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progression of fibrosis
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progression of fibrosis

From what I am able to see there do not seem to be a lot of studies that accurately gauge the time it takes to progress from one stage of fibrosis to another. Of course this is not an easy task since it would require many patients, several biopsies and many years of follow up to give us an accurate representation. Perhaps there is a lot more information out there then I was able to find, I would love to see it. I am always amazed at the collective resources of the people in this forum.

The average rate of progression will always include the patients estimate of when they were exposed which in itself is often not precise. It almost seems impossible to measure, and my experience is that the hepatologists are fairly ambiguous about answering this question. I have personally seen four hepatologists since diagnosis 12 years ago.

Since this disease does not progress in a linear manner it becomes even more difficult to determine the rate of progression. There are so many variables about the individuals health and genetics and other factors that even trying to predict or tell a patient an average rate of progression seems a difficult task at best.

It seems that most information we have shows that getting to stage 1 if that ever happens can take approximately 15-40 years. How do we know the average time for progression from stage 1-2, 2-3, 3-4 and through the different stages of cirrhosis. The information I have seem suggest that it might progress more quickly as more damage to our livers has occurred making it even more difficult to determine an average.

This information suggests that it takes about 6.6 year to progress a stage which is what my hepatologist told me was the average earlier this year.  

http://www.medscape.com/viewarticle/498114_3
" The median estimated rate of fibrosis, based on the known or estimated duration of infection, was 0.15 stages per year (interquartile range 0.37). Note that five patients had stage 5 fibrosis."


I was diagnosed 12 years ago. I have been drug free for 30 years. I stopped drinking alcohol when I was diagnosed 12 years ago but only drank moderately until that time. My general health appeared to be excellent at that time, I was asymptomatic and only found out I had hep c because of blood work I did to obtain life insurance which was denied.

I guess for me the average is meaningless and so I go to the hepatologist to access my condition rather then depending on the average to assure me of my condition.  I have had three biospsies in the past 12 years. I thought I would post my results not for someone else to decided how long they will take to progress, but because I believe many of us have had a completely different experience of progression.

My hepatologist believes that my second biopsy was not accurate. Either poorly interpreted or poorly sampled. My first two biopsies were performed at UCSF by a very experienced hepatologist. My last biopsy was performed locally, but was accessed by two pathologists the second was working at CA Pacific with the gish team of hepatologists.

According to this information since I have progressed from stage 0 to stage 2.5 at the rate of either 4.8 years a stage or 2.4 years a stage depending on the accuracy of the biopsies. Either way that appears to be quite a bit less then the average 6.6 years.

Biopsy 1, 41 years of age, about 20 years after exposure - Stage 0 firbrosis. grade 2 inflammation

Biopsy 2, 46 years of age, about 25 years after exposure - Stage 0 firbrosis. grade 2 inflammation

Biopsy 3, 52 years of age, about 31 years after exposure - Stage 2-3 firbrosis. grade 3 inflammation
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18 Comments Post a Comment
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96938_tn?1189803458
If it's that important that you understand the progression, you have an option.  You should be able to get your hands on the slides from biopsy #2 and have the person who reviewed the specimens of biopsy # 3 take a comparative look.  It should not be that hard to track down the slides if you know the location and and date of the procedure.  Other around here have scrounged up those things before.  Expect to sign a release to get them in your possession.  But, in the end does it really matter?  I'd expect that the Gish gang are pretty adept at what they do.
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Avatar_m_tn
It's actually not that important to me personally. I have never spent a lot of time worrying about my disease except when I was first diagnosed and didn't really understand it.

The reason I posted was because I have read a few posts lately where people asked how long they have before their disease gets more serious, and were responded with average time of 10 years. I thought it might be interesting or informative to someone who had those questions. Perhaps not.
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96938_tn?1189803458
I hear you.  This disease is so confounding sometimes with a lot of gray area.  Although people wait many years to deal with HCV, logically so for them, I'm one who believes that the seriousness exists sooner than the results of a biopsy may infer.  Being a host to a chronic disease, I think, is not an entirely benign event.
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1477908_tn?1349571310
That's the million dollar question for us with HCV and I doubt there is a one size fits all answer. Like you say, "There are so many variables about the individuals health and genetics and other factors that even trying to predict or tell a patient an average rate of progression seems a difficult task at best."

I was dx'd early in 2004 and even though I researched it extensively, I chose to believe that I was OK - I felt pretty darn good - and passed on a bx, citing lack of funds (no Insurance), bad timing, and a host of other excuses. By the time I did have a bx four years later, a stage 4 dx. Understandably, I don't have a prior bx to base anything upon, but in my gut, I believe I put myself at a higher risk for liver AND tx failure by waiting so long.

