Disease progression statistics

[mike716]

Does anyone know where I can get some statistics on how many people with hepatitis progress to end-stage liver disease, particularly with reference to genotype, age, ALT/AST, etc.?

Thanks!

Mike

[Dee1956]

While old this was a very good port.  Thank you all for your contributions
I "think" I got HCV in 1977, 30 years later when dx I was going into cirrhosis
I think treatment sooner rater than later is key
Dee

[mike716]

Thanks for the pointer!.

[mike716]

Thanks!

[BelB64]

The stat I quoted was from a medscape study. It stated that ON AVERAGE(Not everyone unfortunately) women with genotype non 1 who got the disease before age 37 would not get cirrhosis until age 89. I listed the study URL in an earlier message on this thread if you would like to read it. Actually according to the study most people who don't fit the aforementioned population ON AVERAGE will get cirrhosis at about age 65 whether male, female or genotype 1, 2 or 3. I wish the onset of cirrhosis at year 89 had been true for you as well.

[Texas714]

For what it's worth...
Someone ask/said in a female with type 2 or 3, they would not get cirrhosis till they were 89years old...on that topic...
I am a female type 2 with cirrhosis at 50. Good general health.  Not overweight.  Had this over 30 years....maybe closer to 36 years.

[Mr Liver]

Anyone who is interested in fibrosis progression should do a search for Thierry Poynard at PubMed, google, etc. No one has researched the topic more thoroughly than he has. Besides a huge volume of work as a principal investigator, you will often see him cited by others in their abstracts, as well.
Mr Liver

[Andromedae]

I have no stats to contribute - just wanted to say thanks to all for an extremely informative discussion :) .  I've learned a lot.

Andromeda

[scoop49]

ill have to get back to you on some of the older blood counts
but i can tell you that platelets were not an issue until approx "04-'05 (approx 30 years after contracting hep c)
then platelets fell alarmingly down to 50 to 60 counts
they would not start me on tx so i was in the 'tween zone of not quite unhealthy enough for transplant.
platelets continued to vary but were up two months running to 75- 80 early this year and i started tx 4-18'08. since then platelets went from in the 60's to 50's then at week 7 to 29. now (staying on tx) there is at least a temporary hole at high 20's to mid 30's (they will now go slightly below 25 at this hospital.
reason? don't really know- have always been in good physical shape-jog etc. i did go from one glass of wine with dinner to no alcohol at all and stopped taking allergy pill and aleve daily.
alt #'s were never real high-(maybe mid 80's?) on combo tx are now mid 30's
just got your message today- good luck

[mike716]

Hi, Scoop. Sorry it's taken me so long to reply to your post, but I've been layed up with the flu for the past week.

Your story interested me a lot. I've got a coupla questions, okay?

First, what were your test scores (ALT, platelets, PCR, etc.) in 97 when they discovered you were HCV+?

Second, how low were your platelets in 2006?

Last, how did you get your platelets back up again so you could go on tx?

Glad to hear your holding up good with minimal sx. If I run into Duval at the tango salons, I'll say hi to him for ya.

Mike

[Rockerforlife]

Recent studies suggest that chronic infection with HCV will almost invariably result in cirrhosis. It is the time that this takes that varies. For those people who develop a chronic or long term infection (between 70-80% of those infected with HCV) around 20-30% will develop cirrhosis within 20 years. For some it may be quicker but for others it may take up to sixty years so they may well die of unrelated diseases beforeha

[scoop49]

everybody's got an opinion

me-contracted hepc in 1974 settled down-raised a wonderful family-worked hard-was not a stranger to the evening bottle

hep c discovered '97-quit drinking-stayed in very good physical shape-thought f-it the bad stuff only happens to people who ignore the wall scribblings.
2006- wham! i had known for a year or so that my platelet count was way down (result of hep c) and discovered i cannot go on treatment even if i chose to and i gained 20 bloated pounds, felt as if i'd faint walking up stairs and basically thought it was the beginning of the end. (this after at age 57 running 3-5 miles at a good clip and working construction full time and feeling fine)
i am now 59 in week 10 of treatment and as i hold my breath every week hoping my blood counts allow me to stay on tx. (for me the side effects are very tolerable-just bit of fatigue and headaches)

so-i guess -to quote yossarian- there's another country heard from
quantity/quality? who knows

i wish you well-say hi to duval
scoop49

[mike716]

These histories from Brent, somuchmore2, and others about a decision not to treat followed by more-or-less rapid progression are frightening. I'm going to translate them into Spanish and force my hep MD to listen and give me a reply, the next time I see him. I'm very concerned that he and the other hepatologists here in Buenos Aires are judging things by old, bad information.

