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Hepatitis Monthly Editorial Board Comment 2
Kamran Bagheri Lankarani 1, Seyed-Moayed Alavian 2
1.Associate professor of gastroenterology and hepatology, Namazi Hospital, Shiraz University of Medical Sciences, Shiraz, I.R.Iran
2.Associate professor of gastroenterology and hepatology, Baqiyatallah University of Medical Sciences, Tehran, I.R.Iran
We read with interest the article titled" Peginterferon Alfa-2a Alone, Lamivudine Alone, and the Two in Combination in Patients with HBeAg-Negative Chronic Hepatitis B" by Marcellin et al. (N Engl J Med. 2004; 351:1206-17). It was very interesting for us to understand the efficacy of new drugs in chronic hepatitis B (CHB) patients, especially in CHB with HBeAg negative. Treatment of chronic hepatic B infection in the absence of HBe antigen is very challenging. Marcellin and his colleagues in their recent study used pegylated interferon alfa (PEG IFN) in these patients (1), but several points in their study need more clarification. First of all, there is no comparison with standard interferon. Available data indicate prolonged course of standard interferon for ³12 months has 20-30% sustained virologic response which is almost the same as what is reported with PEG IFN in this study with a much lower cost (1, 2, 3). It seems that we need a protocol to compare between the standard interferon alfa with pegylated interferon in HBeAg negative CHB by considering the costs. The second point is that there was one death in PEG IFN group which needs more consideration. While it was claimed that all treated patients had elevated ALT before treatment, the baseline data in table one indicate ALT level in all treatment groups included normal values!?. If this is the case then indication of treatment in these cases with normal ALT level is not clear (4). As mentioned in the article, rate of HBsAg loss and HBsAg seroconversion at week 72 occurred in seven and five patients who received peginterferon alfa-2a monotherapy respectively and; in five and three patients who received peginterferon alfa-2a plus lamivudine, respectively and in no patients in lamivudine group. However, the authors concluded the importance of dual immunomodulatory and antiviral effects of interferon-based therapies in the treatment of HBeAg negative CHB. We think this benefit belongs to interferon alfa and not to lamivudine, which is in accordance with what the authors mentioned in another part of discussion. The results with peginterferon alfa-2a monotherapy were better than combination therapy. The best conclusion is that response rate to lamivudine is lower than that of interferon-based therapy. Several studies suggests that HBV genotypes may influence response to anti-viral therapy and genotypes A and B have been reported to be associated with higher rates of response to interferon alfa than genotypes D and C, respectively (5).There are also no data on genotypes in this article which may affect response to treatment. By considering these points, we believe that while this is an excellent response rate with peginterferon alfa-based therapy in comparison with lamivudine, it is still a long way to conclude that peginterferon alfa is the first-line therapy for HBeAg negative CHB and it needs more studies.
