Eur J Clin Microbiol Infect Dis (2013) 32:11–18
DOI 10.1007/s10096-012-1723-6
REVIEW
Lamivudine versus telbivudine in the treatment of chronic
hepatitis B: a systematic review and meta-analysis
H. Jiang & J. Wang & W. Zhao
Received: 28 June 2012 / Accepted: 1 August 2012 / Published online: 17 August 2012
# Springer-Verlag 2012
Abstract The purpose of this study was to evaluate the
efficacy of lamivudine (LAM) versus telbivudine (LdT) in
the treatment of chronic hepatitis B (CHB). Randomized
controlled studies (RCTs) involving the use of LAM versus
LdT in CHB patients were included in the study. Data were
obtained from the Cochrane-controlled trials register,
EMBASE and MEDLINE databases (1/1990 to 12/2011).
Two reviewers performed quality assessment and extracted
data independently. Eight RCTs were included in the main
analysis. Eight eligible trials were included in the analysis.
At the end of one-year treatment, LdT was better than LAM
at the virological response (RR01.43, 95 % CI01.12–1.84,
P00.005), while less than LAM at the viral breakthrough
(RR00.34,95 % CI00.25–0.48, P<0.00001), viral resis-
tance (RR 00.41,95 % CI 00.28–0.58, P < 0.00001), but
H. Jiang (*)
Department of Geriatric Oncology, The Second Affiliated
Hospital, Southeast University,
1-1 Zhongfu Street,
Nanjing, Jiangsu 210003, People’s Republic of China
e-mail: gfdsa_1234567@sohu.com
J. Wang
Department of Hematology, The Affiliated Drum Tower Hospital,
Nanjing University Medical School,
Nanjing, Jiangsu 210008, People’s Republic of China
W. Zhao
Department of Hepatology, The Second Affiliated Hospital,
Southeast University,
1-1 Zhongfu Street,
Nanjing, Jiangsu 210003, People’s Republic of China
there was no statistically significant difference in the bio-
chemical response (RR 01.13,95 % CI 00.99–1.29, P 0
0.06), HBeAg seroconversion (RR01.13,95 % CI00.92–
1.39, P00.25), therapeutic response (RR01.22,95 % CI0
1.00–1.50, P00.05) and adverse events (RR01.07,95 %
CI01.00–1.14, P00.05). The creatine kinase (CK) elevation
occurred more frequently in the LdT group than in LAM
group (RR02.43,95 % CI01.57–3.75, P<0.0001). When
treatment prolonged to 2 years, LdT was better than LAM
at the HBeAg seroconversion (RR01.29,95 % CI01.12–
1.50, P00.0007) and therapeutic response (RR01.34,95 %
CI01.21–1.49, P<0.00001). LdT was more effective in
inhibiting HBV replication and promoting HBeAg sero-
conversion than LAM for CHB patients, whereby
adverse effects such as CK elevation must be paid
attention to.
Introduction
Chronic hepatitis B virus (HBV) infection is a serious global
public health problem associated with liver fibrosis, cirrho-
sis, liver failure and hepatocellular carcinoma (HCC) [1].
Worldwide, approximately 350 million people have chronic
hepatitis B (CHB) [2]. Approximately 1 million patients die
of end-stage liver disease and HCC as a result of HBV
infection each year [3]. The sustained suppression of
serum HBV DNA to very low or undetectable levels has
been associated with the prevention of liver disease pro-
gression and inhibition of the development of long-term
12 Eur J Clin Microbiol Infect Dis (2013) 32:11–18

