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Changes in patient backgrounds may increase the incidence of HCC after SVR in
the era of IFN-free therapy for HCV - Letter to the Editor
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Hepatology May 2 2016
Hidenori Toyoda, hmtoyoda@spice.ocn.ne.jp
Takashi Kumada, hosp3@omh.ogaki.gifu.jp
Toshifumi Tada, tadat0627@gmail.com
Department of Gastroenterology, Ogaki Municipal Hospital, Ogaki, Japan
To the Editor,
We read with interest the study by El-Serag et al. on the incidence of
hepatocellular carcinoma (HCC) in hepatitis C virus (HCV)-infected patients who
achieved sustained virologic response (SVR), the eradication of HCV [1]. As in
previous reports [2,3], they reported that high age and the presence of cirrhosis at SVR
were two important factors associated with high likelihood of the development of HCC
after SVR. These were also unfavorable factors for achieving SVR in interferon
(IFN)-based antiviral therapy for HCV, and therefore there was a lower percentage of
patients with high age or cirrhosis among those who achieved SVR by IFN-based
therapy.
With the emergence of direct-acting antiviral drugs and IFN-free therapy as a
standard antiviral therapy for HCV, patients with high age or cirrhosis can also achieve
SVR at similar rates as younger patients or those without cirrhosis, because of the high
tolerability and antiviral efficacy of these drugs. This has resulted in dramatic changes
in the backgrounds of patients who achieve SVR, and consequently, may change the
incidence of HCC after SVR.
We compared age and the presence of cirrhosis between two groups treated at our
institution (located in Japan): 578 patients who achieved SVR by IFN-based therapy between 1990 and 2012, and 413 patients who achieved SVR by IFN-free therapy between 2014 and 2015 (Table 1). The percentages of patients who were older than 65 and those who had cirrhosis were significantly higher in the IFN-free group (both, p<0.0001). The annual incidence of HCC after SVR was calculated based on patient age and the presence of cirrhosis using the incidences reported by El-Serag et al., and was found to be 0.28-.035% among patients who achieved SVR by IFN-based therapy, which was compatible with their report. In contrast, the estimated annual incidence of HCC after SVR in patients who achieved SVR by IFN-free therapy was 0.62-0.85% (Table 1). The annual incidence of HCC after SVR in patients receiving IFN-free therapy may be more than two-fold higher than that in patients achieving SVR by IFN-based therapy.
There will be factors other than age and cirrhosis that can influence the incidence
of HCC after SVR. The backgrounds of patients with SVR by IFN-based and IFN-free therapies will vary among countries. In addition, it is unclear whether the eradication of HCV by these two treatment types will have same impact on the suppression of HCC development after SVR. Nonetheless, changes in the backgrounds of patients with SVR in the era of IFN-free therapy may change the incidence of HCC after SVR. The incidence of HCC after SVR may increase in the near future with the use of IFN-free therapy in some countries. Conversely, an analysis of changes in the backgrounds of SVR patients can contribute to the estimation of the incidence of HCC after SVR.
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