Updated data re hepatocellular carcinoma recurrence post DAA

[lporterrn]

For those of you who heard the EASL data regarding hepatocellular carcinoma recurrence post DAA treatment, this suggests we don't have enough evidence to make the connection:
http://www.natap.org/2016/HCV/061716_01.htm][url]http://www.natap.org/2016/HCV/061716_01.htm[/url]

[Philadelphia]

Interesting! The link is a little funky - any chance you can edit it?

[KimInTheForest]

Here is an unfunkied version of the link:

http://www.natap.org/2016/HCV/061716_01.htm

[Philadelphia]

I mean ... I like funk, I'm all for funk. But I prefer it in my music not my links. Thanks Kim.

[lporterrn]

Thanks Kim - I am on vacation and losing my media skills. 

[Lynn K]

FUNKY 

[Mike716]

For those of you who heard the EASL data regarding hepatocellular carcinoma recurrence post DAA treatment, this suggests we don't have enough evidence to make the connection:
[url]http://www.natap.org/2016/HCV/061716_01.htm]http://www.natap.org/2016/HCV/061716_01.htm][url]http://www.natap.org/2016/HCV/061716_01.htm[/url]

I take exception, lporterrn, with your statement above regarding these studies, that "we don't have enough evidence to make the connection" between DAAs and recurring HCC. It suggests that there is a connection but that we simply haven't enough evidence yet to prove it. I read the French paper and, on the contrary, the French study presents plenty of evidence, more and more convincing than the study presented at EASL or the others with similar conclusions, that it is simply untrue.

In support of its contrary conclusion (that DAA treatment does not increase the risk of recurrence of HCC), the French study states: "The prospective follow-up of a large number of patients included in three distinct cohorts of patients reflecting various clinical profiles ensures the quality of our analyses and the confidence in our conclusions."

The heading of the NATAP webpage cited above - "Lack of evidence...(etc.)" - is misleading. Not finding evidence that supports a certain conclusion, after a broad and in-depth study searching for such evidence, is not the same thing as "lack of evidence" or "we don't have enough evidence".

In scientific matters it pays to be careful with language. Catch-phrases like "lack of evidence" can easily be misused. Scientific studies are often done to disprove a certain hypothesis by looking for evidence of it and, finding none, concluding it thereby disproved. This in no way suggests that there was any "lack of evidence" in the study. A double negative is positive. If evidence means anything, a thorough study finding no evidence to show that x is negative is a partial proof, at the very least, that x is not negative. To say that there was no evidence to support such a conclusion is absurd.

After reading the French study, I believe we can safely say that the information presented at EASL was based on an insufficient and inaccurate study, and that, so far as we know, treatment with DAAs does not increase the risk of a recurrence of HCC.

[Mike716]

I neglected to mention that I found the French paper's discussion of possible errors in procedure leading to mistaken conclusions in previous studies highly interesting. It is worth a read, for anyone concerned with this rather serious subject.

[Philadelphia]

I interpreted what Lucinda said very differently to you. My take on her words was that she was saying was that the quoted French study was showing the original study by Buonfiglioli did not have enough evidence. If that makes sense ...

[Mike716]

If that makes sense ...

Yeah, well, it sorta makes sense, Philly. :-)

The point I was trying to make is that they all present evidence, it's just that not all of them present valid evidence. The French study was done very well and its conclusions are justified. The others weren't done well and their conclusions aren't justified.

If you read the French paper I think you will find their discussion of the faults of the previous studies particularly interesting. For example, the study presented at EASL included patients who had received non-curative HCC treatments, that is, patients who had HCC after Tx with DAAs not because the DAAs promoted HCC but because they were never cured of their pre-existing HCC.

In any case, there's plenty of evidence floating around, it's just that some of it is tosh. If you get my point.

M.

[Mugwump]

What would be more informative is a study of how the level of liver damage in general increases the risks of HCC. If there is a comparison of rates of HCV infected individuals who have less liver damage and then go on after cure to develop HCC in comparison to those who have greater liver damage.

Either way some of the data seems to indicate that some people lose their ability to effectively fight off HCC post treatment and this is a huge concern. It is looking more and more like curing HCV does effect the human immune system in ways that we do not completely understand.

My suspicion is that the levels of natural cancer fighting interferon are effected by a sudden proportional increase in healthy liver cells. And those who have cells that are already becoming pre cancerous then do not have as great an ability to clear the troubled cells.

It is ironic that it is the death of liver cells that triggers interferon production and is a natural mechanism to fight off whatever agents are causing the liver cells to die. Essentially, to some extent, it was the death of liver cells that helped keep HCV in check, just perhaps it also kept HCC in check as well.

There is so much to learn about liver chemistry and we are just starting to understand the extremely complex interdependent nature of how the organ works.