complications [4]. Therefore, the main goal of CHB
treatment is the achievement of early and durable
viral suppression, as described in current international
guidelines [5].
The antiviral is critical, and standard antiviral treatment
should be carried out. The main concern of long-term anti-
viral therapy is the emergence of drug resistance. Currently
antiviral drugs include lamivudine (LAM), adefovir, enteca-
vir, telbivudine (LdT) and tenofovir. Although LAM was
the first nucleoside analog inhibitor to be approved for
treatment of CHB, the rate of LAM resistance is approxi-
mately 25 % after 1 year and 76 % after 5 years [6–9].
Newer nucleotide analogues with lower resistance rates
currently recommended by international guidelines may
provide better viral suppression and potentially even better
long-term outcomes [10]. LdT is an L-nucleoside that is
structurally related to LAM and acts as HBV polymer-
ase inhibitor and preferentially inhibits HBV DNA syn-
thesis [11]. A recent meta-analysis of 11 randomized
controlled trials compared the efficacy of LAM and
LdT in the treatment of CHB, where LdT treatment
was associated with a significant inhibiting HBV repli-
cation and preventing drug resistance as compared to
LAM for CHB patients [12]. However, only randomized
controlled trials (RCTs) published until 2010 were in-
cluded in the meta-analysis, and it included one non-
randomized study report. To better assess the value of
LAM versus LdT in the treatment of CHB. We con-
ducted the present meta-analysis based on prospectively
published RCTs in this area.
Materials and methods
was performed on the Cochrane-controlled trials register
and the MEDLINE and EMBASE databases. Some subject
headings were employed: “Hepatitis B”, “lamivudine”, “tel-
bivudine”, “randomized-controlled trial”. Only RCTs
involving CHB patients were included. Studies published
by December 2011 were eligible.
Inclusion and exclusion criteria
The following inclusion criteria were used: (1) RCTs, (2)
study population consisting of CHB patients with viral
replication, and (3) intervention therapies consisting of
LAM versus LdT. Patients were excluded if they (1) were
not adults, (2) were co-infected with either hepatitis C,
hepatitis D virus or human immunodeficiency virus (HIV),
(3) presented with serious concurrent medical illness includ-
ing concomitant renal failure, decompensated liver disease,
evidence of cirrhosis, HCC or organ transplantation
history, and (4) used anti-viral drugs within the preced-
ing 6 months.
Data extraction and quality assessment
Publication trials included in the final meta-analysis were
assessed for validity by two independent reviewers. Data
were independently abstracted by two reviewers, and con-
sensus were reached on any disagreement. They examined
and recorded the trial characteristics and outcomes, using a
10-point scoring system (Table 1) that had been used in a
previously published meta-analysis to examine the reliabil-
ity of RCTs [13]. It included information such as allocation
concealment, the randomization method, the inclusion and
exclusion criteria, etc.

Literature search Data analysis

Only studies published as an abstract or journal article in Two reviewers independently extracted data and used the
English were eligible for this analysis. The literature search program Review Manager for analysis of data (RevMan

Table 1 Description of the trial characteristics and outcomes by using a 10-point scoring system. Score “0” if not described or inadequate or
unclear and “1” if appropriately described ITT intention to treat

Study, first Randomization Allocation Blinding Inclusion and Similar baseline Treatment Cointervention Outcome Extent of ITT Final
author and year concealment exclusion at study entry protocol that could definition follow-up analysis score
criteria defined Clearly affect described
described outcome clearly

