Also agree this article is very incomplete. Inactive group seems to have very low hcc but what exactly do they mean by inactive in this study?
I think the info is incomplete. Some questions to be answered:
1) did the hcc inceptions start before, during or after DNA UND by treatment?
2) what were the health state for treatment group before treatment? I believe they were weaker than inactive group
3) how many years did the treatment last? Does long term viral suppression help?
no i think it is more correlated with immune function decline, after 50yo the immune system is much much weaker and even acute hbv has a very high death rate in very old people
also the increase of hcc on cirrhosis might be due to weak immune system, cirrhotics are severely immune suppressed with even bacteria superinfections
i experienced this immune suppression myself with never ending flu infections, candida and so on
but all this is just a guess we have no data to confirm this....my idea is we have it since birth so i dont think the 50yo limit can be due to more or less hbv integration
It seems like if we have this virus in our liver for decade, it is more likely that cccDNA will integrate into our genome.
So, it is reasonable that if you have this for a long time, it is greater risk to embed into your gene.
it is just study results, the reason of these results is not known
Can you explain why age matters that much that seems there is no point to clear hbsag after 50 yo ? If in future myrrcludex or replicor hit the market these drugs will be of no use for hcc lowering in patients over 50 yo also ?
yes of course hbsag clearance is the best endpoint this is welknown since decades for lowest risk of any related liver disease
clearance after 50yo does not lower risk
Age at which srv happened matters a lot in terms of hcc statistics. Clearance before getting 45 seems to be best.
of course hbsag level/liver cancer is for hbeag negative only.
So if patient cleared hbsag then should be at very minimum risk right? Have you seen studies on patients cleared hbs in relation to hcc?
they even found high viral load baseline has lower cancer risk
to me it is hbsag and liver immune suppression to drive everything, there was even an animal or vitro study who found cancer regression just lowering hbsag
Baseline viral load must be of significance, why they do not mention about it?
there are studies already with direct correlation hbsag level and liver cancer risk with lowest cancer risk on hbsag less than 1000iu/ml.
since inactive carriers have hbsag less than 1000iu/ml they should make this research on hbsag levels and liver cancer risk.it would be good to check also nagalase and liver cancer risk but i dont think they will never check this, they had decades to check it and never did