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livers arn't usually at risk of cancer unless some damage has already been done...just becouse we clear the virus does not mean all damage will disapear all the time...it's like a scar any where else on your body...these celluar changes open you up to the possibitlity of HCC, more so than the average person...so they always will want you to have fetoprotien blood tests periodically and occassional c-sans or mri type imaging done...
if your biopsy showed no damage when you got it done...keep in mind that your liver is a big organ and they only biopsied a very small portion...this means there could be some scarred areas that it missed and they are just being careful...
if you are getting these tests that is good...that means if they see something in there or numbers getting high they can discover the cancer befor it spreads and remove it...so that is the worse case senario...
all of us should have these checkups regularly instead of assume we will completely rid ourselves of all scar tissue after clearance of hcv...
all above is my oppinion based on my reading...i am no dr.just giving it my best shot....hope it helps...perhaps others will know more and have articles...and correct me if i'm mistaken...
Whatever, I know it’s clear! This road has sure been worth it. Thanks everyone and Never give up.
Tony
i figured all this out by trying to figure out how my mom died of liver cancer after being off alchohol for 20 years...
had her drs been as smart as your she'd be alive today...but, no one kept an eye on her liver or alt ast or fetoprotien...what a shame...
sounds like you have a protective dr...so that is a reason to rejoice...and by the way..... MAJOR CONGRADULATIONS ON CLEARANCE!!!!!...THIS PUTS YOU IN THE "NOT LIKELY" TO DEVELOP ANY FUTURE LIVER PROBLEMS CLUB!!!!
I have always followed you bill sense way back when cause we were the same genotype...i didn't clear though and am going on try 2 with higher dose interferon...
BLESSINGS TO YOU!!! FOR YOUR NEW HEP FREE LIFE!!! NOW YOU CAN BLEED ON ANYONE YOU WANT!!!:o)
<u>mrbill</u> - just think about it - you and SVR are now best buds!!!
<u>freedomsoon</u> - and you are mere inches away from calling SVR your own!!! One thing you should ask for when you get your next round of testing done (in a few weeks) is to have them do a qualitative test on you - which is a very sensitive (in many cases more sensitive and accurate than a PCR and TMA) test that will tell you a 'Yes' or a 'No' as to the presence (or lack there of) of any HCV virus in your blood. At this stage of your treatment (nearly 6 months post-tx) you are no longer most concerned as to how much virus is in your bloodstream, as to being more concerned as to is there ANY virus in the bloodstream. In other words - who cares about measuring the overall numbers of virons when the more important question is: Is there any there at all?
TnHepGuy
GODBLESS
MRBILL
this is pure elation!
enjoy your freedom.
mr bill
I found an italian article about cirhhosis (at an early stage, that’s my case) and prevention of liver cancer. I’ll try to translate the lines that might be interesting also for you. the bibliography (what I have noted with numbers in brackets) is in the classic (not on-line) shape, but I believe it should not be difficult to find the articles at any medical library and maybe also on the web (I haven't searched).
The complete article is available here:
http://www.med.unifi.it/didonline/Anno-IV/spec-medchirII/oncologiamed/HCCMARA.htm
I understand that you have NO cirhhosis. But please take note that this article (in another section) quotes the mere INFECTION by HEP C as a major risk factor for hepatocellular carcinoma, together with other ones like cirrhosis or alcohol abuse. My opinion is that as long as the exams are non-invasive, like ultra-scan or blood tests, one may wisely do them. A last recommendation that I just got from my hepatologist: even in the case that you result positive to alphafetoprotein, don’t panic. That test often gives a false-positive result and so every positive must be checked again before one starts to get worried.
here come the article excerpts:
“Probably hepatic cirrhosis represents the most important risk factor for hepatocellularcarcinoma (HCC = liver cancer) in the human being. The cumulative incidence risk at 5 years is between 15 and 20 %. (1).
The annual incidence of HCC in patients with cirhhosis HBV correlated is 2%, and this value decreases to 0.4/0.8 % when the infection occurred without sclerogenic hepatopathy. IN THE CASE OF HEPATIC CIRRHOSIS HCV CORRELATED, THE ANNUAL RISK IS BETWEEN 3 AND 8 %. (1)
[...Early diagnosis of] all cirrhotic patients represents the only strategy that can potentially reduce mortality for HCC, as it can spot the cancer at an early stage. (2)
Currently ultrasound is the most recommended test (sensitivity = 71%, specificity 93%), together with alpha-fetoprotein (sensitivity = 39-64%, specificity =76-91%) every six months. In this way 40-80% of cancers are diagnosed at the stage of solitary knot, even if only the half of them will be able to be treated radically. (2)
(1)
Bruix J, Sherman M, Llovet J, Beaugrand M, Lencioni R, Burrhoughs A, Christensen E,
Pagliaro L, Colombo M, Rodes J. Clinical Management oh Hepatocellular Carcinoma. Conclusions of
tha Barcelona-2000 EASL Conference. Journal of Hepatology 35 (2001) 421-430
(2)
Ryder SD Guidelines for the diagnosis and treatment of hepatocellularcarcinoma (HCC) in
adults GUT 2003; 52 (Suppl III) : iii1-iii8
~dtr.
