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
Thanks for posting the study Cory, interesting information.
-Dave
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
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.
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.
"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
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.
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.
No but I heard about the Eskimo's who spontaneously cleared chronic hepc. :)
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 ?
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.
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
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.
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.
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.