Fibrosure

[rivll]

Hi
I am completing tx for Hep.C at the end of the month with GL 7797 and Riba. I have been feeling particularly bad and I think it is more than the riba. I asked the study Dr. for my fibrosure results to get an indication of the severity of the cirrhosis. I don't think it looks very good, but I am not an expert in test matters.
Fibrotest score is 0.94 and APRI is 8.10.
1. How severe is it by these results?
2. Can my liver improve?
Thanks

[Dee1956]

So sorry you aren't feeling well. you are so close to finishing that is good news.
The last two weeks I felt really bad, I think in my case it was anxiety to be done.  I was tired of being so sick

Hector gave some great advice that helped me understand a bit more.  I am glad you asked the question

Thank you
D

[HectorSF]

2. "Can my liver improve?"

It's complicated...

Hepatology. 2006 Feb;43(2 Suppl 1):S82-8.
Reversal of hepatic fibrosis -- fact or fantasy?
Friedman SL, Bansal MB.
Source
Division of Liver Diseases, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA. Scott.***@****

...“Regression of fibrosis and cirrhosis is a controversial topic. Part of the issue stems from terminology, and failure of some investigators to distinguish between resolution (or reversion), defined as a return to the normal state, and regression, defined as a decrease in matrix (the scarring) content.

Cirrhosis regression is more complicated. While regression of fibrosis does occur in the cirrhotic liver, the vascular manifestations of cirrhosis, especially shunting, appear to persist even after significant decreases in liver matrix content. Reversing the vascular changes of cirrhosis will require more than antifibrotics, in particular antiangiogenic iInhibiting the growth of blood vessel) agents. While the “point-of–no–return” along the spectrum of fibrosis and cirrhosis has not been defined, it may occur in the later stages of cirrhosis and reflect the characteristics of local cell populations, the matrix, and particularly the vasculature.

Clinical Features of Fibrosis and Cirrhosis

Fibrosis per se is asymptomatic and its major clinical importance is the potential for progression to cirrhosis. Cirrhosis, in particular the development of portal hypertension, is responsible for the clinical manifestations of chronic liver disease, although it is heterogeneous both histologically and clinically, and one of the flaws of current histological scoring systems is that cirrhosis is represented as one or at most two stages. Clinically Patients with cirrhosis may be symptomatic or near death. Complication of cirrhosis include portal hypertension, with the development of ascites, varices, and hepatic encephalopathy. Protein synthetic function is decreased, with abnormal clotting. Jaundice and thrombocytopenia are common in late stages, as is the hepatorenal syndrome. Death typically results from progressive liver failure, from complication of portal hypertension (bleeding), or from hepatocellular carcinoma.

Whether or not a patient is symptomatic from cirrhosis depends largely on the HVPG. A normal HVPG is 5 is associated with significant fibrosis. Multiple studies have now made clear, however, that patients do not develop complications of cirrhosis (ascites, varices) until the HVPG is >10, and that HVPG is an accurate predictor of clinical decompensation. Noninvasive tests to categorize cirrhosis include the Child-Pugh score (also called the Child-Turcottee-Pugh score) It was originally developed as a means to predict survival during surgery, but is now used to predict the clinical course of patients with cirrhosis. The score is determined from serum bilirubin, serum albumin, prothrombin time or INR, the degree of ascites, and the degree of of hepatic encephalopathy, and assigns patients to categories A, B, or C, representing well-compensated, severely functionally impaired, and decompensated liver disease, respectively. Patients with Childs A cirrhosis have an excellent 1 year survival, while patients with Childs C have a 1 year survival of <50% with conservative treatment. Once patients have decompensated, the model of end-stage liver disease (MELD) score, is a more accurate way to predict 6 month mortality. The MELD is based on INR, serum bilirubin, and creatintine, is also widely used to prioritize patients on liver transplant waiting lists.”


So in a nutshell...while the structural fibrosis may be able to be reversed the vascular complications of cirrhosis may or may not. A lot would depend upon how much portal hypertension you currently have. Grade of varices, enlargement of spleen, collateral veins, etc. These complications can continue to damage the liver even though the cause of the original injury to the liver has been eliminated. Obviously more knowledge is needed about how cirrhosis develops and studies need to be done to follow patients with cirrhosis after clearing the hepatitis C virus. For your particular case time will tell. Having periodic staging of your liver will help to show any changes in in the stage of your liver disease. If would be good to have it done every couple of years after you have achieved SVR.

Hector