simvastatin use on hbv

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the suggested dose is 40mg, but it is better to start at 20mg for some weeks.remember to check alt/ast before and after weekly and then monthly

4. Discussion
The HBV infected liver makes a trillion virions every day. SIM is
an ideal drug to target the liver since 93% of an oral dose is extracted
on the first pass through the liver (Mauro, 1993). Liver tissue levels
of SIM have not been reported in humans. In a mammalian model,
the hepatic concentration of SIM was observed to be 44× that of
serum after 60 min (Germershausen et al., 1989). SIM given as a
single dose of 40mg to humans produced peak serum levels of
10 ng/ml; if 44-fold hepatic concentration also occurs in humans,
the resulting liver tissue level would then be 3.2M (Pentikainen
et al., 1992). Thus, the ambient molar concentrations needed to
reduce in vitro virion production listed in Table 1 appear to be
achievable in vivo with doses that are currently approved by the
FDA for cholesterol lowering.

An anti-cholesterol effect provides a ready explanation as to
how SIM inhibits extracellular virion production (i.e. structural
assembly) of HBV. How SIM reduces DNA intracellular intermediates
of HBV remains to be elucidated. It is unlikely that SIM is
working as a polymerase inhibitor, since it does not appear to be
structurally related to nucleosides/tides. Thus, the mechanism of
anti-HBV action by SIM needs further investigation.
Most hepatologists no longer consider statins to have any significant
hepatotoxicity (Cohen et al., 2006). Millions of people
have taken SIM safely. While there are rare adverse effects, these
side-effects are well delineated. Moreover, it is even possible that
SIM may become useful in the treatment of portal hypertension.
Abraldes et al. have extensively investigated SIM as an agent to treat
portal hypertension (Zafra et al., 2004). They recently reported a 30-
day double-blind randomized controlled trial using 20–40 mg/day
of SIM. A significant lowering of portal hypertension and fewer
side-effects than placebo were seen in 59 patients with advanced
cirrhosis (Abraldes et al., 2009).
Statins have been noted in two large epidemiologic studies
in veterans to reduce the risk of HCC by 50% (El-Serag et
al., 2009; Khurana et al., 2005). Moreover, because of Veteran’s
Administration pricing policies during the latter study periods, the
predominant statin being prescribed (77%) was SIM (El-Serag et
al., 2009). The possibility that SIM may possess anti-HCC activity
provides additional rationale for combination therapy.
HBV resistance to the NAs is becoming an increasing problem.
We have previously shown equal in vitro efficacy of SIM against
wild-type and the clinically relevant HBV resistant strains that
encode rtL180M, rtM204V, rtM204I, rtN236T (Bader and Korba,
2008).