for hepatocellular carcinoma (HCC) in patients with nonalcoholic steatohepatitis (NASH). The authors state that patients with NASH cirrhosis have a greatly increased risk of HCC and that the most significant factor related to this increase seems to be alcohol consumption. Although this study is important and intriguing in a number of ways and provides insight into the risk factors involved in HCC development, we would like to add one additional comment to the authors’ discussion that is noteworthy in several respects. In their article,1 the authors attempt to discuss comprehensively the incidence and risk factors for NASH-related and hepatitis C virus–related cirrhosis and HCC. Although it is obvious that evaluating the mechanisms for these diseases is beyond the scope of their study, it would have been worthwhile for the

authors to mention a potential underlying mechanism for these conditions that could lead to a better understanding of the results achieved in their report. For this reason, we would like to draw attention to the possible role of adipocytokines in the development of HCC, which could elucidate the risk factors associated with the development of HCC. Among the great number of mechanisms that have been proposed to explain the link ABT-263 solubility dmso between NASH-related cirrhosis and HCC, adipocytokine dysregulation offers new and promising perspectives for a wide range of liver diseases. Adipose tissue is a major source of bioactive substances learn more known as adipocytokines, which

include resistin, leptin, tumor necrosis factor α, and adiponectin.2 Hypertrophied adipocytes in obesity release chemokines that induce the accumulation of macrophages in visceral adipose tissue, which then produce nitric oxide and proinflammatory cytokines. These inflammatory changes induce adipocytokine dysregulation, which is characterized by a decrease in insulin-sensitizing and anti-inflammatory adipocytokines and an increase in proinflammatory adipocytokines.2 Disturbed adipocytokine secretion due to inflammatory changes in obese adipose tissue might, therefore, promote hepatic steatosis, inflammation, fibrogenesis, or hepatocarcinogenesis of the liver.3 Moreover, alcohol, which induces cell death and inflammation in the liver, can cause the development of HCC in NASH patients because of the liver injury already triggered by adipocytokine dysregulation. In conclusion, on the basis of the aforementioned mechanisms, it is reasonable to expect increased rates of HCC in NASH patients, especially those with increased alcohol consumption.