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Despite Antiviral Treatment, Liver Cancer Risk Persists
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Despite Antiviral Treatment, Liver Cancer Risk Persists

Despite Antiviral Treatment, Liver Cancer Risk Persists
Researchers have hoped that treating hepatitis B patients with antivirals would reduce both their viral loads and their liver cancer risk. However, a new study that followed 1,378 treated and 1,014 untreated patients over five years found antivirals did not reduce liver cancer rates as hoped.

The study tracked new liver cancer cases among patients infected with the hepatitis B virus (HBV) (average age 47, 65% male) who had been treated primarily with entecavir (Baraclude) for their high viral loads and liver damage. They compared that group's liver cancer occurrence to those of patients whose "inactive" HBV infection did not require treatment.

Among the treated group, 70 patients (6.2%) developed liver cancer during the study period compared to only 11 (1.1%) in the untreated group. Notwithstanding  the ability of antivirals to reduce viral load, a life-long history of HBV infection and liver damage appeared to increase cancer risk, despite the reduction in viral load later in life.

What is especially disappointing is that liver cancer developed even in treated patients who had no history of cirrhosis (severe liver scarring) which increases cancer risk. Among the antiviral-treated patients:

20 of 223 HBeAg-negative patients who had cirrhosis at the start of treatment developed liver cancer.
15 of 316 HBeAg-negative patients who had no cirrhosis also developed liver cancer.
Among the treated patients who developed liver cancer, 30 were positive for the hepatitis B "e" antigen (HBeAg) and 30 were HBeAg-negative.
How well the antiviral worked in patients also determined who remained cancer-free. Of the 246 patients who failed to achieve low or undetectable viral loads as a result of treatment, 36 (18.8%) patients developed liver cancer over the five-year study.

The risk of cancer was increased overall by male gender, underlying cirrhosis and older age in the treated group. Curiously, having high viral loads (HBV DNA) at the start of treatment did not appear to increase liver cancer risk.

The key message for doctors is that liver cancer risk remains despite a dramatic reduction in viral load, researchers noted. "...Patients on (antiviral) treatment that effectively suppressed viral replication are still at higher risk of liver cancer compared with patients with inactive stage chronic hepatitis B," they concluded in the study published in the March issue of the journal Gut.

Persistent liver damage before the start of antiviral treatment, evidenced by elevated alanine aminotransferase (ALT) levels, may predispose patients to liver cancer, they also noted.

"The inactive group may have more intact immune response to HBV and therefore may also have entered the inactive stage early in life, with a shorter period of high viral replication and active hepatitis," they wrote.

Source: www.ncbi.nlm.nih.gov/pubmed/24615378
13 Comments Post a Comment
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Avatar_m_tn
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
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Avatar_m_tn
Baseline viral load must be of significance, why they do not mention about it?
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Avatar_m_tn
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
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Avatar_m_tn
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?
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Avatar_m_tn
of course hbsag level/liver cancer is for hbeag negative only.

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Avatar_m_tn
Age at which srv happened matters a lot in terms of hcc statistics. Clearance before getting 45 seems to be best.
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Avatar_m_tn
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
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Avatar_m_tn
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 ?
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Avatar_m_tn
it is just study results, the reason of these results is not known
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Avatar_m_tn
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.
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Avatar_m_tn
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
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Avatar_m_tn
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?

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Avatar_m_tn
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?
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