I inwardly cringe when people ask about progression probabilities and that old standby crops up that most of us will die with HCV, not from it. I think that over age 50 all bets are off  -  not that we're all going to croak tomorrow by any means, but we will see it affect our lives in one way or another either in a direct way or via secondary issues like diabetes. Hopefully the new drugs will eliminate that dodgy question, 'should I or shouldn't I' and get the job done once and for all.

Pam
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Avatar_f_tn
By all accounts, particularly with the 6.6 yr  -  1 stage progression theory I should have decompensated cirrhosis and I don't, not even close. There was a whole lot of drinking going on back in the day so it really depends on the person.
  
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979080_tn?1323437239
Has anybody ever heard this story of a large number of Korean war veterans that got
infected and those who adapted a healthy life style lived an average life span
and those who did`nt (alcohol , bad diets ect...) had trouble from Hep C ?
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Avatar_f_tn
No but I heard about the Eskimo's who spontaneously cleared chronic hepc. :)
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Avatar_f_tn
I was reading some study abstracts recently, and from what I was able to understand, there seemed to be the thought that people's bodies respond differently based on the particulars of the genotype and various aspects of the genotype, along with the more obvious prior medical condition.  I think there is a great deal still to be discovered and hope that happens quickly.
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Avatar_n_tn
For one thing,  there is different typed of Hep-c, and viral load different for people, how old how long also determines. Alot of aspects. Good book to help anyone with this is,"the Hepatiis Handbook> by: Matthew Dolan. Its like the Bible for Hep-c people. You can order it on line, Barnes and Noble or any book store. And get a well educated docter. Gasterolist,or internist. but one that knows because I have been to alot of Docters that dont know much if anything especially a family practioner.  you need a specialist. And if you can get the treatment, it works, depending on type, viral load, and lifestyle.I have had hep-c for 40yrs, I did take the treatment, , but I am type 1A and it is not responsive to treatment.,my viral load was over a million. But this thing duplicates itself and so its hard to cure.But  biopsy is the Gold standard to see how much liver damage there is.. good luck everyone.
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Avatar_f_tn
"but I am type 1A and it is not responsive to treatment.,my viral load was over a million."

A viral load of a million or higher is quite average. 1A is responsive to treatment.  Nearly half the people with genotype 1a who undergo antiviral therapy with the current standard of care achieve SVR.  I went undetected for for around 57 out of 72 weeks which means I responded but the interferon and ribavirin did not work effectively enough with my immune system to suppress the virus after stopping therapy.  The protease inhibitors which we are all hoping will be released in 2011 will give us geno 1's around a 75 percent chance of SVR.

Trinity
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1542388_tn?1293855413
Dear Spec,
I was surprised to learn my husband's cirrhosis had progressed from a 2 in 2003 to a 4 of 4 this last month. He drank some over those years, but not much, and has a typical American lifestyle of a poor diet and high stress. He attempted tx in '03 but after 3 months, dropped out because of the severe side effects of the Inteferon/Rib. It came down to making a living or staying on tx. He was a builder and since the housing bubble burst, that stressor has been eliminated (had to go on disability). Now I'm a full time nursing student trying to figure out tx while his health is still reasonable. He developed DM after quitting the HCV tx and I fear that the many of diabetes drugs and the other scripts he takes has escalated the cirrhosis. For us, it becomes a strategy trying to figure out symptom management and collateral damage for his liver. He also has deg disk disease in his back, arthritis, gallbladder disease, some peripheral neuropathy from the DM, HTN, depression, diverticulosis, and some other issues from the impaired liver like spenomegaly, portal htn, esoph varicies, some hep enceph, etc.  All of the meds he takes to manage the pains and blood glucose are pretty scary when the liver is impaired. I just found this forum and have found more info here that the visits to the docs. Anyway, there seems to be so many factors for escalation of this disease that the window of treatment opportunity knocks, but like Pam, we had lots of excuses why we couldn't do it "right now". Sad reality to  know the window is closing.
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Avatar_f_tn
Very interesting post.  I assume to contracted hep C 1971.  My biopsy in 2/10 was stage 1 grade 1.  I stopped drinking after my dx this year.  So who knows why I progressed as slowly as I did.  But I don't count on it staying that way.  This liver doc I met with recently indicating the progression will remain slow.  I don't believe him.  But a good question for the new doc I'm seeing at Mayo in March.
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Avatar_m_tn
All of the patients had the final liver biopsy taken more than 5 years after the initial one and almost two-thirds of them showed fibrosis progression, development of advanced fibrosis/cirrhosis being observed in 27% including more than one-third of those with F1 (portal fibrosis) in the initial biopsy. These results clearly indicate that chronic hepatitis C is a progressive disease in many patients who initially present with no/minima l fibrosis and that progression to advanced fibrosis does occur in a significant number of cases within 5-10 years...Progression to F3 or cirrhosis was seen in 36% of those with F1 initially......

