B Positive – all you wanted to know about - ASHM

Executive Summary
variable course of chronic infection. noninvasive
methods of fibrosis assessment,
such as algorithms based on biochemical
markers in serum, or the use of non-invasive
scans, such as the fibroscan® technique to
quantify hepatic fibrosis, are currently under
assessment and may become a useful adjunct
to (and in some cases avoid the need for) liver
biopsies in the future (chapter 3: Hepatitis b
virus testing and interpreting test results).
as virological tests for the diagnosis and
monitoring of hepatitis b have improved, the
goalposts for treatment continue to change.
indications for treatment are discussed in
chapter 7: treatment of chronic hepatitis b
virus infection. treatment should currently be
considered for patients in the immune active
phase of chronic hepatitis b (high HbV dna
> 20,000 iu/mL, elevated aLt and fibrosis or
inflammation on biopsy), but not for patients
in the immune tolerant phase (high HbV dna
> 20,000 iu/mL and normal aLt). treatment is
also recommended for patients with pre-core
mutant disease (Hbeag negative, elevated
aLt and HbV dna > 2000 iu/mL) and should
be considered in all patients with cirrhosis
and any level of detectable HbV dna. the
primary goal of treatment is virological
suppression (particularly in the Hbeag
negative group), but other goals include
Hbeag seroconversion (in Hbeag-positive
patients), and histological improvement.
these goals are often related, but may occur
independently. the therapeutic endpoint
is Hbsag seroconversion, but this outcome
occurs infrequently.
HbV treatment is based around two main
classes of therapy: immunomodulating
agents (interferon based-therapy) and
direct antiviral agents. standard interferon
therapy has now been replaced by the use
of pegylated interferon. therapy is given
by weekly subcutaneous injection for a
fixed duration of 12 months and results in
Hbeag seroconversion in just under a third
of Hbeag-positive patients. it may also have
a role in some Hbeag-negative patients in
whom it is able to induce sustained viral
control. Pegylated interferon has a significant
10 b Positive – all you wanted to know about hepatitis b: a guide for primary care providers
side effect profile and is contra-indicated in
decompensated cirrhosis.
the other mainstay of HbV treatment is the use
of antiviral agents, an increasing number of
which is now available. Lamivudine has been
used for the treatment of chronic hepatitis b
infection for many years. While active against
HbV, it results in an increasing rate of drug
resistance when used as monotherapy for any
length of time. additional potent anti-HbV
agents now licensed for use in australia are
entecavir and adefovir; other agents not yet
available here include telbivudine, tenofovir
and emtricitabine. the use of these agents is
discussed in detail in chapter 7: treatment of
chronic hepatitis b virus infection. a major
concern with the use of any antiviral agent is
the development of drug resistance. in chronic
hepatitis b, drug resistance may lead to viral
rebound, hepatic flare and, in patients with
cirrhosis, potential hepatic decompensation.
an understanding of the mechanisms of
HbV resistance development will guide the
appropriate use and combination of these
agents in the future (chapter 2: Virology: viral
replication and drug resistance).
a number of special situations exist in which
the management and therapeutic options
for HbV may be more complex than usual.
these include the management of pregnant
women, children and people who have a
hepatitis c, hepatitis d (delta) or human
immunodeficiency virus (HiV) co-infection
(chapter 10: Managing hepatitis b virus
infection in complex situations). in patients
with HiV co-infection, a number of antiviral
agents have activity against both HbV and
HiV (lamivudine, emtricitabine, adefovir,
tenofovir and entecavir) and thus their
effect on both viruses must be carefully
considered before treatment for either is
initiated. another group in need of careful
management is that of people with HbV
infection undergoing immunosuppressive
therapy (including cancer chemotherapy),
transplant recipients and patients treated
with immunosuppressive agents for autoimmune
disease, steroids, or antimonoclonal
agents such as rituximab. the aggressive