Cingles Info

Hi Dana,
Here's what I found at http://www.hcvadvocate.org
Can Liver Fibrosis Be Reversed? Still A Widely Debated Topic
Alan Franciscus
Editor-in-Chief
Cirrhosis is a result of late stage scarring in chronic liver
disease. Cirrhosis occurs as a result of progressive damage to the
liver tissue starting with subendothelial or pericentral fibrosis
(hepatic fibrosis) and progresses to panlobular fibrosis with nodule
formation (cirrhosis). Up until now it has been generally thought
that once fibrosis is established it is irreversible. Until recently
the clinical diagnosis of cirrhosis was made based upon the signs and
symptoms of end stage liver disease. Such symptoms include variceal
bleeding, jaundice, ascites, muscle wasting and encephalopathy.
Clinically these symptoms continue to indicate a poor prognosis in
the absence of liver transplantation and are used to classify
severity for patients waiting transplantation. However, due to
advances in the management of liver disease and the impact that
hepatitis C disease management is having, liver biopsies have led to
fibrosis and cirrhosis being diagnosed at an earlier stage. It has
been demonstrated in some studies that early stage fibrosis, and even
advanced cases of cirrhosis can regress during treatment of hepatitis
C even without the benefit of a sustained virological response (SVR)
to treatment with interferon.
Basically, treatment gives the liver a vacation or rest from
inflammation caused by HCV. Providing that the cirrhosis is not at
such an advanced stage that treatment is not an option, treatment is
often used to improve the health of the liver even if the disease
cannot be eradicated.
In February 2001 issue of the New England Journal of Medicine, Hammel
et al discussed a group of patients with liver fibrosis who had
surgery to decompress an obstructed biliary system. In this patient
population, some patients had their liver fibrosis regress
significantly after decompression, which was confirmed by pre and
post liver biopsy. Until this publication the natural history of
histologic changes after biliary decompression had not been discussed
in humans. This study certainly implies that fibrosis caused by
biliary obstruction is reversible in some cases, but studies similar
to this one need to duplicate results to rule out variations in
sampling on liver biopsy. As well, this study was criticized for not
having a control arm or strict selection criteria. Regardless of the
criticism, the apparent improvement in fibrosis after biliary
decompression adds another example to a growing list of specific
interventions, which result in histologic improvements including
fibrosis regression.
There have been consistent reports on the reversibility of liver
fibrosis in humans when the cause of the underlying liver disease is
eliminated. These include abstinence from alcohol, surgical reversal
of jejunoileal (removal of a portion of the small intestine) bypass,
immunosuppressive therapy for autoimmune hepatitis, long term
treatment with lamivudine for chronic hepatitis B, treatment of
hepatitis C and hepatitis D with interferon and, finally, treatment
of primary biliary cirrhosis with methotrexate plus ursodiol.
Over the past decade or so there has been major progress in
understanding the cellular and molecular regulation of hepatic
fibrosis. It has been determined that the build up of scarring in
fibrotic diseases of the liver is not static or a unidirectional
event but a dynamic and regulated process that works well with
intervention.
The growing amounts of clinical and scientific data provide us with
the knowledge that extensive fibrosis or cirrhosis in patients that
still have compensated liver function should no longer be considered
untreatable. Both currently available as well as future therapies
have the potential for preventing the progression of disease by
regression of fibrosis.
Despite growing knowledge on whether liver fibrosis is reversible,
there are still some unanswered questions. Liver fibrosis does not
develop at the same rate in all patients and the fibrotic responses
to therapy will vary from patient to patient. What are the host or
disease specific factors that are linked to both a slower progression
of fibrosis and a positive response to treatment? In addition,
should treatment strategies be better designed to reverse fibrosis
and improve liver health, rather than to only treat when there's a
good probability of a cure? For example, long-term therapy with
alpha interferon may improve fibrosis in patients with chronic
hepatitis C even in those patients who do not experience a virologic
response. With that finding wouldn't long-term alpha interferon
therapy be well justified in patients that do not gain a virologic
response to treatment? It certainly seems to make a case for
physicians to partner with patients to make these important treatment
decisions.

else. Now I am a little confuse hear, so bear with me and don't
attack me!! LOL I did not think that liver damage could be
reversed. I thought treatment was to illiminate the Virus from
attacking the liver. Am I missing something. I hate this should you
or should you not go on treatment and this only confuses me more when
I hear things like this??? Someone help??....................Dana