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Hep C Discussion Forum -> General Discussion -> Liver Fibrosis
Post Info TOPIC: Liver Fibrosis
mallani


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RE: Liver Fibrosis
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Joanne, I'm not happy either! Wish I'd given up the booze earlier. However,' accept the things we cannot change'. You're correct, cirrhosis is not a death sentence. We need to look after ourselves, watch for HCC and find comfort in the fact that Rx is helping our liver heal.



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Geno 1b, IL28B CT,  x3 prior relapser,  ex-cirrhotic, 75 yo, did 48 weeks with Victrelis/Peg./Riba.  VL 1.28m at start, UNDET. at 8 ,12 ,16 ,24 ,30  and 48 weeks.  EOT 15 Feb 2013 , UNDET. at EOT + 28 weeks. SVR!  Still Undet. at EOT +5 years

Malcolm
JoAnneh


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Malcomb, I have heard of people living a long time w chirrosis.
But first we need SVR. I don't like knowi g I am in the 20 percent
That reached this stage but I just can't think about it as it would
Sadden me. I just want to ride bikes, play outside and swim again:)
JoAnne

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JoAnne

Genotype 1a, Triple therapy w/Invicek started May 19, 2012

DET 4 wk. UND 2,6,12,24 48 treatment. Achieved SVR 2013!
mallani


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Correct, LC. Much has been published using biochemical markers, various formulae, imaging parameters (ultrasound, CT and MRI). Various docs have differing views on these.



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Geno 1b, IL28B CT,  x3 prior relapser,  ex-cirrhotic, 75 yo, did 48 weeks with Victrelis/Peg./Riba.  VL 1.28m at start, UNDET. at 8 ,12 ,16 ,24 ,30  and 48 weeks.  EOT 15 Feb 2013 , UNDET. at EOT + 28 weeks. SVR!  Still Undet. at EOT +5 years

Malcolm
LC


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You said they can only accurately assess that with the Fibroscan or a liver biopsys right?

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Genotype 1a, VL 1,151,923.  51 years old.  Started treatment on AbbVie TOPAZ II clinical trial Oct 10, 2014!  Undetected at weeks 2 and 4! 
mallani


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Increasingly, the decision of when to treat, how to treat and how long to treat, is being based on the degree of liver damage(fibrosis). The hepC virus does not directly cause liver damage. It is our bodies reactive response that causes our problems. Many patients with chronic HCV never develop significant fibrosis. Others develop progressive fibrosis, but do not progress to cirrhosis. Up to 20% do progress to cirrhosis. Identifying who will progress to cirrhosis has been the subject of much research. Genetic and biochemical markers have been identified- Steff has posted a new one in the 'Knowledge Base'.

It is well known that fibrosis can be accelerated by alcohol, fatty liver, coexisting HIV and HBV, and any other liver inflammation. It is also more common in males. The time interval between the fibrosis stages is non-linear, meaning it may take 20 years to progress from F0 to F2, 10 years from F2 to F3, but only 5 years from F3 to F4. (only a guide).

To understand how fibrosis develops, we need a brief understanding of liver anatomy. The basic liver unit is the lobule. Rows of liver parenchymal cells (hepatocytes) are bathed in blood filled sinusoids. 75% of the blood comes from the portal vein (draining the gut) and 25% from the hepatic artery (from the heart). Blood drains back to the heart via the hepatic veins. The liver thus has a luxurious blood supply. Each lobule is surrounded by the portal tracts, containing tiny branches of the hepatic artery, portal vein and bile duct. When our virus enters an hepatocyte to replicate, chemicals called cytokines are released from the hepatocyte. These stimulate normally inert stellate cells (lying near the sinusoids), and these start to lay down collagen (precursor of fibrous tissue). As time goes on, more collagen is deposited giving more fibrous tissue. Initially the fibrous tissue is confined to the portal tracts, and thickens the lining of the sinusoids. Other chemicals attract inflammatory cells, and hepatocyte death occurs. The dead cells are replaced by collagen, and this eventually extends beyond the portal tracts into the lobule forming fibrous septae. When these extend from one lobule to another, we have reached F3.(bridging fibrosis)

The classification of liver fibrosis is used on liver biopsy specimens. The Metavir system is the oldest and is still widely used. F0 means no fibrosis, F1 means some portal tract fibrosis, F2 means more extensive fibrosis with a few septae, F3 is extensive septae with some interlobular fibrosis, and F4 is cirrhosis with widespread fibrosis disrupting liver architecture. The degree of inflammation is given as A0-3, but I am not discussing this.

Obviously, fibrosis affects liver perfusion. Decreased perfusion means less exposure to the drugs and is probably the reason for the decreased SVR's in F3's and F4's, as well as the need for longer Tx. If SVR is obtained, 60% of patients can expect an improvement of at least 1 stage at 2 years post Rx.

In summary, find out your fibrosis stage before treatment. Cheers.



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Geno 1b, IL28B CT,  x3 prior relapser,  ex-cirrhotic, 75 yo, did 48 weeks with Victrelis/Peg./Riba.  VL 1.28m at start, UNDET. at 8 ,12 ,16 ,24 ,30  and 48 weeks.  EOT 15 Feb 2013 , UNDET. at EOT + 28 weeks. SVR!  Still Undet. at EOT +5 years

Malcolm
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