Continue Baraclude Treatment?

[anyone76]

Anyone have been taking Baraclude for more than 2 to 3 years?

I am still unable to achieve undetectable viral load after 2.5 year of Baraclude treament. Both Dr and I are struggling whether I should move on to another drug. Since I have been taking Baraclude for 3 years, there are couple options,
1. Increase to 1mg, and treat it as Epivir resistant (took Epivir before but viral load has not change after 3 months)
2. Change to another drug Telbivudine
3. Change to Hepsera

Anyone has experience, comment or suggestion? Really appreciate.

[stevenNYer]

Hopefully your doctor knows what he / she is doing?

It is hard to suggest what you should consider doing without a series of labs (HBV DNA and ALT) over time.  List your labs pre and post treatment in chrono order.

Also, your age, age of infection, ethnicity, and your eAntigen and eAntibody status.  

[cajim]

Does this help?

"An appropriate time to alter therapy by switching to or adding another drug is treatment failure, either primary treatment failure or an inadequate response while receiving treatment with oral agents.  The definition of primary treatment failure is a serum HBV DNA decline of less than 1 log10 IU/mL from baseline at week 12 of treatment, whereas an inadequate virologic response is defined as a serum HBV DNA ≥ 2000 IU/mL at week 24 of treatment.  The first step in the evaluation of potential primary treatment failure is to exclude patient nonadherence to prescribed therapy as a potential cause. With respect to oral antiviral therapy, if the agent has indeed been taken on a regular/prescribed basis, the patient is considered to have primary treatment failure and should be switched to a more potent drug or possibly a combination of drugs.  An inadequate virologic response (serum HBV DNA ≥ 2000 IU/mL after 24 weeks of oral antiviral therapy) is a much more common reason for altering therapy, and a "roadmap" outlining the management of these patients was recently published.  Patients who have an inadequate response need to have their treatment changed to an alternative regimen, with either a different drug that is more potent and not cross-resistant or the addition of a second drug. Patients who only achieve a partial response after 24 weeks of treatment (serum HBV DNA ≥ 60 IU/mL to < 2000 IU/mL) may also need to change to a different therapeutic regimen. For some, a second drug can be added that is not cross-resistant with the first drug. However, if patients are being treated with a drug that has a low rate of resistance development, such as entecavir, they can continue treatment to and beyond 48 weeks. In this situation, patients should undergo serum HBV DNA testing every 3 to 6 months. Some drugs, such as adefovir, have a delayed antiviral effect. These patients should remain on therapy but be monitored every 3 months, with further assessment after 48 weeks of therapy. If their response remains partial or becomes inadequate at this time point, as defined by the "roadmap" concept, therapy should be changed.  Chronic hepatitis B patients with an inadequate response after 24 weeks of therapy with a drug with a risk of resistance, such as telbivudine, need to switch to a different, more effective drug.  Alternatively, a second drug without cross-resistance to the first drug can be added to the regimen. The patient should then be monitored every 3 months up to week 48. If the serum HBV DNA falls to undetectable levels by week 48, HBV DNA testing may occur every 6 months. However, patients with advanced disease should continue to be monitored every 3 months, regardless of their response to treatment.  Another appropriate time to alter therapy by switching or adding another drug to the treatment regimen is when there is development of HBV antiviral drug resistance. Treatment with adefovir is associated with a 29% rate of resistance in HBeAg-negative patients after 5 years of therapy.  Entecavir is associated with one of the lowest cumulative rates of resistance in treatment-naive patients, < 1% after 4 years of therapy.  Resistance with telbivudine occurs at intermediate rates, with 25% of HBeAg-positive patients and 11% of HBeAg-negative patients experiencing resistance after 2 years of therapy.  The pivotal telbivudine trial demonstrated that the greater the degree of viral suppression at week 24 of therapy, the better the outcomes after 1 and 2 years of therapy in terms of undetectable serum HBV DNA, HBeAg seroconversion, ALT normalization, and rate of HBV antiviral drug resistance.  Finally, HBV antiviral resistance was not noted in the tenofovir pivotal trials in HBeAg-positive and HBeAg-negative patients treated for 1 year.  Table 4 summarizes the potential management of HBV antiviral resistance based on the US treatment algorithm and the AASLD guidelines. The general principle of the recommendations outlined in Table 4 is to add a second drug that is not cross-resistant with the first (eg, adding a nucleotide drug such as adefovir or tenofovir when resistance to a nucleoside agent such as lamivudine, telbivudine, or entecavir is detected. The opposite concept applies to the patient with adefovir resistance (ie, add a nucleoside agent). This strategy of adding a second drug vs sequential treatment is supported by studies showing that the rate of subsequent adefovir resistance is considerably higher using the switch strategy in the setting of preexisting lamivudine resistance."

From "Treatment of the HBV-Infected Patient: When to Start, When to Stop, and When to Change Therapy," Keeffe, E.B.  March 5, 2008.