1829. Determinants of Response to Pegylated Interferon and Ribavirin for Acute Hepatitis C Virus Infection in Patients with Human Immunodeficiency Virus
Session: Oral Abstract Session: Hepatitis C
Saturday, October 5, 2013: 3:00 PM
Room: The Moscone Center: 250-262
Background: Acute hepatitis C virus (HCV) treatment success rates are high in HIV-infected MSM with peginterferon (pIFN) and ribavirin (R), but a substantial portion still fail.  Direct-acting antiviral (DAA) use has been reported in acute HCV.  Since available DAAs may increase drug interactions and side effects, predicting which patients will fail treatment with pIFN/R could better inform use of DAAs in this population.

Methods: From 2004-13, 75 HIV-infected MSM with acute HCV were treated with pIFN/R via ongoing NYC cohort studies, with SVR data available on 57 subjects. Subjects were: median age 40.5 years, 18% black, 82% white, 25% Hispanic. All but 5 were genotype 1. Median pre-treatment CD4 was 559 cells/μL, 72% were on ARVs, 60% had HIV RNA <200 copies/mL.  52% with available IL28 data were genotype CC.  Via conditional logistic regression, risk factors for failure to achieve rapid virologic response (RVR) and SVR were assessed.

Results: 58% and 32% of subjects did not achieve RVR and SVR, respectively.  While all 25 subjects with RVR achieved SVR, 18/32 subjects without RVR did not.  Factors associated with failure to achieve RVR were: CD4 (OR 1.4 per 100 cells/mL decrease (CI 1.4 – 1.8), p 0.10), pre-treatment HCV RNA >106 IU/mL (22.5 (5.6 – 90.4), <0.001), peak HCV RNA >106 IU/mL (13 (3.1 – 55.1), 0.001), nadir HCV RNA >105 IU/mL (15.6 (4.0 – 61.5), <0.001), HCV viral load flux <1 log (1.8 (1.2 – 2.7), 0.009), duration of HIV > 8 years (3.1 (1.0 – 9.2), 0.045), time to HCV treatment >12 weeks (2.6 (0.9 – 7.7), 0.092). In multivariate analysis, the duration of HIV > 8 years and baseline HCV RNA <106 remained significant for failure to achieve RVR.  All non-genotype 1 subjects achieved an SVR.  Predictors of not achieving an SVR included: IL28B genotype (OR 2.8 (95% (0.8–9.7), p 0.096), CD4 (1.31 per 100 cells/mL decrease (0.99–1.72), 0.053), pre-treatment HCV RNA >106 (7.3 (1.8 – 29.8), 0.005), peak HCV RNA >106 (10.9 (1.3–91.3), 0.027), nadir HCV RNA >105 (6.5 (1.6–27.1), 0.010).  In multivariate analysis, IL28 genotype and baseline HCV RNA <106 were predictive of failure to achieve SVR.

Conclusion: In patients with poor prognostic predictors as described above, the addition of a DAA to pIFN/R should be considered from time of initiation of treatment or if no RVR is achieved.

Leah Burke, MD1, Daniel Fierer, MD2, David Cassagnol, M.S.3, Rosanne Hijdra, B.S.4, Wouter Van Seggelen, M.D.4 and Kristen Marks, MD5, (1)Infectious Diseases, New York Presbyterian Hospital - Weill Cornell, New York, NY, (2)Mt. Sinai Sch. of Med., New York, NY, (3)Weill Cornell Medical College, New York, NY, (4)Amsterdam Medical Center, Amsterdam, Netherlands, (5)Medicine, Division of Infectious Diseases, Weill Medical College of Cornell University, New York, NY

Disclosures:

L. Burke, None

D. Fierer, None

D. Cassagnol, None

R. Hijdra, None

W. Van Seggelen, None

K. Marks, None

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