Very sad. He was very brave, courageous and selfless… Very, very sad…

It is interesting. There is an association between increased coffee consumption and better liver health, mentioned in studies, yes. But, in my understanding, “association” itself does not mean “causative relation”. Is “reverse” causal relation possible? For example, people having healthier liver, without cirrhosis – may just better tolerate coffee (and, consequently, may have statistically higher coffee consumption).

Yes, pack of straws is more peaceful analogy… Great movie, great guitar…

Gaj
Sorry if “russian roulette” analogy seems as some “over-melodramatic” “negative connotation” or something like that. I had read mentioned by you Dr.James’s posting with similar analogy and decided that this analogy is ok for this forum.

James, thank you. Yes, probably we spoke about different studies. Some studies show 7% initial risk, some studies show only 3% risk (as cited by you http://ilc-congress.eu/high-rate-cancer-recurrence-hepatitis-c-patients-despite-successful-virus-eradication-direct-acting-antiviral-therapy/) for “HCC-naive” patients. Situation seems not well-studied yet…

Regarding to additional 3% mortality risk with interferon, if i correctly understand, this finding was made in Cochrane analysis of HALT-C and EPIC3 trials (http://www.cochrane.org/CD003617/LIVER_interferon-for-interferon-nonresponding-and-relapsing-patients-with-chronic-hepatitis-c). But these trials used long-term (during 3 years, for example) “supportive” interferon monotherapy treatment for patients with cirrhosis. Of course, interferon is a serious medication with many side effects, and its long-term (for several years) administration with cirrhosis may cause decompensation and/or additional mortality risk. But, if I correctly understand, this does not mean that “short” courses of interferon (for example, 12-24 weeks) will give similar 3% of additional mortality.

Another question is possible – if we possibly have initial 7% blip of HCC risks after treatment, then, does it mean that treatment with DAAs with cirrhosis looks like some sort of “Russian roulette” game with 1 “HCC-bullet” per 13 empty chambers?

James, thank you. Yes, I agree that “There are no right answers, only informed speculation”. There is a situation of uncertainty… But possible 7% blip with subsequent 3% rate seems quite high compared to results of HCC risks after SVRs, achieved with interferon-ribavirin treatment (1-1.4%). Is it possible that interferon-ribavirin treatment is more safe in terms of HCC risks? Probably, it may be possible – because we did not hear about increased HCC risks after interferon-induced SVRs. If it is correct, then more safe (than DAAs-only) treatment in terms of HCC risks may be possible.

Is it possible that combinations of interferon-ribavirin with DAAs (for example, sof-peg-rib) are more safe than “DAAs-only regimens” in terms of HCC risks?

One thing that seems to getting missed is that most of that 7% was made up of 21% of people who HAD PREVIOUSLY HAD AN HCC.

Could you please clarify – what is the reason for such conclusion? In a study http://dx.doi.org.sci-hub.cc/10.1016/j.jhep.2016.07.027 with 7.4% HCC occurence rate “Those with “non-characterized nodules” and a previous diagnosis of HCC were excluded.”

Hi Gaj!

So 6.6% dropping to 1.9% may indicate an increased initial risk followed by a rapid decline….or it may just be within the normal spread of statistical data over any period of time.

Yes, I am not sure about this too. Drugs are under review by european regulator now, and, hope, we will have some decision and additional information in near future. Personally, I decided to wait, at least several months. Of course, I had read https://fixhepc.com/forum/experts-corner/320-why-am-i-afraid-to-take-the-medications.html#2770 – but this posting was written before emerging of data of possibly increased risk of HCC occurence/recurrence shortly after DAA treatment with cirrhosis. If there is an increased possibility (for example, 1:13 chance) of getting HCC in first year after treatment, then decision looks not so obvious for my situation (“well-compensated” cirrhosis during 10 years).

Then have a look at the graph marked DC below that one which shows a large and continuing decrease in the rates of liver decompensation for this same group of patients…

Yes. But if we will focus on question whether benefits of treatment outweigh harm or not, probably, we need to take into account that treatment itself may cause decompensation in some cases, mostly in sub/decompensated cirrhosis. For example, one study (http://www.natap.org/2015/EASL/EASL_34.htm) show that albumin < 35 or age > 65 in Child B or C cirrhosis are associated with more risks than benefits in terms of liver function, measured by MELD score. This may be a cause of recommending treatment after liver transplantation for some patients, for example. Each case is individual…

P.S. If you feel that discussing of possibility of increased HCC occurence (not only HCC recurrence) after DAA treatment in cirrhotics is some “offtopic” in this thread – please feel free to edit my messages.

Hi beaches,

of course, patients with cirrhosis have some risk of HCC (several percents per year)… But main question – whether treatment is worse than disease or not… Sofosbuvir was approved in 2013 – and many people was treated with DAAs during 2013-2016 (and earlier, in clinical trials). Hope that retrospective studies are possible to determine HCC risk after DAA treatment.

most people with HCV develop cirrhosis and HCCs.

If i correctly understand, from point of view of current medical evidence this is not correct. “The majority of patients with chronic HCV infection are fortunate not to develop cirrhosis and the need for liver transplantation” (http://www.journal-of-hepatology.eu/article/S0168-8278(13)00598-9/fulltext ) In some studies, there are such data that only 20% (or something like that) of HCV-infected will develop decompensated cirhhosis and/or HCC during lifetime without treatment. Really, we dont know this percent with 100% certainty – because this requires very long observation (lifetime long), and virus was discovered only several decades ago. Also, there are many contributing factors which affects fibrosis progression – alcohol consumption, body weight…