Lai (2007) 1 1 1 1 1 1 0 1 0 1 8
Hou (2008) 1 1 1 1 1 1 0 1 0 0 8
Azam (2011) 1 0 0 0 0 1 0 0 0 0 2
Rasenack (2007) 1 0 1 0 1 1 0 1 0 0 5
Jia (2007) 1 0 1 1 1 1 0 1 0 1 7
Chen (2009) 1 0 1 0 0 1 0 0 0 0 3
Liaw (2009) 1 1 1 1 1 1 0 1 1 0 8
Eur J Clin Microbiol Infect Dis (2013) 32:11–18
Version 5.0 for Windows). The differences observed be-
tween the two groups were expressed as the relative risk
(RR) with the 95 % confidence interval (CI). The presence
of heterogeneity between trials was assessed by chi-square
statistics and I2 statistics. The chi-square statistics with P<
0.1 was considered significant across trials. Treatment
effects across trials were combined using a random effects
model (I2 >0.25) and a fixed effect model (I2 <0.25). Sensi-
tivity analyses were conducted to check whether excluding
one study with low quality of this meta-analysis would
affect the final results. The publication bias was assessed
using a Begg’s and Egger’s test.
Results
The electronic database search yielded 1,098 potentially
relevant publications, and the process for relevant trials
was assessed as shown in Fig. 1. Finally, eight RCTs ful-
filled the inclusion criteria and were subject to meta-analysis
[14–21]. The study quality was assessed for using the 10-
point scale, the quality score ranged from 2 to 8, in which a
higher score is associated with better quality. Table 2 lists
the key features of the studies included in this meta-analysis.
Biochemical response
According to treatment time, our analysis is divided into two
subgroups. A one-year treatment group (group A) and a
Fig. 1 Flow diagram of
reviewed randomized
controlled trials (RCTs)
13
two-year treatment group (group B). Four trials [14–17]
demonstrated the biochemical response rate in group A. A
summary estimate of the relative risk of LdT versus LAM
using a random effects approach demonstrated that the rate
of ALT normalization in the LdT group was higher than the
LAM group [RR 01.13, 95 % CI 00.99–1.29, P 00.06]
(Fig. 2a). When a low quality study [17] was removed, the
response rate between the two groups was not statistically
significant by used a random effects model [RR01.12,
95 % CI 00.96–1.30, P 00.16]. Three trials [18–20]
demonstrated the biochemical response rate in group
B. The biochemical response rate in the LdT group
was higher than the LAM group [RR 01.14, 95 %
CI01.08–1.21, P<0.00001] (Fig. 2b). When a low qual-
ity study [19] was removed, the response rate between
the two groups was still statistically significant by use
of a random effects model [RR01.16, 95 % CI01.05–
1.27, P00.003].
HBeAg seroconversion
Three trials [14–16] demonstrated the HBeAg serocon-
version rate in group A. The rate of seroconversion in
the LdT group was similar to the LAM group [RR0
1.13, 95 % CI 00.92–1.39, P 00.25] (Fig. 2c). When a
low quality study [14] was removed, the rate of sero-
conversion between the two groups was not statistically
significant. Three trials [18–20] demonstrated the
HBeAg seroconversion rate in group B. The HBeAg
14 Eur J Clin Microbiol Infect Dis (2013) 32:11–18

Table 2 Description of included

randomized controlled trials Study Study design Treatment options Dosage of drugs LAM LDT Treatment

Lai 2005 [14] RCT, DB LAM VS LDT 100 mg 600 mg 12 months

Hou 2008 [15] RCT, DB LAM VS LDT 100 mg 600 mg 12 months
Lai 2007 [16] RCT, DB LAM VS LDT 100 mg 600 mg 12 months
Azam 2011 [17] RCT LAM VS LDT 100 mg 600 mg 12 months
Liaw 2009 [18] RCT, DB LAM VS LDT 100 mg 600 mg 24 months
Rasenack 2007 [19] RCT, DB LAM VS LDT 100 mg 600 mg 24 months
Jia 2007 [20] RCT, DB LAM VS LDT 100 mg 600 mg 24 months
Chen 2009 [21] RCT, DB LAM VS LDT 100 mg 600 mg 24 months

