Here's a recent article that cautions about the "completely reversed"
label, but is very optimistic otherwise:

Reversibility of Hepatic Fibrosis and Cirrhosis--Is it all Hype?
Scott L Friedman

Now that the idea that hepatic fibrosis is reversible is taking root,
many clinicians are beginning to ask why, if fibrosis is reversible, is
there so little progress in the clinical setting, and will patients ever
really benefit from antifibrotic therapies? Underlying such questions is
a subtle cynicism that the reversibility of fibrosis and cirrhosis has
been overhyped—yet another example of the medical media 'spin machine'
giving false hope to desperate patients. The situation has been fueled
by the actions of ambitious institutional press relations officers. One
such example is the worldwide media focus on the use of sulfasalazine to
treat hepatic fibrosis, with claims that half of all liver deaths could
be avoided[1] even though the drug's reported efficacy was based on a
single study in rodents.

So what is the truth, and how do we maintain perspective? First of all,
progress has been tremendous. The mere idea that fibrosis can regress
when the initial disease is controlled or cured is exciting, given the
decades of dogma that suggested scar formation was a unidirectional
pathway. Ample evidence that fibrosis regresses with control of
hepatitis B, hepatitis C, or other chronic liver diseases[2] attests to
the tremendous regenerative power of the liver, and the rapid progress
made in the development of targeted antiviral and disease-specific
treatments. Without such advances a discussion of reversibility would
have been moot, but this discussion has raised some semantic issues that
sow controversy and obscure continued progress. Specifically, use of the
term 'reversal' implies a complete return to normal histology, whereas a
better term would be 'regression'—a more accurate and relevant term that
indicates improvement in fibrosis without necessarily a return to normal
histology. Of equal importance, stasis of disease or delayed progression
are clinically meaningful, as they might prevent the development of
cirrhosis, which is the only stage of chronic liver disease associated
with significant and predictable complications.[3] A related issue is
the failure of some clinical studies to distinguish between cirrhosis,
which connotes distinct architectural and structural changes (including
nodules of fibrosis that encapsulate hepatocytes), and advanced
fibrosis, which lacks these features.
[...]

Complete text at
http://www.medscape.com/viewarticle/556253?src=mp
(Requires free registration)

Thomas