Abstract
The aim of this study was to analyze serum changes in mediators of fibrogenesis and in non-invasive markers of liver fibrosis among HIV/HCV-coinfected patients starting maraviroc (MVC)-based antiretroviral therapy. Patients included in this prospective pilot study met the following criteria: (1) HIV-infection, (2) detectable serum HCV-RNA, and ((3) started MVC. Transforming growth factor-β1 (TGF-beta1), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) were measured in serum samples at baseline and 6 months after starting MVC. AST-to-platelet ratio index (APRI) was assessed at the same time points. Twenty-four patients were analyzed. Median (IQR) serum levels at baseline and after 6 months on MVC of TGF-beta1 were 27,295 (20,562–36,844) and 33,753 (18,973–46,130) pg/mL (p = 0.116), of MMP-2 were 216 (186–274) and 241 (194–306) ng/mL (p = 0.247), and of TIMP-1 were 237 (170–284) and 216 (171–271) ng/mL (p = 0.415). APRI levels were 0.99 (0.53–3.46) at baseline and 0.83 (0.48–2.34) at 6 months (p = 0.16). Serum mediators of liver fibrogenesis and fibrosis do not change significantly in HIV/HCV-coinfected patients in the short-term after starting MVC. As TGF-beta1 levels have been shown to increase over time in HCV infection and liver fibrosis worsens rapidly in HIV/HCV coinfection, these parameters seem to evolve in a different way in MVC-treated patients.
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Acknowledgments
This study has been partly supported by grants from Pfizer and the Spanish Health Ministry (ISCIII-RETIC RD06/006). JAP received an intensification grant from the Fundación Progreso y Salud of the Consejería de Salud de la Junta de Andalucía (Reference AI-0021). JAP received an intensification grant from the Spanish Health Ministry (Programa-I3SNS).
Conflicts of interest
Juan Macías has been an investigator in clinical trials supported by Roche, Bristol-Myers Squibb and Abbott Pharmaceuticals. He has received lectures fees from Roche, Gilead, Boehringer Ingelheim and Bristol-Myers Squibb, and consulting fees from Boehringer Ingelheim, Bristol Myers-Squibb, Merck Sharp & Dome and Schering-Plough.
Joaquín Portilla has been an investigator in clinical trials supported by Abbott Pharmaceuticals, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead, GlaxoSmithKline, Janssen Cilag, Merck Sharp & Dome and Roche. He has received lectures or consulting fees from Abbott Pharmaceuticals, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead, GlaxoSmithKline, Janssen Cilag, Merck Sharp & Dome, Roche, and Schering-Plough.
Ignacio de los Santos has been an investigator in clinical trials supported by Roche, Bristol-Myers Squibb and Abbott Pharmaceuticals. He has received lecture fees from Gilead, Boehringer Ingelheim, Jansses-Cilag and Bristol-Myers Squibb, and consulting fees from Boehringer Ingelheim, Bristol Myers-Squibb, and Merck Sharp & Dome.
Antonio Rivero reports having received consulting fees from Bristol-Myers Squibb, Abbott Pharmaceuticals, Gilead, Roche and Boehringer Ingelheim.
Manuel Márquez has been an investigator in clinical trials supported by Bristol-Myers Squibb, Boehringer Ingelheim and GlaxoSmithKline. He has received lectures fees from Gilead, Boehringer Ingelheim, Jansen Cilag, Bristol-Myers Squibb, GlaxoSmithKline and Abbott Pharmaceuticals and consulting fees from Boehringer Ingelheim, Abbott Pharmaceuticals and Merck Sharp & Dome.
Juan A. Pineda reports having received consulting fees from GlaxoSmithKline, Bristol-Myers Squibb, Abbott Pharmaceuticals, Gilead, Merck Sharp & Dome, Schering-Plough, Jansen Cilag and Boehringer Ingelheim. He has received research support from GlaxoSmithKline, Roche, Bristol-Myers Squibb, Schering-Plough, Abbott Pharmaceuticals and Boehringer Ingelheim and has received lecture fees from GlaxoSmithKline, Roche, Abbott Pharmaceuticals, Bristol-Myers Squibb, Gilead, Merck Sharp & Dome, Jansen Cilag, Boehringer Ingelheim and Schering-Plough.
The rest of the coauthors report no conflicts of interest.
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Macías, J., Viloria, M.M., Rivero, A. et al. Lack of short-term increase in serum mediators of fibrogenesis and in non-invasive markers of liver fibrosis in HIV/hepatitis C virus-coinfected patients starting maraviroc-based antiretroviral therapy. Eur J Clin Microbiol Infect Dis 31, 2083–2088 (2012). https://doi.org/10.1007/s10096-012-1546-5
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DOI: https://doi.org/10.1007/s10096-012-1546-5