2197. Hepatitis B Reactivation in Patients with Malignancies Undergoing Treatment for Hepatitis C Infection with Direct-Acting Antivirals. (26th November 2018)

• Record Type: Journal Article
• Authors: Pritchard, Haley; Hwang, Jessica P; Torres, Harrys
• Is Part Of: Open forum infectious diseases. Volume 5(2018)Supplement 1
• Page Start: S648
• Page End: S649
• Publication Date: 2018-11-26
• Subjects: Communicable diseases -- Periodicals; Medical microbiology -- Periodicals; Infection -- Periodicals; 616.9
• DOI: 10.1093/ofid/ofy210.1851
• Languages: English
• ISSNs: 2328-8957

Abstract

Abstract: Background: Reactivation of hepatitis B virus (HBV) can occur in patients after cancer therapies. Direct-acting antivirals (DAAs) are the effective therapies for hepatitis C virus (HCV) infection, and HBV reactivation in HCV/HBV co-infected patients treated with DAAs has been reported. We analyzed the risk of HBV reactivation among HCV/HBV co-infected cancer patients being treated with DAAs. Methods: We prospectively followed patients with any type of cancer and HCV treated with DAAs between January 2014 and January 2018 at MD Anderson Cancer Center. Information on demographics, use of radiation, chemotherapy, immunotherapy, or anti-CD20 antibodies, and anti-HBV therapy were collected. All patients had the following tests at baseline, 2 and 4 weeks after initiation of DAAs, at end of treatment (EOT), and 12 weeks after completion of DAAs: alanine aminotransferase, total bilirubin, HBV surface antigen (HBsAg), hepatitis B core antibody (anti-HBc), and HBV DNA and HCV RNA levels. We defined the following outcomes by AASLD-recommended parameters: HBV reactivation (HBsAg reverse seroconversion, HBV DNA >2 log compared with baseline, HBV DNA >3 log if HBV DNA was undetectable, or >4 log if baseline was unavailable), hepatitis flare (ALT increase ≥3 times baseline and >100 U/L), and HBV-associated hepatitis (HBV reactivation and hepatitis flare). Patients were followed for 12 weeks after completion of DAAs. Results: Of 169 cancer patients treated for HCV infection, 2.4% ( n = 4) had chronic HBV infection (HBsAg+/anti-HBc+), and most (3/4) of these were on anti-HBV therapy. Past HBV infection (HBsAg-/HBcAb+) was noted in 30% (51/166), and none received anti-HBV therapy. Of these, 37% (19/51) had cancer therapy within 6 months prior to DAA treatment. HBV reactivation did not occur in any co-infected patients. Two patients had hepatitis flare, but none developed HBV-associated hepatitis. Conclusion: This is the first prospective study evaluating HBV reactivation in HCV/HBV co-infected cancer patients receiving DAAs. The risk of HBV reactivation in these patients seems to be low. Future studies with a larger cohort of co-infected cancer patients allowing personalized risk stratification are needed. Disclosures: J. P. Hwang, Gilead Sciences: Investigator, Grant recipient; Merck & Co., Inc.: Investigator, Grant recipient. H. Torres, Gilead Sciences, Merck & Co., Inc.: Grant Investigator, Grant recipient; Vertex Pharmaceuticals: Grant Investigator, Grant recipient.