We thank Drs. Wang and Kao for their interest and comments regarding our study of the effect of chronic hepatitis C infection and its resolution on serum lipid levels.1 They raise several important issues.

The authors raise the issue that the rebound in serum cholesterol and low-density lipoprotein (LDL) that occurred after successful treatment-induced viral clearance may have been the result of recovery of hepatic function following the resolution of hepatic inflammation rather than a specific effect of hepatitis C virus clearance. We acknowledge that the liver plays an important role in lipid metabolism and that lipid metabolism may be influenced by hepatic inflammation. However, we believe that the alterations seen in our study were specific to hepatitis C infection. For instance, several studies found patients with chronic hepatitis C to have significantly lower cholesterol levels than those with chronic hepatitis B infection, suggesting that the alteration in lipids observed in hepatitis C infection is virus-specific.2–4 Further, when stratifying by pretreatment levels of alanine aminotransferase or hepatitis C RNA, we found no difference in rebound levels of cholesterol or LDL, suggesting that the degree of hepatic inflammation or level of viremia does not influence cholesterol or LDL levels. We are not aware of any studies evaluating the change in serum LDL and cholesterol levels following viral suppression during hepatitis B therapy, but agree that such evaluation would allow this question to be definitely answered.

We acknowledge that lipid levels may fluctuate over time and can change in response to lifestyle or dietary changes. Although multiple post-treatment measurements would be helpful in furthering our findings, we disagree that a single measurement is not sufficient. Clinical management of hyperlipidemia is frequently based on a single measurement of lipids, and benefit of treatment based on a single initial measurement has been demonstrated.5, 6 In addition, we would expect to see random fluctuations in both the clearance and nonresponse groups and thus such fluctuations should impact both groups equally.

Finally, we agree that there are conflicting data regarding the role of hepatitis C infection as a risk factor for coronary artery disease (CAD). A possible explanation is that all studies of CAD in hepatitis C that we are aware of have used hepatitis C seropositivity alone to diagnosis hepatitis C. These studies are thus limited by a lack of ability to discern the presence of active infection. In addition, none of the previous studies has specifically evaluated the role of treatment of hepatitis C on CAD outcomes.7, 8 Long-term studies to assess the impact of hepatitis C treatment on CAD remain warranted.


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    Maggi G, Bottelli R, Gola D, Perricone G, Posca M, Zavaglia C, et al. Serum cholesterol and chronic hepatitis C. Ital J Gastroenterol 1996; 28: 436440.
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    Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344: 13831389.
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    Alyan O, Kacmaz F, Ozdemir O, Deveci B, Astan R, Celebi AS, et al. Hepatitis C infection is associated with increased coronary artery atherosclerosis defined by modified Reardon severity score system. Circ J 2008; 72: 19601965.

Kathleen E. Corey M.D., M.P.H.*, Raymond T. Chung M.D.*, * Department of Gastroenterology, Massachusetts General Hospital, Boston, MA.