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Hepatitis C virus infection is associated with endothelial dysfunction in HIV/hepatitis C virus coinfected patients

de Castro, Isabel Fernándeza; Micheloud, Darielaa,b; Berenguer, Juanc; Guzmán-Fulgencio, Maríaa; Catalán, Pilard; Miralles, Pilarc; Álvarez, Emilioe; López, Juan Carlosc; Cosín, Jaimec; Lorente, Raquelf; Muñoz-Fernández, M Ángeles; Resino, Salvadora

doi: 10.1097/QAD.0b013e32833ce54d
Clinical Science

Objective: To quantify serum levels of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in HIV/HCV coinfected patients to examine their association with several clinical and epidemiological characteristics and the therapeutic responsiveness to interferon (IFN)-α and ribavirin therapy (IFN-α + RBV).

Design: Retrospective study.

Methods: We carried out a cross-sectional study with 183 IFN-α-naive patients on HAART, and 24 healthy controls. We also analyzed 30 out of 183 patients on IFN-α + RBV for the duration of 48 weeks.

Results: HIV/HCV coinfected patients had higher levels of sICAM-1 and sVCAM-1 than the healthy control group (P < 0.05). Patients with HCV-genotype 1, advanced fibrosis (F≥3) or moderate to severe activity grade (A≥2) had the highest values of sICAM-1 and sVCAM-1. When we carried out a multivariate analysis, we found a significant positive relationship between both HCV-genotype 1 and advanced fibrosis (F≥3) with sICAM-1 (R = 0.549; P < 0.001); and a significant positive relationship between HCV-genotype 1 and advanced fibrosis (F≥3) with sVCAM-1 (R = 0.624; P < 0.001). We also found a positive relationship of sICAM-1 or sVCAM-1 levels with transaminases and alkaline phosphatase circulation levels (P < 0.05). Nonresponder patients had higher sICAM-1 and sVCAM-1 serum levels, and patients with sustained virologic response had significantly lower levels of sICAM-1 (P = 0.001) and sVCAM-1 (P = 0.019).

Conclusion: HIV and HCV coinfection induces alterations in sICAM-1 and sVCAM-1 serum levels, which were higher in patients with HCV-genotype 1 and advanced stage of HCV infection. However, response to IFN-α + RBV may reduce these cardiovascular risk markers.

aLaboratory of Molecular Epidemiology of Infectious Diseases, National Centre of Microbiology. Instituto de Salud Carlos III, Majadahonda, Spain

bInternal Medicine Department, Spain

cInfectious Diseases-HIV Unit, Spain

dMicrobiology Department, Spain

ePathology Department, Spain

fMolecular Immunobiology Laboratory, Hospital General Universitario ‘Gregorio Marañón,' Madrid, Spain.

Received 12 February, 2010

Revised 10 May, 2010

Accepted 6 June, 2010

Correspondence to Salvador Resino, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda); Carretera Majadahonda-Pozuelo, Km 2.2; 28220 Majadahonda, Madrid, Spain. Tel: +34 918 223 266; fax: +34 915 097 946; e-mail: sresino@isciii.es

This work has been accepted as a poster presentation at the CROI 2010: Fernández de Castro I, Berenguer J; Micheloud D, Catalán P, Miralles P, Álvarez E, Lorente R, Muñoz-Fernández MA, Resino S. HIV and hepatitis C infection induce endothelial dysfunction in HIV/HCV coinfected patients. 17th Conference on Retroviruses and Opportunistic Infections (CROI 2010). San Francisco, USA. February 16–19, 2010.

© 2010 Lippincott Williams & Wilkins, Inc.