One hundred and six patients (mean age 41.65 ± 12.83 years) with chronic hepatitis C virus infection and no/minimal fibrosis in the initial liver biopsy (F0/F1 by METAVIR score) were followed prospectively while untreated with repeated biopsy after 5 or more years (mean interval 7.8 ± 1.51 years). Patients showing fibrosis progression were compared with nonprogressors for baseline and follow-up parameters.

As shown in Fig. 1, comparison between the initial and final liver biopsy demonstrated no changes in fibrosis stage in 42 cases (39.6% nonprogressors: 14 with F0 and 28 with F1) and variable degree of liver fibrosis progression in the remaining 64 patients (60.4% progressors: 13 with F0 and 51 with F1 in the initial biopsy). The ΔF was 1 stage in 27, 2 stages in 24 and 3 stages in 13 of these progressors. The probability of being nonprogressor or progressor did not differ significantly between cases with F0 or F1 in the initial biopsy (P = 0.201) and, among progressors, mean ΔF/year was 0.212 ± 0.66 in patients with F0 and 0.266 ± 0.91 in those with F1 (P = ns). However a ΔF of 3 stages as well as progression to F3 or to F4 (cirrhosis) were observed only in patients with F1 in the initial biopsy. Overall, fibrosis progression was observed in 13 of 27 cases with F0 (48.1%, including 5 to F1 and 8 to F2) and in 51 of 79 with F1 (64.5%, including 22 to F2, 16 to F3 and 13 to F4). Thus, among those with F1 initially, 20% progressed to F3 and 16% to F4 (cirrhosis)

http://www.natap.org/2010/HCV/041510_06.htm
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Avatar_m_tn
Thanks for posting the study Cory, interesting information.
-Dave
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Avatar_m_tn
I've cited an additional source to this study, now it provides more pertinent info than was once presented.  36% of patients with Stage 1 progressed to Stage 3/4 within 5 years.  Given that, the estimated time of infection in individuals becomes more important, and the progression to stage3/cirrhosis is closer than once previously thought.      

" In a study from the Journal of Viral Hepatitis, 2006, It was found that the rate of fibrosis progression was higher then once thought.Often treatment was delayed if the patient had no fibrosis, but if you read the summary below it may make you think twice about starting treatment before liver damage/fibrosis developes. "

"PEG-IFN plus Ribavirin, the current standard of therapy for hepatitis C,..... use in HCV carriers with no/minimal liver fibrosis has been questioned mainly because this has been assumed to be a benign, stable condition with minimal risk of progression to 'clinically significant' liver disease......All our patients had the final liver biopsy taken more than 5 years after the initial one and almost two-thirds of them showed fibrosis progression, development of advanced fibrosis/cirrhosis being observed in 27% including more than one-third of those with F1 (portal fibrosis) in the initial biopsy.
Fibrosis:
F1 or Stage 1 none or mild peri-portal fibrosis
F2 or Stage 2 peri-portal fibrosis with/without extension and portal-portal bridging
F3 or Stage 3 portal-central bridges but no nodular formation
Stage 4 probable or definite cirrhosis

These results clearly indicate that chronic hepatitis C is a progressive disease in many patients who initially present with no/minimal fibrosis and that progression to advanced fibrosis does occur in a significant number of cases within 5-10 years.....Progression to F3 or cirrhosis was seen in 36% of those with F1 initially.....Fibrosis is facilitated by older age and alcohol and associated with inflammatory activity and ALT levels.....By multivariate analysis high alcohol intake (>40 g/day) and steatosis correlated independently with fibrosis progression (data not shown)......The ALT profile during follow-up was also found to have a significant association with fibrosis progression. Thirty-one patients had persistently normal ALT during the entire follow-up period and nine of them (29%) showed fibrosis progression (3 from F0 to F1, 5 from F1 to F2 and 1 from F1 to F3) compared with 55 of 75 (73.3%) of those with elevated ALT.. Antiviral therapy should be considered in mild chronic hepatitis C."

http://hepatitiscnewdrugresearch.com/fibrosis.html
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