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HCC among patients with Entecavir VS Lamivudine
Abstract
Background
& Aims: Little is known about whether the antiviral agent entecavir is more effective than a less potent drug, lamivudine, in reducing the risk of death and hepatocellular carcinoma (HCC) in patients with chronic hepatitis B (CHB).

Methods
We performed a retrospective analysis of data from 5374 consecutive adult patients with CHB, treated with entecavir (n=2000) or lamivudine (n=3374) at a tertiary referral hospital in Seoul, Korea from November 1, 1999 through December 31, 2011. Data were collected from patients for up to 6 years and analyzed by multivariable Cox proportional hazards model for the entire cohort and for propensity score matched cohorts.

Results
During the study period, 302 patients (5.6%) died, 169 (3.1%) received a liver transplant, and 525 (9.8%) developed HCC. Multivariable analyses showed that compared with lamivudine, entecavir therapy was associated with a significantly lower risk of death or transplantation (hazard ratio [HR], 0.49; 95% confidence interval [CI], 0.38–0.64), but a similar risk of HCC (HR, 1.08; 95% CI, 0.87–1.34). In the 1792 overall propensity-matched pairs, entecavir was again associated with a significantly lower risk of death or transplantation (HR, 0.49; 95% CI, 0.37–0.64) and a similar risk of HCC (HR, 1.01; 95% CI, 0.80–1.27). Entecavir also reduced risk of death or transplantation, compared with lamivudine, in 860 pairs of patients with cirrhosis (HR, 0.42; 95% CI, 0.31–0.57) but there were no differences in risk for HCC (HR, 1.00; 95% CI, 0.78–1.28). However, entecavir and lamivudine did not have significantly different effects on clinical outcome in 878 pairs of patients without cirrhosis.

Conclusions
In a retrospective study of 5374 patients with chronic hepatitis B virus infection, entecavir therapy was associated with a significantly lower risk of death or transplantation than lamivudine. However, the drugs did not have different effects on HCC risk.

http://www.sciencedirect.com/science/article/pii/S0016508514002443
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I assume all patients had und viral load if taking  entecavir for long,  would be interesting to see how hbsag levels corresponded to hcc occurrence!
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During the long-term ETV, HBVDNA keeps undetectable, no serious liver damages, how does HCC develops?
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Hbvdna is und in your blood stream but detectable inside liver
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It's already very very low and no abnormal liver damage, why develops HCC? Generally we thought HCC is developing with long-term ALT abnormal?
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Some long-term studies found that even most potent NA (TDF) could not cut risk of HCC. Especially, when we have had this virus for a long time and it already integrated in our genome.

HCC is very complicated if cure (cccDNA - & anti-hbs +) could not achieve, the risk of HCC remains higher.
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What if one of the potential treatments currently being tested actually works to reduce HBsAg significantly, even if not a cure? Would that lower HCC risk significantly?
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The only way to reduce risk significantly is hbsag clearance with or without seroconversion to anti-hbs. Nowadays the only way to obtain that status is through interferon therapy but unfortunately inf doesn't work for everyone.
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As I know, long-term TDF can also reduce cccDNA slowly, by 10 years, reduce to only 1%-10% volume compare with baseline. So HCC risk is reduced?
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Please see this link.

http://www.gastroenterologyupdate.com.au/latest-news/hcc-risk-remains-high-with-hep-b-antivirals
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To be honest, the article is quite general, no detailed information. After 42 months of NUCs, 7.7% patients developed HCC, too general.
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Andrey is correct peg add on is the best solutions and peg is even active on liver tumors so in case of hbsag clearance its effect is very considerable

peg is a tumor therapy for melanoma and other tumors too

it is also interesting to see how nagalase goes once hbsag is cleared, my guess is that presence of nagalase during hbv infection is one of the main tumors effectors, afterall if immune system is fully functional we can have all the hcc we want in the liver...that it will get cleared by the immune system
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By the way any study on nucs with less durability than 10 years is of zero significance for 2 reasons:
tumors take decades to escape immune detection and become visible to us

nucs take at least 5 years to change viral numbers in the liver, i d say even more than 5 years
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Impact of hbv therapy on hcc incidence , very good presentation
http://www.aphc.info/pdf/2014/pleniere_14012014/1430/Massimo_COLOMBO.pdf

Hbsag clearance before being 50 years old seems to have best prognosis. Age at which hbsag was cleared plays very important role.
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From this report we can see ETV or TDF at least reduce HCC risk especially on non-cirrhosis patients. So conflict with the lines above...
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