Telbivudine: A valuable treatment option in chronic hepatitis B

Abstract

The last five years have emerged as a new era in the treatment of chronic hepatitis B (CHB). Advances in therapeutics and the approval of new drugs have been accompanied by a better understanding of the natural history and pathogenesis, as well as better diagnostics. In the treatment of CHB, no therapy has been proven to eradicate the virus completely from the human body due to the persistence of the covalently closed circular hepatitis B virus (HBV) DNA in the hepatocytes. Long-term maximal viral suppression is of utmost importance for the prevention of disease progression and hepatocellular cirrhosis development. Telbivudine is one of the more potent options, with phase III studies indicating its antiviral potency with 6- to 6.5-log 10 copies / mL reductions in HBV DNA levels at year one, comparable to other potent agents such as entecavir or tenofovir. The increasing rates of hepatitis B e antigen (HBeAg) seroconversion were achieved in HBeAg-positive patients during periods of up to four years of continuous telbivudine treatment, and seroconversion was durable in most patients throughout a two-year, off-treatment follow-up, indicating the potential for a finite treatment period in this group of patients. Long-term telbivudine treatment offers effective viral suppression to CHB patients, with certain baseline characteristics and on-treatment virological response. It is also one of the few drugs in the treatment of CHB under FDA pregnancy Category B. Telbivudine is well-tolerated, with elevations in creatine phosphokinase being the most common abnormality observed in the clinical trials. Most often, elevations have been asymptomatic. There are few new drugs for hepatitis B in the pipeline, with the agent farthest along in development, clevudine, halted for problems with muscle toxicity. Future research in hepatitis B will focus on the best ways to use the existing therapies, including telbivudine, sequentially or in combination, in order to maximize viral suppression and minimize the development of antiviral resistance.