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HLA-B18 as risk factor of liver fibrosis progression in HIV/HCV treatment-experienced patients

The Pharmacogenomics Journal volume 17, pages 479–480 (2017)Cite this article

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We recently published an association between the presence of human leukocyte antigen-B18 (HLA-B18) and fibrosis progression in HIV/HCV non-cirrhotic patients who had never received treatment for HCV infection.1 We found that 73.2% of HLA-B18pos patients with liver fibrosis showed progression, and only 38.2% of HLA-B18neg patients showed progression of fibrosis in the follow-up period. This fact could have implications for the timing of therapy in patients with absent or minimal liver fibrosis. Nevertheless, the population included in that study consisted only of treatment-naive patients. Patients with interferon-based therapy who experienced treatment failure have shown higher liver fibrosis progression compared with treatment-naive patients.2, 3 Here, therefore, we analyze the role of HLA-B18 in liver fibrosis progression among patients with previous HCV treatment failure.

We retrospectively included HIV/HCV co-infected patients with prior HCV treatment failure attending our hospital between January 2007 and December 2014. Patients who fulfilled the following inclusion criteria constituted the study population: i) Failure associated with PEGylated interferon plus ribavirin with/without boceprevir or telaprevir; ii) detectable HCV-RNA at baseline and during follow-up; iii) two determinations of liver stiffness (LS) separated by at least one year. The exclusion criterion was liver cirrhosis at baseline, defined as LS⩾14.6 kPa. Transient liver elastography (FibroScan, Echosens, Paris) was used to measure LS. The cutoffs used to define the liver fibrosis stage were as follows: <6.5 kPa (F0–F1, minimal or absent fibrosis); 6.5–9.4 kPa (F2, significant fibrosis); 9.5–14.5 kPa (F3, advanced fibrosis) and ⩾14.6 kPa (F4, cirrhosis).4 HLA-B was genotyped. The endpoints were: i) the proportion of patients who increased liver fibrosis by at least one stage, and ii) the proportion of F0–F2 patients who progressed to severe liver fibrosis (F3–F4). Patients were censored for the following reasons: i) achievement of the outcome variable; ii) initiation of new HCV treatment, including combinations; iii) loss to follow-up; and iv) end of study (31 December 2014).

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References

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Acknowledgements

The authors thank Laura Ruiz and Ismael Zafra for their technical support in this study. This study was funded by the Fundación Progreso y Salud, Consejería de Salud de la Junta de Andalucía (grants for health research projects: 0430/2012), the ISCIII-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo (ISCIII-RETIC RD06/006 and RD12/0017).

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Authors and Affiliations

  1. Infectious Diseases Unit, Hospital Universitario Reina Sofía de Córdoba, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Universidad de Córdoba (UCO), Cordoba, Spain

    M Frías, D Rodríguez-Cano, F Cuenca-López, A Gordon, Á Camacho, J Torre-Cisneros, A Rivero-Juárez & A Rivero

  2. Infectious Diseases and Microbiology Unit, Hospital Universitario de Valme, Seville, Spain

    J Macías & J A Pineda

  3. Immunology Unit, Hospital Universitario Reina Sofía de Córdoba, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Universidad de Córdoba (UCO), Cordoba, Spain

    B Manzanares-Martín & J Peña

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  1. M Frías
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Corresponding author

Correspondence to A Rivero-Juárez.

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Competing interests

AR received consulting fees from Bristol-Myers Squibb, Abbott, Gilead, Roche, Boehringer Ingelheim, GlaxoSmithKline, Merck Sharp & Dohme, and Janssen-Cilag. He also received lecture fees from GlaxoSmithKline, Roche, Abbott, Bristol-Myers Squibb, Boehringer Ingelheim and Schering-Plough. The remaining authors declare no conflict of interest.

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Frías, M., Rodríguez-Cano, D., Cuenca-López, F. et al. HLA-B18 as risk factor of liver fibrosis progression in HIV/HCV treatment-experienced patients. Pharmacogenomics J 17, 479–480 (2017). https://doi.org/10.1038/tpj.2016.80

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