Re biopsies, I've read a lot of articles that say they can't be trusted. It's not just that different people with different experience are analyzing the biopsy samples, but the very nature of a biopsy - a very small specimen of the liver - makes it untrustworthy. An article in the February issue of Hepatology on a new test, FibroTC, is especially interesting for the light it throws on this point, in regard to the often non-homogeneous nature of liver fibrosis, which makes biopsies appear seriously unreliable. Here's the URL: http://www.ncbi.nlm.nih.gov/pubmed/18098299?dopt=Abstract

By the way, got a copy of that article from the authors andI posted an image from it on my forum webpage, if anyone wants to look at it. It's the multi-colored graph. Click on it to make it bigger (or just go to http://www.medhelp.org/user_photos/show/8507). The image shows a FibroTC analysis of an HCV-infected liver that has four different stages of fibrosis in it. What good would a biopsy be on that person's liver? Depending on where the needle went in, anything from F2 to F4 could be diagnosed.

Re upbeat's post, I believe there is evidence that treating HCV runs the risk of powering up the virus if it isn't eliminated. It's the old "what doesn't kill you makes you stronger" idea, and it's as true for microbes as it is for humans, I believe. It's always dangerous to treat and not cure. That's why they tell you not to stop taking antibiotics before finishing the box, even if the infection you're taking them for has cleared up.

I don't really know how interferon and ribavirin work, on a molecular level, but the suppression of viral genotype breakouts is not the only concern. There's the problem of the drugs pushing the present genotype into a more virulent mode. Viruses have different virulences (power to cause cellular harm) just like bacteria do. Normally a microbe doesn't evolve a higher virulence than infection/transmission allows, on the principle that if it is so virulent that it kills its victim before he or she transmits the infection then it dies off with the victim. But taking drugs can alter that equilibrium. And the evolution of HCV is super fast. It has a huge reproduction rate.

I think a lot of interesting discussion has come out of this thread and the forum in general on these questions, particularly the treat/wait thing. It's too bad there isn't more being done by research to solve them, like coming up with a really good non-invasive liver damage test. As long as the medical community sticks to their age-old biopsy belief, we aren't going to make much progress.

Mike

[Upbeat]

I have heard the same story of rapid stage increase after treatment.  I sometimes wonder if the treatment may have something to do with it.  Just thinking out loud.  I don't have a clue.

                                                                                                                    Ron

[somuchmore2]

OK. Below is a little history on my stuff.

Likely first infected 1972/73.
Diagnosis 1998 while buying more life insurance.
STOP are alcohol (prior I would have 8 to 12 beers on weekends)
Biopsy 1998 0/2.
Treated with interferon-riba but non-responder.
At this point heard and thought oh well only 20% get cirrhosis.
Second treatment peginterferon-riba but again non-responder.
Biopsy 2003 2/3
Discussed progression from 0/2 to 2/3 and realized it happens.
In 2005 through 2006 I was followed-up with 6 months blood, ultra-sound and one CT.
Early 2006 Fibro-Metavir score indictated F2-F4.
In early 2007 I had a major life threating event of grade III varices bleed.
Many worked hard and saved my life ( along with the help of my Lord) while in ICU.

So, I think 10 years from 0/2 biopsy to where I am at now is quick.
Current no need for another biopsy the watch now is all about MELD score factors and liver cancer via regular MRI.

[Willy50]

I presented some stats, just because I thought they were compelling.  The problem with loking at the picture is that we must rely on statistics, records and assumptions and they can all be bent a little to provide a sometimes a contrasting portrayal of fact through different interpretation of "facts".

Here is a current article which suggests that things could be getting better;

http://www.hivandhepatitis.com/2008icr/ddw/docs/060608_b.html

I'm no scientist but I wonder how well they screened people in 1994? (from where the earliest of these stats origionated).  The sad fact is that if the data is faulty, then the conclusion reached may also be faulty.

When I was first suspicious that I had HCV I went to visit my a doctor.  I told them I had elevated liver enzymes and that it was possible that I had HCV as I had a few factors of transmission risks in my past.  I had to argue with the guy to test me (he thought my enzymes were too low to merit an elisa test.  When he got the results he failed to mention to me that I had tested "reactive" for HCV antibodies.  I only found this out later, 7 months later, when the CDC called me.  How on top of HCV were doctors in the 90's?  Probably even less schooled than my doctor was.  I really wonder how much you can trust some of these articles.  In a sense, the only thing we can really get a handle on is our own health and liver staging.  

IF we care for ourselves we might expect different results than the aggregate of people who didn't know they had HCV.  On the flip side, the problems experienced by Brent are really chilling.  One never knows whether the damage progression can move so quickly or also whether biopsy interpretations can also play into the equation.  I've heard a few people express that all slides are not interpreted the same, leading to what can appear to be a rapid shift in staging over a few years.  

More questions raised than answers sometimes....

best,
Willy

[IAmTheWalrus]

I think the researchers are putting very precise numbers on the data they have. It still doesn't paint a clear picture, or at least the picture we want to see.