Your five month result pretty much tells the story. You will get a more definitive result at the six month point by doing a 'Qualitative' test as TnHepGuy suggested. My doc has both a super-sensitive qualitative AND quantitative test done for me, at each testing interval post-tx. Both tests measure down to 5 IU/ml. Just to be 100% sure, these would be good tests to do at the 6 month point...especially the qualitative.
By most patients experiences, if you have <200 IU/ml. after five months the 99.99% odds are that it IS gone! Almost always the virus rebounds quickly to pre-tx load levels, or higher within a few months after tx. The sensitive test will give you the definitive answer, so I would push for a <5 IU, OR <10 IU 'qualitative' test....and if the doc will allow you...also a similarly sensitive 'quantitative' test....to confirm each other's result.
Breathe much easier at this point....the odds look better than great!!!!
Congratulations!!!!!!!
With your history of little or no damage, you should be in great shape regardless....but err on the cautious side if anything......there is still lots that we do NOT know about the effects of this virus...and the interferon tx! Our systems may well be altered in substantial ways that may call for much more attention to health and moderation.
My very best wishes to you..... I know you must feel like crying and celebrating...at the same time!!!!!
Doubledose
all the best to you guys and try not to worry to much about other things that follow enjoy the moment. We can all slip on a banana peel and go tomorrow so don't worry.
Bob L
<b>Duke Researchers Show How Hepatitis Infection Leads To Liver Cancer</b>
DURHAM, N.C. -- Hepatitis B and C infections slowly eat away at a person's liver, severely damaging liver function and greatly increasing the risk of liver cancer. Now researchers at Duke University Medical Center have discovered the hepatitis virus makes the liver into a cancer time bomb by converting the organ into billions of cancer-prone cells.
The finding, published in the Sept. 16 issue of the Proceedings of the National Academy of Sciences, demonstrates that once a hepatitis infection takes hold in the liver, even apparently healthy cells have lost one of two copies of a protective tumor suppressor gene called M6P/IGF2R, making them highly vulnerable to further genetic damage. Without a working copy of this suppressor gene, cancerous cell growth can't be stopped.
"This finding demonstrates that hepatitis infection somehow favors survival of a subset of liver cells that are defective in a key cancer protective gene we know is an early marker for development of liver cancer," said Randy Jirtle, lead investigator of the study. "This is a first step in understanding how the hepatitis virus damages the liver and greatly increase the chance of developing liver cancer."
In addition, he said a test for the gene may help surgeons determine how much tissue surrounding cancerous liver lesions needs to be removed. Some of that "normal-looking" tissue may already be on the path to cancer, he said.
The discovery is particularly relevant because hepatitis, particularly hepatitis C, is responsible for about 85 percent of liver cancer cases in the United States. The Centers for Disease Control and Prevention (CDC) estimates that 3.9 million Americans are infected with hepatitis C. Complications from hepatitis C are blamed for 10,000 deaths per year, but the CDC estimates the fatality rate could triple or quadruple within 15 years.
There is no effective treatment for hepatitis C, which is transmitted through contaminated blood. Most people become infected through intravenous drug use, which accounts for half of all infection. But nearly half of the people who become infected have no identifiable risk factors. Eighty percent of those who become infected develop chronic hepatitis, in which symptoms may be vague or missing for a decade or more.
During this silent period, the viral infection is slowly killing off healthy liver cells. The cells that remain, the researchers discovered, are genetically damaged, but still capable of regenerating the liver. The result is that much of the liver becomes a clone of genetically identical pre-cancerous cells. Eventually, one of those cells may sustain additional genetic damage during its normal function of detoxifying chemicals. Since these cells are already cancer-prone, they may not be able to "fix" the genetic damage, said Jirtle, and they become cancerous tumors.
The research was supported by a grant from the National Institutes of Health, and in part by Sumitomo Chemical Co. and Zeneca Pharmaceuticals. The research team included Jirtle, professor of radiation oncology at Duke; Tomoya Yamada of Sumitomo Chemical Co., Osaka, Japan; Angus De Souza of Zeneca Pharmaceuticals, Cheshire, U.K.; and Sydney Finkelstein of the University of Pittsburgh Medical Center.
Previous studies by Duke researchers showed the tumor suppressor gene M6P/IGF2R, which stands for mannose 6-phosphate/insulin-like growth factor II receptor, is often mutated in early-stage liver tumors, demonstrating that it plays an important role in the initial progression to liver cancer. The new study now links loss of the gene to hepatitis infection.
Normally, people have two copies of this cancer-fighting gene. Even if one copy of the gene has a mutation, the other good copy can usually compensate. But when the remaining good copy becomes deleted through a second mutation, the protein's tumor-fighting ability is lost completely.
The M6P/IGF2R protein is present in all cells of the body, where it performs several important functions that control cell growth, Jirtle said. It deactivates the potent growth promoter, IGF2, and it helps to activate a potent growth inhibitor called transforming growth factor beta 1 (TGFB1).
Hepatitis infection may favor survival of defective cells that lack one copy of this growth inhibitor gene because these cells have a growth advantage, Jirtle said. Another possibility is that these cells are somehow protected from viral infection, he said.
"Our finding that M6P/IGF2R inactivation is an early event in the development of liver cancer may provide a powerful approaches for diagnosis and treatment of liver cancer," said Jirtle. "We now have a marker for one of the earliest events in the progression to liver cancer in hepatitis-infected patients."
http://www.sciencedaily.com/releases/1997/09/970920100223.htm
Maj Neni