459. Effect of Sorafenib on Hepatitis C Viremia in Cirrhotic Patients with Hepatocellular Carcinoma
Session: Poster Abstract Session: Hepatitis C
Thursday, October 27, 2016
Room: Poster Hall
Background:

Sorafenib is a kinase inhibitor approved for the treatment of advanced primary liver cancer. It also inhibits hepatitis C Virus (HCV) replication in vitro through different mechanisms including alteration of viral entry into the cells and interruption of production of viral particles. In clinical practice, conflictive results have been reported on the antiviral activity of sorafenib in HCV-infected patients with hepatocellular carcinoma (HCC). Herein, we aimed to study the effect of sorafenib on HCV viremia in such patient population.

Methods:

HCV-infected HCC patients presenting to MD Anderson Cancer Center between 11/2012-3/2016 were enrolled in a prospective observational study. Only viremic patients with HCC receiving sorafenib were included. HCV-RNA levels were measured before, during and after sorafenib administration. Since chronically infected patients have stable HCV RNA levels that only varies ∼0.5 log10 IU/m, a significant change in HCV viremia was defined as a variation of HCV-RNA ≥ 1 log10IU/ml from baseline following sorafenib therapy.

Results:

Sixteen patients were studied. The majority were men (75%), white (68%) and had HCV genotype 1 (68%). None of these patients received antiviral therapy along with sorafenib. Mean duration of sorafenib treatment was 14 months (range, 2 - 41 months). Mean HCV RNA was 6.3 log10IU/ml (range, 4.2 – 7.2) before sorafenib therapy (baseline) and 5.9 log10IU/ml (range, 4.4 – 6.5) at the end of such therapy. The variation between baseline and nadir viral loads was 0.89 log10IU/ml (range, 0.05 – 4.2). A significant change in viral load was noted in 5 patients (31%), mainly at week 4 of treatment with a mean viral load of 4.7 log10IU/ml (1.5 - 6.2) and a mean decline of 1.6 log10IU/ml compared to baseline levels. These changes were not sustained after 4 weeks of treatment. Viral load became undetectable in one patient at week 12 of treatment before returning to its baseline level after discontinuing sorafenib.

Conclusion:

Sorafenib is a weak inhibitor of HCV replication in infected patients with HCC. However, further research will determine if the addition of direct-acting antiviral agents to sorafenib could improve the virologic outcome of this difficult-to-treat group of cirrhotic patients with HCC.

Jeff Hosry, MD1, Ahmed Kaseb, MD2, Minas P. Economides, MD1, Manal Hassan, MD2 and Harrys Torres, MD, FIDSA1, (1)Infectious Diseases, The University of Texas MD Anderson Cancer Center, Houston, TX, (2)Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX

Disclosures:

J. Hosry, None

A. Kaseb, Bayer: Investigator , Research support
Amgen: Investigator , Research support
Pfizer: Investigator , Research support
Merck: Investigator , Research support
BMS: Investigator , Research support

M. P. Economides, None

M. Hassan, None

H. Torres, Gliead Sciences: Investigator and Scientific Advisor , Research grant
Merck & Co.: Investigator and Scientific Advisor , Research grant
Vertex Pharmacuticals: Investigator and Scientific Advisor , Research grant
Janssen Pharmaceuticals: Scientific Advisor , Consulting fee
Genentech: Scientific Advisor , Consulting fee
Novartis: Scientific Advisor , Consulting fee
Astellas Pharma: Scientific Advisor , Consulting fee
Pfizer: Scientific Advisor , Consulting fee

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