(INF-P12) A national study of risk for non-liver cancer in people with hepatitis C treated with direct acting antivirals or an interferon-based regimen


Charlotte LybeckInfektionskliniken, ÖrebroÖrebro Universtitet, Universitetssjukhuset i ÖrebroÖrebro1
Daniel BruceScandinavian development servicesStockholm2
Scott MontgomeryAvdelningen för klinisk epidemiologi och biostatistikÖrebro UniversitetÖrebro3
Soo AlemanInstitutionen för medicinKarolinska universitetssjukhuset/Karolinska InstitutetStockholm4
Ann-Sofi DubergInfektionskliniken, ÖrebroÖrebro Universtitet, Universitetssjukhuset i ÖrebroÖrebro1


Background and Aims: Direct acting antivirals (DAA) against hepatitis C virus (HCV) have been shown to have an immune modulatory effect, with a possibly decreased tumour specific CD8 T cell response. Reports indicative of a high risk for hepatocellular carcinoma early after DAA treatment, have raised concerns about an increased risk also for non-liver cancer. Our aim was to study the early incidence of non-liver cancer after initiation of DAA or interferon therapy in a national HCV cohort.

Method: All diagnosed HCV-infected persons in Sweden, their antiviral treatments, non-liver cancer or death/emigration were identified retrospectively, using the national HCV-surveillance register and other national registers. Cox regression was used to compare persons treated with DAAs (n=1,920), interferon (n=2,586) or no HCV therapy (n=13,872) between 2009 and 2015. Persons with a previous cancer diagnosis (5.7%) were studied separately. Age was used as the time-scale, analyses were stratified by sex and adjusted for the Charlson comorbidity index.

Results: In total 492 non-liver cancers were diagnosed. Among persons with no previous cancer, 21, 24 and 177 developed non-liver cancer following DAA, interferon and no treatment, respectively. The corresponding numbers for those with previous cancer were 25, 20 and 225, respectively. The hazard ratios (and 95% confidence intervals) for non-liver cancer in the no previous cancer group are 1.35 (0.66-2.76; p=0.41) for men and 1.75 (0.59-5.18; p=0.31) for women with DAA treatment, compared with interferon treatment. For those with previous cancer, the corresponding hazard ratios are 1.03 (0.41-2.57; p=0.95) for men and 0.86 (0.35-2.13; p=0.75) for women with DAA treatment.

Conclusion: This study did not demonstrate any significantly increased risk for non-liver cancer early after DAA therapy initiation. The hazard ratio was slightly increased among those without previous cancer, but the cancers were few and the results were not statistically significant.

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