Although their results provide important data to improve our understanding about the interactions between HCV infection and lipid metabolism, several issues deserve further discussion.

First, the most important finding was the LDL and cholesterol rebounded in patients with chronic hepatitis C who achieved sustained virologic response after discontinuation of therapy. However, this fact could be simply explained by the recovery of hepatic function after resolution of hepatic inflammation. Liver is known to mediate lipid metabolism including the uptake of circulating free fatty acid and the secretion of very low density lipoprotein into peripheral blood, which may influence serum concentration of cholesterol and LDL. Our previous case-control study consistently showed lower cholesterol and LDL levels in patients with chronic hepatitis C than in uninfected controls.2 However, HCV infection was LDK378 solubility dmso associated with a higher cholesterol level in patients with normal alanine aminotransferase (ALT) Sorafenib clinical trial levels,2 suggesting ALT level, a biomarker of hepatic inflammation, may play a role in modulating the relationship between HCV infection and lipid metabolism. Another study also reported a significant

decrease of cholesterol level in patients with chronic active hepatitis compared to healthy controls.3 Therefore, the authors should perform analyses comparing patients with lipid rebound with those who were not stratified by pretreatment ALT levels or HCV viral load, in order to clarify the causal relationship between HCV clearance and cholesterol

rebound. Second, cholesterol and LDL levels physiologically fluctuate with the changes of diet, exercise, or lifestyle. Although their cohort adopted complete paired lipid data before and after hepatitis C treatment to directly evaluate these changes in a given individual, it is still difficult to differentiate physiological fluctuation from significant Unoprostone lipid rebound by one spot measurement. To solve this issue, the authors should provide more lipid data during the follow-up period to exclude possible biases from the physiologic fluctuation of serum lipid concentrations. Finally, a previous cohort study found HCV infection was associated with a higher risk of CHD after adjustment for traditional risk factors.4 Furthermore, HCV infection may independently predict an increased severity of CHD based on Reardon severity score in a population of individuals with angiographically determined CHD.5 In this article, the authors demonstrated the association between HCV infection and relative hypolipidemia in several contexts. Paradoxically, this hypolipidemic effect could not provide appropriate explanation for the increased risk of CHD in patients with chronic hepatitis C. In addition, our previous data also indicated a positive association of HCV RNA level with insulin resistance in patients infected with chronic hepatitis C.