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Clinical Practice Pearls
P R O B E
• V o l . L I I I • N o . 3 • A p r – J u n 2 0 1 4
Liv.52 Update
Safety and Efficacy of HD-03/ES
*
Therapy in Patients
With Chronic Hepatitis B
Singh J, et al
Indian J Clin Res
. 2006;17(5):39–43.
*
HD-03/ES is marketed as Liv.52 HB
A B S T R A C T
In vitro studies indicated that HD-03/ES
has surface antigen suppression and hepatitis
B virus (HBV) elimination activities. Acute and
subacute toxicity studies indicated that HD-03/ES is
devoid of significant toxicity following acute and repeated
administration in rats. This study was undertaken to evaluate
the safety and efficacy of HD‑03/ES capsules in the management
of chronic hepatitis B (CHB) infection. An open clinical study
was carried out in 14 patients with CHB infection and was treated
with HD-03/ES capsules twice daily in the morning and evening for
a period of 6 months. Clinical, biochemical, and HBV markers were
monitored before and after initiation of therapy. Statistically significant
improvements were observed in clinical, biochemical, and HBV markers
after administration of HD-03/ES capsules. Adverse effects were
mild and never warranted withdrawal of the drug. The results of this
preliminary study indicate that HD‑03/ES is safe and effective in the
treatment of CHB.
Key Words:
Chronic hepatitis B, HD-03/ES, IFN-
α
, lamivudine,
HBsAg, HBeAg
Introduction
Despite the existence of safe and
efficient vaccines against hepatitis
B infection for almost 20 years,
hepatitis B virus (HBV) infection
remains a major public health problem
worldwide with 400 million chronic
carriers, who are exposed to the risk
of developing liver cirrhosis and
hepatocellular carcinoma (HCC).
1,2
To date, IFN-
α
and lamivudine are
the only approved drugs for chronic
HBV infection in India. IFN-
α
therapy is only partially effective and
its use is frequently limited by adverse
effects.
3
Lamivudine, a cytidine
analog, is a very efficient inhibitor
of HBV replication.
4
Although it
efficiently inhibits HBV replication,
the slow kinetics of viral elimination
during lamivudine therapy and
the spontaneous viral genome
variability lead to the emergence
of drug-resistant mutants, which
carry mutations affecting the reverse
transcriptase domain. Approximately
50% of treated patients develop viral
resistance after 3 years of treatment
with lamivudine.
5
In order to better
control viral replication and delay
the emergence of virus resistant