Fig. 2 a Effect of telbivudine vs. lamivudine at the end of one-year of telbivudine vs. lamivudine at the end of one-year treatment on
treatment on biochemical response. b Effect of telbivudine vs. lamivu- HBeAg seroconversion. d Effect of telbivudine vs. lamivudine at the
dine at the end of two-year treatment on biochemical response. c Effect end of two-year treatment on HBeAg seroconversion
Eur J Clin Microbiol Infect Dis (2013) 32:11–18
seroconversion rate in the LdT group was higher than
the LAM group [RR 01.29, 95 % CI 01.12–1.50, P 0
0.0007] (Fig. 2d). When a low quality study [19] was
removed, the response rate between the two groups
was still statistically significant [RR 01.26, 95 % CI 0
1.04–1.52, P 00.02].
Virological response
Four trials [14–17] demonstrated the virological response
rate in group A. A summary estimate of the relative risk of
Fig. 3 a Effect of telbivudine vs. lamivudine at the end of one-year
treatment on virological response. b Effect of telbivudine vs. lamivu-
dine at the end of two-year treatment on virological response. c Effect
15
LdT versus LAM using a fixed effects approach demonstrat-
ed that the response rate in the LdT group was higher than
the LAM group [RR01.43, 95 % CI01.12–1.84, P00.005]
(Fig. 3a). When a low quality study [17] was removed, the
response rate between the two groups was not statistically
significant by use of a random effects model [RR01.33,
95 % CI00.99–1.79, P00.06]. Three trials [18–20] demon-
strated the virological response rate in group B. The re-
sponse rate in the LdT group was higher than the LAM
group [RR 01.46, 95 % CI 01.35–1.58, P < 0.00001]
(Fig. 3b). When a low quality study [19] was removed,
of telbivudine vs. lamivudine at the end of one-year treatment in
virologic breakthrough. d Effect of telbivudine vs. lamivudine at the
end of one-year treatment on therapeutic response
16
the difference between the two groups was still sta-
tistically significant [RR 01.48, 95 % CI 01.35–1.62,
P<0.00001].
Virologic breakthrough
Three trials [14–16] demonstrated the virologic break-
through rate in group A. A summary estimate of the relative
risk of LdT versus LAM using a random effects approach
demonstrated that the rate of virologic breakthrough in the
LAM group was higher than the LdT group [RR00.34,
95 % CI00.25–0.48, P<0.00001] (Fig. 3c). When any one
of two low quality studies [14] was removed, the difference
between the two groups was still significant. Only one trial
[18] demonstrated the virologic breakthrough rate in group B.
The results of the study showed the virologic breakthrough
rate in the LdT group as 23.4 %, compared to 41.9 % in the
LAM group. The difference was statistically significantly
[RR00.56, 95 % CI00.47–0.66, P<0.00001].
Therapeutic response
Three trials [14–16] demonstrated the therapeutic response
rate in group A. The response rate in the LdT group was
similar to the LAM group [RR01.22, 95 % CI01.00–1.50,
P00.05] (Fig. 3d). When the low quality study [14] was
removed, the response rate between the two groups was still
not significant [RR01.19, 95 % CI00.95–1.48, P00.14].
Four trials [18–21] demonstrated the therapeutic response
rate in group B. The response rate in the LdT group was
higher than the LAM group [RR01.34, 95 % CI01.21–
1.49, P<0.00001] (Fig. 4a). When a low quality study
[19] was removed, the response rate between the two groups
was still significant [RR01.33, 95 % CI 1.18–1.50, P<
0.00001].
Adverse events
Some side effects were reported in patients such as influen-
za, nausea, headache and diarrhea. Three trials [14–16]
reported the adverse events rate in group A; the result of
the LdT group was similar to the LAM group [RR01.07,
95 % CI01.00–1.14, P00.05] (Fig. 4b). When a low quality
study [14] was removed, the difference between the two
groups was still not significant. Two trials [18, 21] demon-
strated the adverse events rate in group B; the result of the
study was not statistically significant [RR01.15, 95 % CI0
0.94–1.40, P00.17].
Creatine kinase (CK) elevation
Three studies [14–16] showed Grade 3 or 4 CK elevations in
group A. The CK elevation rates in the LdT group was
Eur J Clin Microbiol Infect Dis (2013) 32:11–18
higher than the LAM group [RR02.43, 95 % CI01.57–
3.75, P<0.0001] (Fig. 4c). When a low quality [14] was
removed, the difference in CK elevation rate was still sta-
tistically significant [RR02.51, 95 % CI01.61–3.92, P<
0.0001]. Only one trial [18] demonstrated the CK elevation
rate in group B; the result of the study showed the CK
elevation rate in the LdT group as 12.9 %, compared to
4.1 % in the LAM group. The difference was statistically
significant [RR03.18, 95 % CI02.10–4.79, P<0.00001].
Viral resistance
Tow studies [14, 15] showed viral resistance rate in group
A. The viral resistance rates in the LAM group were higher
than the LdT group [RR00.41, 95 % CI00.28–0.58, P<
0.00001] (Fig. 4d). Only one study [18] demonstrated the
viral resistance rate in group B; the result of the study
showed the viral resistance rate in the LdT group as
20.4 %, compared to 35.1 % in the LAM group. The
