” The fibrosis index is the stage of liver scarring divided by the number of years the patient has presumably been infected. For example, if someone had a blood transfusion in 1968, and is diagnosed with HCV in 2003, it is presumed that they have been infected for 35 years. If they have a liver biopsy revealing stage 1 fibrosis, their Fibrosis Index is calculated as: stage 1/35 years or 0.029 stages of fibrosis per year infected. This suggests that it will take another 35 years to progress to stage 2."
I have been diagnosed for 3 years and was contemplating starting treatment soon, but since I'm Grade2, Stage 1 and have not changed in 3 years (had another biopsy last week). I'm pretty sure I was infected 25 years ago. Which if this is accurate should means that it will take another 25 years to get to stage 2. I'll be 75 then. I have to admit that I'm terrified of tx. Have a history of intermittent depression and do not tolerate antidepressants at all. I've managed without them well, but the doctors tell me that they want me to start back on them 2 or 3 months before starting tx. Is anyone else out there waiting and do you think this is a well calculated risk at this point?
Thanks for any input.
I have no knowledge/comment on the "fibrosis index" you mention although it does sound interesting. What I do know is that fibrosis progresses differently in different people. That said, from what I've read, if someone was infected at a relatively young age and is only stage 1, 25 years later -- especially if it's a woman -- then the chances are progression is going to be very, very slow, if at all. As to your question, personally I would not treat if in your shoes (never did look good in high heels anyway :) ). But seriously, what I would do would be to take a watch and wait approach, monitoring my liver, including periodic (every 3-5 years) biopsies or alternatively more frequent Fibroscans which hopefully will more or less replace biopsies in the not too distant future.
Sometimes these scales can be deceptive. However, it is a good sign that you've had it for so long and haven't had a fast rate of progression. I've heard that some people never really progress. Then, there are other who go for a long time w/o progressing and then, all of a sudden, start progressing a lot. The best thing to do is weigh all the factors w/you doctor and make the right decision for your life and your situation. I've also heard that after age 50 that the rate of progression and bump up. There's just so much that they don't know. Another thing to consider is that the more years that you have Hep C actively-the more at of risk you get for liver cancer. So, it's in everyone's best interest to try to get an SVR. There are some new treatments coming out in the next 3-5 years, so if you were to wait, you might have a better chance with some of the newer drugs.
also another thing to consider is how HCV effects other organs, i.e. extra hepatic manifestations. like jim said i would wait and monitor LFT's, etc. although they say ALT is not a good indicator of progression if you are in normal range for many years then jump past 100 then i would treat. something to keep your eye on. good luck
Like you, I am Stage 1, Grade 2. , and had this for 30 years or more. I asked my gas. about the stage progression and he said it could take 10 - 20 years to move to stage 2. However, he did add theres really no way to know that for sure. Some people can stay at the same level for years, providing you take care of yourself and don't drink. He also stated once progression starts it could move from stages quickly.
Throughout the years alcohol was a big part of my life and was very surprised there was little damage to my liver. I have quit drinking since finding out I had hep C. If drinking all those years did not cause much damage I figure my odds of stage progression would be slow.
I am going to hold off on treatment unless I can get into VX950 trial. Also will monitor my blood yearly, and get biopsy or fibroscan every 3 years if I do not get into the Vertex trail.
Jim -- She's a kayakgirl. She's not wearing high heels, she's wearing Teva's. (just kiddin' Jim, but we don't all pain ourselves that way)
Hey Kayak girl -- kayaked first time this past weekend on a fast moving river. Supposed to be rated class 1 but had quite a few class 3 rapids because of all the rain we have had in Texas. It was a ball. Now I want to buy one! But seriously, to your question. like Jim, I have never heard of that index. What I have heard is that fibrosis is non-linear -- that is, it may progress slowly for decades and then you may start a quick decline. Also what happens with hep C as we age, is we develop what is called comorbidity. That is, we develop other health issues that may impair the success of treatment such as insulin resistence and auto immune issues. Therefore, one might meet with greater success treating earlier in life.
Progression to Cirrhosis in Hepatitis C Patients: An Age-dependent Process
"Several studies have previously reported an association between age at infection and rate of fibrosis progression,[10–16] with a higher rate of progression in patients with an older age at infection. In a study on 2313 untreated HCV patients, Poynard et al. found that alcohol consumption of 50 g or more per day, and male gender were also independently associated with a faster progression. Viral genotype, however, does not seem to be associated with the rate of fibrosis progression.
