RT Book, Section A1 Dienstag, Jules L. A2 Jameson, J. Larry A2 Fauci, Anthony S. A2 Kasper, Dennis L. A2 Hauser, Stephen L. A2 Longo, Dan L. A2 Loscalzo, Joseph SR Print(0) ID 1178426858 T1 Chronic Hepatitis B Treatment T2 Harrison's Principles of Internal Medicine, 20e YR 2018 FD 2018 PB McGraw-Hill Education PP New York, NY SN 9781259644016 LK accesspharmacy.mhmedical.com/content.aspx?aid=1178426858 RD 2024/03/29 AB Although progression to cirrhosis is more likely in severe than in mild or moderate chronic hepatitis B, all forms of chronic hepatitis B can be progressive, and progression occurs primarily in patients with active HBV replication. Moreover, in populations of patients with chronic hepatitis B who are at risk for HCC (Chap. 78), the risk is highest for those with continued, high-level HBV replication and lower for persons in whom initially high-level HBV DNA falls spontaneously over time. Therefore, management of chronic hepatitis B is directed at suppressing the level of virus replication. Although clinical trials tend to focus on clinical endpoints achieved over 1−2 years (e.g., suppression of HBV DNA to undetectable levels, loss of HBeAg/HBsAg, improvement in histology, normalization of ALT), these short-term gains translate into reductions in the risk of clinical progression, hepatic decompensation, HCC, liver transplantation, and death; regression of cirrhosis and of esophageal varices have been documented to follow long-term pharmacologic suppression of HBV replication. In addition, restoration of impaired HBV-specific T-cell function has been shown following successful suppression of HBV replication with antiviral therapy. To date, seven drugs have been approved for treatment of chronic hepatitis B: injectable interferon (IFN) α and pegylated interferon (long-acting IFN bound to polyethylene glycol, PEG [PEG IFN]) and the oral agents lamivudine, adefovir dipivoxil, entecavir, telbivudine, and tenofovir disoproxil fumarate (TDF).