Stage 3/4 Bridging Fibrosis/Fattty Liver

[uncledudeness]

assuming that i get to UND and then SVR, what is the process of reversal of liver damage. is it safe to assume that the liver will regenerate at some point and become a healthy organ? i'm a geno 1a, at 9 weeks, and my ast/alt are now in the normal range. at last PCR, viral load was 4689. another question is about fatty liver. i've lost about 15 lbs and i understand that it's helpful, but how is fatty liver affected, should i reach svr?

i've read a bit about liver regeneration, but it's still a bit fuzzy..

thanks again for everything.

[crossroadsec]

@ Charlie and unclududeness - The MRE sounds like a great test. Sounds like you're doing well. Are you on a low sodium diet? Good sources of protein that don't overtax the liver are helpful too. My doc upped my protein after tx to help with regeneration of the liver. Best to you!
Karen :)

[charlie2247]

I am in the same boat. 3/4 early cirrhosis. My doctor at UCLA say's " you are cured, you liver will get better". He has ordered a CT scan in 6 months to check on a couple of small lesions.The test I want is an MRE elastography that can accuratly test the stiffness of the liver and really show the extent of fibrosis/ cirrhosis. The only place I can find it is at the Mayo Clinic.I am expecting a slight regeneration over time, maybe to bring me to a 2/3 type situation. My liver functions are good so I will be fine if that is the end result.

[uncledudeness]

thank you to all that responded. it's encouraging that there seems to be signs that early cirrhosis can improve. i sure hope so.

now that i am treating for the second time i have more hope than i did the first time.....

[desrt]

Update to my posting on this thread:
Ultrasound 9+ post-tx showed no fatty liver. So sometime between 5 years post and 9 years post the steatosis resolved. Geno 3 minimal fibrosis.

[frijole]

It would probably be best to click on the individuals' names and leave messages to them since this thread is rather old.  Otherwise kristina538 and ozgirl may not see your questions.  Or... start a new thread.  the topic always has relevance. I too am hoping my stage 3 & 4 early cirrhosis can improve although my hepatologist will absolutely not give me that confirmation.
frijole

[pugdaddy]

Hi Kristina, I was reading your post above.  Congratulations on SVR!
I did too - but am left with very scarred liver & mild portal hypertension.
Did you ever have any sumptoms of liver disease prior to your treatment?
Thanks!

[pugdaddy]

Dear Ozgirl -
I'm reading your 2011 post where your husband has improved from cirrhosis.  Do you mind if I ask what stage cirrhosis he was in?  
What were his worst symptoms?
Many thanks,
Pugdaddy

[Ozgirl707]

My husband had cirrosis, HCV geno 2, he did tx and SVR'd.

That was about 6 years ago.

He has 6 mnthly scan and liver cancer tests. His liver has improved heaps. His specialist says it is healing well! :)

So if you live a healthy life style and do exercise, which he does, the liver must improve itself!! Also he has Milk Thystle sup. that might help.

Good luck with SVR,
All the best,

~Ozgirl

[Kristina538]

I managed SVR with Stage 3 (possibly more) bridging fibrosis.  I had spleen problems and portal vein enlargement; both of which have disappeared in subsequent scans.  My specialist said I would heal further over time, and I continue to eat in a 'liver-friendly' manner.  

I do, however, have regular (6-12 months) bloods and an annual ultrasound, as I believe I am a higher liver cancer risk.  

My greatest celebration since SVR is getting regular, normal bowel movements, which shows me, in a very personal way, that there has been improvement.

[frijole]

maybe it is that your encephelopothy makes you so in tune and aware of the issues.  Or maybe it isn't as bad as you think.  In any event your posts are always insightful and informed and I enjoy reading them.
Frijole

[paen53]

The question you pose, I think, is one that many of us "late-stagers" wonder about. I remain hopeful that my Stage 4 liver has stablilized after 72 weeks tx and SVR - and hope that in time it may have reversed some damage. I've thought about running another Fibrosure to see if there's any difference, one way or the other, since my last test a few years back. But the test is not very accurate in the mid-areas of fibrosis from what I read. I'm not so sure about another bx down the line (last one in 2008), but I guess I won't rule it out. Hopefully in the near future there'll be a less invasive means of determining liver damage.

Pam

[uncledudeness]

thank you for your response HectorSF. it was very helpful. I guess it's one of those questions that is unique to each individual.

one of the main reasons for my question is that i am at late stage 3. the biopsy could not rule out stage 4. i am hoping if i clear, that i won't progress to stage 4, and i will live happily ever after...

thanks again for you insightful response.

[desrt]

My experience with fatty liver:
Dx with steatosis/NAFLD by ultrasound one year post successful tx. Also dx as insulin resistent. Started taking Metformin ER, got my IR under control, lost 40 lb, had another US at 5 yrs. post-tx. Steatosis was still there. I asked if it had improved, progressed, or stayed the same. Was told US isn't a very good tool for determining this. Since my fibrosis was not very far advanced in 2001, I've never bothered to get another biopsy. In your case, periodic bx might be justified, so you may be able to track your NAFLD post-tx.

