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Entecavir and tenofovir work well for people with drug-resistant hepatitis B virus

Liz Highleyman
Published:
04 February 2015

A combination of entecavir plus tenofovir effectively suppressed hepatitis B virus (HBV) in people with resistance to other antivirals, according to results from the European ENTEBE study presented at the American Association for the Study of Liver Diseases (AASLD) Liver Meeting last month in Boston. Another study, however, showed that for some people with drug resistance, tenofovir works equally well on its own.

Antiviral therapy using nucleoside/nucleotide analogues such as entecavir (Baraclude), tenofovir (Viread), adefovir (Hepsera), telbivudine (Sebivo/Tyzeka) or lamivudine (Zeffix) is the mainstay of chronic hepatitis B treatment. Although they effectively suppress HBV replication during therapy, they typically do not eradicate the virus and may be used long-term. But HBV often develops resistance to antivirals – especially the oldest drug, lamivudine – which can lead to treatment failure.

Entecavir + tenofovir

Fabien Zoulim of Hospices Civils de Lyon in France and colleagues conducted the phase 3b ENTEBE trial to evaluate the safety and efficacy of entecavir plus tenofovir combination therapy for people with chronic hepatitis B who experienced previous nucleoside/nucleotide treatment failure.

Developing resistance to one antiviral can confer cross-resistance to similar drugs. But combining entecavir (a guanosine nucleoside analogue) and tenofovir (an adenosine nucleotide analogue) may provide a single regimen that works for all patients with prior nucleoside analogue failure, the researchers suggested as background. These two drugs both have high barriers to resistance and non-overlapping resistance profiles.

ENTEBE enrolled 144 previously treated participants in Europe between May 2010 and September 2011, of whom 92 started treatment. Three-quarters were men, most were white and the median age was 42 years. Two-thirds were initially hepatitis B 'e' antigen (HBeAg)-positive and one-third HBeAg-negative. A majority (54%) had HBV genotype D and 32% had genotype A. The median alanine aminotransferase (ALT) level was 36.5 (near the upper limit of normal) and they had compensated liver disease.

Participants had last taken nucleoside antivirals more than seven days ago. Just over half had previously used entecavir, 22% had used lamivudine, 12% had used tenofovir, 4% had used adefovir and the remainder had used telbivudine (Sevibo or Tyzeka) or two-drug regimens. They had experienced treatment failure, defined as HBV DNA >50 IU/ml, with primary non-response (less than a 1-log decline; 10%), partial virological response (57%) or viral breakthrough on therapy (33%). Among participants with available viral sequencing data, 58% had at least one resistance mutation, including 52% with lamivudine resistance, 26% with entecavir resistance and 7% with adefovir resistance.

All participants received 1.0mg entecavir plus 300mg tenofovir once daily. Treatment continued through week 96 and participants were followed for a further 24 weeks off treatment.

A total of 89 people completed 48 weeks of treatment (the primary analysis) and 86 people completed 96 weeks. At 48 weeks, 76% had HBV viral load <50 IU/ml, rising to 85% by 96 weeks in an intent-to-treat analysis.

Prior partial responders were most likely to respond to entecavir plus lamivudine (90%), followed by those with prior viral breakthrough (87%) and prior primary non-response (56%). Response rates were 88% for those who previously received entecavir monotherapy, 82% for those with prior tenofovir monotherapy and 80% for those with prior lamivudine monotherapy.

The 14 people who did not have undetectable HBV viral load at week 96 included six people with HBV DNA >50 IU/ml, six who discontinued treatment before this time point and two with missing data. Among six people who underwent resistance testing, no treatment-emergent resistance mutations were observed through week 96.

Serological response rates were low, as is typically seen with nucleoside/nucleotide therapy. At 96 weeks, 9% experienced HBeAg loss, 2% had HBeAg seroconversion, 2% had hepatitis B surface antigen (HBsAg) loss and just 1% achieved HBsAg seroconversion (HBsAg loss and development of protective anti-HBs antibodies).

Entecavir plus tenofovir was generally safe and well-tolerated. There were no severe adverse events deemed related to study drugs and only one person discontinued therapy due to an adverse event. The most common treatment-related side-effects were fatigue and nausea. No one experienced severe kidney or bone problems (potential side-effects of tenofovir).

"Entecavir combined with [tenofovir] is a highly effective and well tolerated option for rescue therapy, regardless of the type of prior [nucleoside analogues] used," the researchers concluded. They added that lower baseline HBV viral load – but not baseline resistance profile – was a predictor of virological response.

Tenofovir monotherapy

In a related study, Young-Suk Lim of University of Ulsan College of Medicine in Seoul and colleagues compared tenofovir plus entecavir versus tenofovir alone for people with chronic hepatitis B who had entecavir-resistant HBV and who did not achieve viral suppression on current or prior antiviral treatment.

This Korean study included 90 people; 76% were men and the mean age was 51 years. Most (89%) were HBeAg positive and nearly one-quarter had liver cirrhosis.

A majority (57%) had previously been exposed to entecavir, lamivudine and adefovir, with a further 10% also having used telbivudine; 18% had tried entecavir and lamivudine, 8% had used entecavir and adefovir, and 6% had used entecavir alone. About half were currently on entecavir plus adefovir, 32% were on entecavir alone and the rest were on antiviral regimens without entecavir. None, however, had used tenofovir. The most frequently detected entecavir resistance mutations at baseline were M204V/I, L180M, T184 and S202G.

Participants were randomly assigned to receive either tenofovir plus entecavir or tenofovir monotherapy for 48 weeks. This study had a stricter threshold for undetectable viral load, HBV DNA <15 IU/ml.

After 48 weeks of treatment, 73% of participants taking tenofovir plus entecavir and 71% of those taking tenofovir alone achieved viral suppression – not a significant difference.

Among 13 people eligible for resistance testing at week 48, no additional or novel resistance mutations were detected. There was, however, a "marked decrease" in pre-existing resistance mutations.

High baseline HBV viral load and previous use of adefovir were associated with a lower likelihood of virological response in a multivariate analysis (odds ratio 0.33 and 0.14, respectively).

Again, treatment was safe and well-tolerated, with no early discontinuations due to adverse events. Side-effect profiles were similar in both treatment groups.

Comparing people taking tenofovir plus entecavir or tenofovir alone, the researchers concluded that there was no significant difference in either the proportion of people who achieved virological response or in the degree of HBV DNA reduction.

"[Tenofovir] monotherapy may be a reasonable option for the rescue therapy of patients infected with entecavir-resistant HBV," they recommended.

References

Zoulim F et al. The safety and efficacy of entecavir and tenofovir combination therapy for chronic hepatitis B in patients with previous nucleos(t)ide treatment failure: week 96 results of the ENTEBE study. American Association for the Study of Liver Diseases (AASLD) Liver Meeting, Boston, abstract 230, 2014.

Lim Y-S et al. Tenofovir disoproxil fumarate alone or in combination with entecavir in patients with entecavir-resistant chronic hepatitis B: multicenter randomized trial. American Association for the Study of Liver Diseases (AASLD) Liver Meeting, Boston, abstract 231, 2014.