RSS Feeds
Antiviral Therapy for Chronic Hepatitis B
Summaries for Patients are a service provided by Annals to help patients better understand the complicated and often mystifying language of modern medicine.
Summaries for Patients are presented for informational purposes only. These summaries are not a substitute for advice from your own medical provider. If you have questions about this material, or need medical advice about your own health or situation, please contact your physician. The summaries may be reproduced for not-for-profit educational purposes only. Any other uses must be approved by the American College of Physicians.
What is the problem and what is known about it so far?
Hepatitis B is inflammation of the liver that is caused by a virus. The virus spreads through contact with infected body fluids. Most people who get hepatitis B recover within a few months, but some develop chronic infection. Chronic infection increases risk for liver failure and liver cancer. Persons with chronic infection often have virus-related protein substances in their blood (called hepatitis B surface antigens and e antigens) for many years. When an e antigen is present, it usually means that the person has very active liver disease and a lot of virus present. Doctors often treat these patients with powerful antiviral drugs. However, some patients develop viral forms (mutants) that are resistant to 1 or more antiviral drugs. To help suppress virus levels, prevent resistance, and improve outcomes, doctors might use different types of antiviral drugs or switch drugs during treatment. Few studies have assessed the benefits and harms of switching among different antiviral therapies for chronic hepatitis B.
Why did the researchers do this particular study?
To see which of the following 3 treatment regimens best suppresses virus levels in patients with chronic hepatitis B: telbivudine (a thymidine nucleoside analogue), adefovir (an adenosine nucleotide analogue), or adefovir followed by a switch to telbivudine.
Who was studied?
135 adults with chronic hepatitis B who were e antigen positive. Their average age was about 33 years. Most were Asian men. None were co-infected with hepatitis C or D virus or HIV.
How was the study done?
The researchers recruited patients with e antigen–positive chronic hepatitis B from 16 international, academic, gastroenterology clinics. Patients were randomly assigned to telbuvidine for 52 weeks, adefovir for 52 weeks, or adefovir for 24 weeks followed by a switch to telbivudine for 28 weeks. Telbuvidine was taken as 3 daily pills (600 mg total) and adefovir as a single daily pill (10 mg). The researchers asked patients about side effects and tested blood for evidence of actively multiplying virus (HBV DNA levels) several times during follow-up. They then compared the amounts of virus over time in the groups.
What did the researchers find?
Tests at 24 weeks after treatment showed that viral amounts (HBV DNA levels) were reduced more with telbuvidine than with adefovir. At 52 weeks, HBV DNA levels were similar among patients initially treated with telbivudine and among those switched to telbivudine. These levels were lower than those among patients treated continuously with adefovir. Similar types and numbers of side effects were reported across groups.
What were the limitations of the study?
Both the researchers and the patients knew which therapies the patients received. Long-term drug resistance and clinical outcomes were not assessed. We do not yet know whether the findings are generalizable to other geographic areas and populations. Only 2 of several available antiviral agents were tested.
What are the implications of the study?
Telbivudine alone and switching from adefovir to telbivudine both suppressed viral levels more than adefovir alone in adults with e antigen–positive chronic hepatitis B.
Article and Author Information
-
The summary below is from the full report titled “Treatment of Hepatitis B e Antigen–Positive Chronic Hepatitis with Telbivudine or Adefovir. A Randomized Trial.” It is in the 4 December 2007 issue of Annals of Internal Medicine (volume 147, pages 745-754). The authors are H.L.Y. Chan, E.J. Heathcote, P. Marcellin, C.L. Lai, M. Cho, Y.M. Moon, Y.C. Chao, R.P. Myers, G.Y. Minuk, L. Jeffers, W. Sievert, N. Bzowej, G. Harb, R. Kaiser, X.J. Qiao, N.A. Brown, and the 018 Study Group.