[HectorSF]

Thanks for the nice feedback.
Maybe my encephalopathy is quite as bad as I imagine? I may not know what day it is, but I guess I can still put two words together somehow and have it make some sense.

...It's 6 Am. Time to go to sleep. Yikes!

Hectorsf

[frijole]

That was excellent.  Very clearly said and very understandable.  Something we all need around here.
frijole

[HectorSF]

It is fuzzy for everyone! This is an issue that confronts all who work with liver disease as well as those that suffer from it. In the future we will know a lot more about this issue then we do today. "Despite the mounting clinical evidence, the potential for the reversal of cirrhosis remains a debated issue, the methods used in the clinical studies are still criticized, and even the terminology is a matter of controversy." from  the Journal of Pediatric Gastroenterology & Nutrition.

Fibrosis used to be seen as a something that could only get worse over time. It is now known that fibrosis is a dynamic process that can stabilize and reverse itself as well as progress for further degrees of illness. One of the reasons that it is still impossible to quantify regression is that the system used for measuring progression is not an accurate, quantifiable system.

The Metavir scoring system is specially designed to evaluate the liver in people with HCV.
The fibrosis score is assigned a number from 0-4
• 0 = no scarring
• 1 = minimal scarring
• 2 = scarring has occurred and extends outside the areas in the liver that contains blood vessels
• 3=bridging fibrosis is spreading and connecting to other areas that contain fibrosis
• 4=cirrhosis or advanced scarring of the liver

It is well know that this system is a qualitative assessment of the degree of liver disease rather than a quantifiable system. For example stage 4 cirrhosis is divided into two sub-parts that are very different from one another. Compensated cirrhosis and decompensated cirrhosis. When the liver becomes decompensated it is usually considered "the point of no return". This is when the liver is now longer able to perform all of its functions and systems such as ascites, variceal bleeding, etc. occur. Treatment for HCV is no longer recommended by the manufacturers of pegylated interferon and ribavirin as treatment itself may cause the liver to totally fail. The only option available at  this point is a liver transplant.

Since the degree of illness during decompensated cirrhosis is so critical, the MELD system is used to quantify the degree of liver damage and the chances of the patient surviving over a future time period. This is the measurement system used to assess who is the sickest and who needs a transplant most quickly in order to continue living. This is how patients are chosen to qualify for the next available donor liver due to the shortage of livers available. Even the MELD system with its numerical measurement of between 6-40 (40 being gravely ill) doesn't accurately gauge how ill is a patient is. So exceptions are made and points can be given to patients to try to more accurately indicate how ill the patient is and how long they can survive without a transplant.

So since their is no accurate system for measure liver disease throughout  its life-cycle, there is no way to accurately access the reversal of liver damage using the  Metavir scoring system. So if a person has stage 4 cirrhosis and they are able to remove the cause of their liver disease (IE successful treatment of HCV=SVR) then all that can be said is the the patient's liver has repaired itself and  gone from stage 4 to, for example, stage 3. With the MELD system a patients MELD score is constantly varying which is why periodic blood tests are taken to track the patients condition.

Obviously this is an issue that many people are working to overcome and to have a more accurate way of measuring the degree of liver disease as it will help in accessing the degree of illness, if it stable or  progressing or regressing. Remember, most people with HCV never progress through all 4 stages of liver disease in their life times. While others progress at various rates through all 4 stages and then suffer from liver failure or liver cancer and must have a new liver in order too continue living. As more is learned about the nature of liver disease it will help to improve both assessment and treatment of liver disease for patients.

For more information on this topic I would recommend the following article from the Journal of Pediatric Gastroenterology & Nutrition:
http://journals.lww.com/jpgn/fulltext/2007/04000/reversal_of_liver_cirrhosis__a_desirable_clinical.1.aspx

"Cirrhosis is the final stage of chronic liver damage of various etiologies. It used to be considered an irreversible lesion, but enormous advances in our understanding of hepatic cellular and molecular biology in the past 2 decades have challenged this view. There is now substantial evidence that cirrhosis can be a reversible process. This concept is supported by an increasing number of clinical reports showing the disappearance of cirrhotic lesions from liver biopsies taken from patients cured of their liver disease. The reversal of cirrhosis usually occurs in patients with short-lived liver disease, after the successful treatment of the underlying liver damage. Recently, however, we observed the spontaneous reversal of cirrhosis after the loss of hepatitis B viremia in 2 men, 21 and 28 years old, who had developed cirrhosis as young children. Several questions and controversial issues concerning the definition of advanced cirrhosis, the limitations of liver biopsy (eg, sampling, interpretation error), and the applicability of noninvasive methods to the assessment of fibrosis, are being addressed. Future prospects include the possibility of antifibrotic therapy to prevent fibrosis or favor its degradation."

Cheers!
Hectorsf