difference was statistically significantly [RR00.58, 95 %
CI00.49–0.70, P<0.00001].
Publication bias
Begg’s funnel plot and Egger’s test were performed to
assess the publication bias of eight [14–20] studies. Evalu-
ation of publication bias for virological response showed
that the Begg test (p00.881) and Egger test (P00.921) were
not significant.
Discussion
Over the past two decades, treatment of CHB has great-
ly improved with the availability of nucleos(t)ide ana-
logs (NAs). They include LAM, adefovir dipivoxil,
entecavir, LdT and tenofovir. LAM was the first ap-
proved and widely used antiviral drug for the treatment
of CHB, although it induced rapid suppression of serum
HBV DNA to very low or undetectable levels, with the
extension of the treatment time, the potential risk for
the emergence of LAM resistance was increasing year
by year [22]. LdT with low costs was approved and
used worldwide for the treatment of CHB patients who
have elevated serum ALT levels and evidence of viral
activity. A 3-year study has shown LdT treatment
yielded high rates of viral suppression and ALT normal-
ization with a favourable safety profile. High rates of
HBeAg seroconversion were achieved with prolonged
LdT therapy and were sustained in the majority of
patients over 52 weeks off therapy [23]. Recently, some
studies have carried out direct comparisons between the
antiviral efficacies of two drugs. The aim of this
Eur J Clin Microbiol Infect Dis (2013) 32:11–18
Fig. 4 a Effect of telbivudine vs. lamivudine at the end of two-
year treatment on therapeutic response. b Effect of telbivudine
vs. lamivudine at the end of one-year treatment on adverse
events. c Effect of telbivudine vs. lamivudine at the end of
analysis was access to an evidence-based conclusion
based on available data regarding the efficacy of both
drugs.
In this analysis, we compared the efficacy of LAM and
LdT in the treatment of CHB. LdT was superior in main-
taining viral suppression compared to LAM therapy at the
end of one-year treatment, while also it has the advantage of
viral resistance and viral breakthrough, but there was no
significant difference in the biochemical response, HBeAg
seroconversion, therapeutic response and adverse events.
However, the difference between one-year treatment and
17
one-year treatment on CK elevations. d Effect of telbivudine
vs. lamivudine at the end of one-year treatment on viral
resistance
two-year treatment was that LdT was better than LAM at
the HBeAg seroconversion and therapeutic response. Data
from the study suggest that LdT treatment led to a cumula-
tive HBeAg seroconversion rate of 46 % in the three-year
treatment group [23]. The results of this analysis for HBeAg
seroconversion is similar to previous data; the rates of
HBeAg seroconversion increased significantly with pro-
longed LdT treatment. Although the exact mechanism
remains uncertain, some evidence suggests that LdT may
play an immunological effect in HBV viral [24]. The rate of
therapeutic response increased significantly with prolonged
18
LdT treatment; the high therapeutic response rate is consis-
tent with high rates of viral suppression, ALT normalization
and HBeAg seroconversion during the prolonged LdT treat-
ment. This analysis indicated that the total incidence of
adverse events in the LdT group was similar to the LAM
group. But grade 3 or 4 increased CK occurred more fre-
quently during LdT treatment, the research data show that
the possible mechanism of CK elevations is related to mi-
tochondrial toxicity [25].
There are several limitations that should be considered in
our meta-analysis. First, some studies were not double-
blinded, the lack of blinding could affect the outcomes
assessment [17]. Second, studies published in abstract form
did not report sufficient data, so the insufficient data may
affect the final conclusion [17, 21]. Third, only English
studies were included in this analysis which may cause
language bias. Finally, the important limitation was publi-
cation bias. In this analysis, although the assessment of
publication bias for virological response was not significant,
the possibility of publication bias may exist in any research,
because the negative studies and small sample studies may
be less likely to be published.
In summary, LdT was more effective in inhibiting HBV
replication and promoting HBeAg seroconversion than
LAM for CHB patients, for which adverse effects such as
CK elevation must be paid attention to. Further, more high-
quality, randomized controlled trails are clearly needed to
guide the standards of treatment for CHB.
Acknowledgments and disclosures We declare that we have no
financial and personal relationships with other people or organizations
that can inappropriately influence our work, and there is no profes-
sional or other personal interests of any nature or kind in any product,
service, and company that could be construed as influencing the
position presented in, or the review of, the manuscript.
Conflict of interest The authors declare that they have no conflict of
interest.
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