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. 2016 Oct 17;11(10):e0162965.
doi: 10.1371/journal.pone.0162965. eCollection 2016.

Antiviral Treatment of HCV-Infected Patients with B-Cell Non-Hodgkin Lymphoma: ANRS HC-13 Lympho-C Study

Affiliations

Antiviral Treatment of HCV-Infected Patients with B-Cell Non-Hodgkin Lymphoma: ANRS HC-13 Lympho-C Study

Laurent Alric et al. PLoS One. .

Abstract

Hepatitis C virus (HCV) infection is associated with lymphoproliferative disorders and B-cell non-Hodgkin lymphomas (B-NHLs). Evaluation of the efficacy and safety profiles of different antiviral therapies in HCV patients with B-NHL is warranted.

Methods: First, we evaluated the sustained virologic response (SVR) and safety of Peg-interferon-alpha (Peg-IFN) + ribavirin +/- first protease inhibitors (PI1s) therapy in 61 HCV patients with B-NHL enrolled in a nationwide observational survey compared with 94 matched HCV-infected controls without B-NHL. In a second series, interferon-free regimens using a newly optimal combination therapy with direct-acting antiviral drugs (DAAs) were evaluated in 10 patients with HCV and B-NHL.

Results: The main lymphoma type was diffuse large B-cell lymphoma (38%) followed by marginal zone lymphoma (31%). In the multivariate analysis, patients with B-NHL treated by Peg-IFN-based therapy exhibited a greater SVR rate compared with controls, 50.8% vs 30.8%, respectively, p<0.01, odds ratio (OR) = 11.2 [2.3, 52.8]. B-NHL response was better (p = 0.02) in patients with SVR (69%) than in patients without SVR (31%). Premature discontinuation of Peg-IFN-based therapy was significantly more frequent in the B-NHL group (19.6%) compared with the control group (6.3%), p<0.02. Overall, survival was significantly enhanced in the controls than in the B-NHL group (hazard ratio = 34.4 [3.9, 304.2], p< 0.01). Using DAAs, SVR was achieved in 9/10 patients (90%). DAAs were both well tolerated and markedly efficient.

Conclusions: The virologic response of HCV-associated B-NHL is high. Our study provides a comprehensive evaluation of different strategies for the antiviral treatment of B-NHL associated with HCV infection.

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Conflict of interest statement

L. Alric has received consulting and lecturing fees from Bristol-Myers Squibb, Gilead, Roche, Schering-Plough/Merck, Abbott/AbbVie, and grants from Bristol-Myers Squibb, Gilead, Roche and Merck. S. Pol has received consulting and lecturing fees from Bristol-Myers Squibb, Boehringer Ingelheim, Tibotec, Vertex, Gilead, Roche, Schering-Plough/Merck, Novartis, Abbott/AbbVie, Sanofi and Glaxo Smith Kline, and grants from Bristol-Myers Squibb, Gilead, Roche and Merck/Schering Plough. P. Cacoub has received consulting and lecturing fees from Bristol-Myers Squibb, Gilead, Roche, MSD, Servier, and Vifor. D. Bonnet, C. Besson, N. Lapidus, J. Jeannel, J.M. Michot, D. Canioni, F. Davi, P. Rabiega, L. Ysebaert and O. Hermine declare that they do not have anything to disclose regarding conflict of interest with respect to this manuscript. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

Figures

Fig 1
Fig 1. Flowchart.
Peg-interferon-alpha (Peg-IFN), B-cell non-Hodgkin lymphoma (B-NHL) First generation of protease inhibitors (PI1s), Direct-acting antiviral drugs (DAAs).
Fig 2
Fig 2. Sustained virologic response of the patients from the cohort treated by Peg-IFN-based therapy, * p< 0.02.
First generation of protease inhibitors (PI1s). A: global sustained virologic response. B: sustained virologic response according to HCV genotype.
Fig 3
Fig 3. Haematological response of the patients from the B-NHL group treated by Peg-IFN-based therapy with or without sustained virologic response, * p = 0.02.
Fig 4
Fig 4. Overall survival of the patients with B-NHL and controls.

References

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