An old saying is, "Measure it with a micrometer, mark it with chalk, and cut it with an axe!"

Nowhere is this fallacy more evident than in the attempt to bend general statistics to an individual case, precise CI's notwithstanding. There are so many things, known and unknown, in each individual case that can work against the odds.
.

[pvk]

If you don't mind my asking, how long exactly did it take for you to get from I to IV?  Did you have any 'symptoms' along the way?

I'm very curious because I'm a stage 1 as of my Sept 06 biopsy, been infected 30+ years, have an opportunity to get into the telaprevir trial, and am having great difficulty deciding what to do.  

Thanks for any personal information you might be willing to share.

  

[somuchmore2]

I agree no one knows after 30+ or 50+ years.

In my case I was told about the 20% but then ramped from stage I to stage IV quickly.

[pvk]

Thanks for posting that, mikesimon.  Although I don't understand the details, it appears to be positive news.  Can anyone explain the numbers?  For example, if the estimated annual mean transition F0>F1 is 0.117, is that saying that 11.7% of the people with F0 today will be F1 in a year?  Or, does it mean that it will take eight to nine years on the average to go from F0 to F1?  Just wondering...

[mikesimon]

That is better than I usually see. That is why I posted it. Since we can't really know how it is going to go we may as well look at favorable information. We might feel a little better. I hope so anyway.
Mike

[mike716]

Gee, I wouldn't know what to do without a Markov maximum likelihood estimation method and a meta-analysis. And boy am I glad that the impact of potential covariates was evaluated using meta-regression. Of course the estimated annual mean stage-specific transition probabilities were based on the random effects model. What else?

So, the prevalence of cirrhosis after 20 years is 16%, 18%, or 7%? That sure is good bad news. Or bad good news, if you like.

I sure gotta hand it to those researchers for providing "increased precision in estimating fibrosis progression". Yippee!

M.

[mikesimon]

It's all a mystery but everything will be revealed in time - if we're just patient. Mike

[mike716]

"Other studies have provided mixed results, indicating both favorable and poor long term prognosis from chronic hepatitis C virus infection"

I'll say they're mixed. "Mixed up" is maybe more like it. Who does these so-called studies? Who controls them? Is this science, or the numbers racket? "Hey, Vito, what's da odds on F4 at fifty? Ya handicappin it? Yeah, yeah, I saw dat story in the Pamona Hepatitis Scratch Sheet, we put dat in there ta get the odds down, sure. Okay, give 'em twenny ta one, but I don't wanna hear no krap from da losers, ya unnerstand me, youse guys? Cause if de odds are fixed it ain't my fault, I'm jus runnin da book."

M.

[mikesimon]

Estimation of stage-specific fibrosis progression rates in chronic hepatitis C virus infection: A meta-analysis and meta-regression.
Thein HH, Yi Q, Dore GJ, Krahn MD.

University Health Network, Division of Clinical Decision‐Making and Health Care Research, Toronto, Ontario, Canada.

Published estimates of liver fibrosis progression in individuals with chronic hepatitis C virus (HCV) infection are heterogeneous. We aimed to estimate stage-specific fibrosis progression rates and their determinants in these individuals. A systematic review of published prognostic studies was undertaken. Study inclusion criteria were as follows: (1) presence of HCV infection determined by serological assays; (2) available information about age at assessment of liver disease or HCV acquisition; (3) duration of HCV infection; and (4) histological and/or clinical diagnosis of cirrhosis. Annual stage-specific transition probabilities (F0-->F1, ... , F3-->F4) were derived using the Markov maximum likelihood estimation method and a meta-analysis was performed. The impact of potential covariates was evaluated using meta-regression. A total of 111 studies of individuals with chronic HCV infection (n = 33,121) were included. Based on the random effects model, the estimated annual mean (95% confidence interval) stage-specific transition probabilities were: F0-->F1 0.117 (0.104-0.130); F1-->F2 0.085 (0.075-0.096); F2-->F3 0.120 (0.109-0.133); and F3-->F4 0.116 (0.104-0.129). The estimated prevalence of cirrhosis at 20 years after the infection was 16% (14%-19%) for all studies, 18% (15%-21%) for cross-sectional/retrospective studies, 7% (4%-14%) for retrospective-prospective studies, 18% (16%-21%) for studies conducted in clinical settings, and 7% (4%-12%) for studies conducted in nonclinical settings. Duration of infection was the most consistent factor significantly associated with progression of fibrosis. Conclusion: Our large systematic review provides increased precision in estimating fibrosis progression in chronic HCV infection and supports nonlinear disease progression. Estimates of progression to cirrhosis from studies conducted in clinical settings were lower than previous estimates. (HEPATOLOGY 2008.).