The present study reports a median rate of fibrosis progression of 0.13 U of fibrosis/year, giving a median estimated time to cirrhosis of about 31 years, which is very close to what is found by Poynard et al. (0.133 units of fibrosis per year; progression to cirrhosis: 30 years). The rate of progression seems to increase with higher ALT levels, although the difference does not reach statistical significance (P=0.08). The risk of being a fast progressor is increased 4.5-fold if BMI is above 25 kg/m2 but the number of cases analyzed is too small to draw any conclusion. Our study also confirms that the rate of progression increases with age at infection, with a faster progression in older patients. Our results are in agreement with the observation of Poynard et al. showing that age at infection is directly associated with time to cirrhosis. In their study, the authors suggest that fibrosis progression is not linear but shows three phases characterized by little or no progression in the early phase, followed by moderate fibrosis progression in the second phase and finally by rapid fibrosis progression in the late phase of the disease. Patients infected at younger age show a much slower rate of progression from phase 1 to phase 3, whereas patients infected at older ages show a much more rapid progression through these phases. Another prospective study has confirmed that fibrogenesis is not linear but that age is a highly significant risk factor for fibrosis progression in HCV infection, even more closely correlated to fibrosis progression than duration of infection. Thus, there is supportive evidence that age matters considerably but the reason for it, however, remains unclear. As it was recently discussed, one possible explanation is the shortening of hepatocyte telomeres with increasing age leading to hepatocyte senescence, loss of hepatocyte function, exhaustion of hepatocellular regeneration and to a greatly enhanced fibrotic response to injury. Besides hepatocyte senescence, immunosenescence could also play a role. Even though the molecular mechanism behind it remains to be unravelled, it has been observed that HCV-induced liver disease progresses more rapidly in case of immunodeficiency,[19, 20] indicating that immunosenescence might be responsible for faster disease progression in older patients. The current hypothesis for immunosenescence indicates a crucial role of CMV infection,[21, 22] which matches with CMV-infection being a major risk factor for fibrosis progression following HCV recurrence after liver transplantation.[23, 24]
Most reported studies are not population-based but rather represent a selection of patients referred to hepatology centers. Whether the same results would be seen in additional study groups such as the HCV-contaminated anti-D immunoglobulin cohort has to be critically evaluated. These prospective studies have shown that the occurrence of liver cirrhosis was lower than expected.
Even if some factors have been shown to increase fibrosis progression, the key question once a patient is infected by HCV is to estimate when cirrhosis will occur; in other words, how many years will be required before the patient becomes cirrhotic? No previous study has estimated the age at which cirrhosis is likely to occur. In our data, and apart from a particular patient profile (women infected by a non-1 genotype before 37 years of age), it is interesting to note a more or less uniform age at which cirrhosis is expected to occur (65 years). It should be kept in mind, however, that several factors such as heavy alcohol consumption or treatment can accelerate or delay fibrosis progression respectively.
Our results might have important implications in treatment algorithms in terms of when antiviral or eventually antifibrotic treatment needs to be started to prevent development of liver cirrhosis. As a younger age has been reported to be associated with better response to therapy, one strategy is to treat as early as possible to eradicate the virus. On the other hand, given the great improvement in antiviral therapy over the last decade and as further dramatic improvements are expected in the near future, another strategy is to delay therapy until new more efficient drugs become available. Our findings suggest that patient's age should be better taken into account before choosing a therapeutic strategy. A specific active monitoring and a more aggressive therapeutic approach should be adopted in older patients for whom cirrhosis is close in order to prevent progression to end-stage liver disease, especially if there is evidence of significant disease, as it was recently found that treatment of genotype 1 patients with mild disease was not cost-efficient."
Actually I've switched from Teva's to the most awesome flipflops ever... Montrail's :)
Congrats frihole on surviving your whitewater experience. Are you hooked now? The best high there is! And thanks everyone for your input. I have felt so alone with this disease and it's great to have your support and know that you're out there!
Copyright 1994-2016 MedHelp International. All rights reserved.
MedHelp is a division of Aptus Health.
This site complies with the HONcode standard for trustworthy health information.
The Content on this Site is presented in a summary fashion, and is intended to be used for educational and entertainment purposes only. It is not intended to be and should not be interpreted as medical advice or a diagnosis of any health or fitness problem, condition or disease; or a recommendation for a specific test, doctor, care provider, procedure, treatment plan, product, or course of action. Med Help International, Inc. is not a medical or healthcare provider and your use of this Site does not create a doctor / patient relationship. We disclaim all responsibility for the professional qualifications and licensing of, and services provided by, any physician or other health providers posting on or otherwise referred to on this Site and/or any Third Party Site. Never disregard the medical advice of your physician or health professional, or delay in seeking such advice, because of something you read on this Site. We offer this Site AS IS and without any warranties. By using this Site you agree to the following Terms and Conditions. If you think you may have a medical emergency, call your physician or 911 immediately.