OBJECTIVES: We investigated the influence of hepatitis C virus (HCV) therapy with pegylated interferon-α plus ribavirin on cardiovascular disease risk through the serial measurement of several laboratory markers in HCV-monoinfected and HCV/HIV-coinfected patients. METHODS: In a longitudinal study, biomarkers of inflammation, coagulation and oxidative stress were measured during and after therapy. RESULTS: A total of 56 patients were included; 32 (57.1%) were HCV/HIV coinfected and 24 (42.9%) were HCV monoinfected. Compared with baseline, during HCV therapy there was a significant decrease in the concentrations of matrix metalloproteinase-9 (P < 0.001), intercellular cell adhesion molecule-1 (ICAM-1) (P ≤ 0.01) and oxidized low-density lipoproteins (P = 0.002). In contrast, levels of vascular cell adhesion molecule-1 (VCAM-1), monocyte chemotactic protein-1 and fibrinogen increased during treatment. After treatment discontinuation, levels of ICAM-1, VCAM-1 and tumour necrosis factor-α were significantly lower compared with baseline, a change restricted to patients with sustained virological response. Decreases in transaminases and HCV-RNA from baseline correlated positively with the decrease in ICAM-1 concentration 6 months after treatment discontinuation. Changes in biomarkers were similar in HIV-infected and -uninfected patients. CONCLUSIONS: Treatment for HCV induces different changes in several cardiovascular risk biomarkers, most being anti-atherogenic effects, although only the anti-atherogenic effects remain after treatment discontinuation in patients with sustained virological response.
OBJECTIVES: We investigated the influence of hepatitis C virus (HCV) therapy with pegylated interferon-α plus ribavirin on cardiovascular disease risk through the serial measurement of several laboratory markers in HCV-monoinfected and HCV/HIV-coinfectedpatients. METHODS: In a longitudinal study, biomarkers of inflammation, coagulation and oxidative stress were measured during and after therapy. RESULTS: A total of 56 patients were included; 32 (57.1%) were HCV/HIV coinfected and 24 (42.9%) were HCV monoinfected. Compared with baseline, during HCV therapy there was a significant decrease in the concentrations of matrix metalloproteinase-9 (P < 0.001), intercellular cell adhesion molecule-1 (ICAM-1) (P ≤ 0.01) and oxidized low-density lipoproteins (P = 0.002). In contrast, levels of vascular cell adhesion molecule-1 (VCAM-1), monocyte chemotactic protein-1 and fibrinogen increased during treatment. After treatment discontinuation, levels of ICAM-1, VCAM-1 and tumour necrosis factor-α were significantly lower compared with baseline, a change restricted to patients with sustained virological response. Decreases in transaminases and HCV-RNA from baseline correlated positively with the decrease in ICAM-1 concentration 6 months after treatment discontinuation. Changes in biomarkers were similar in HIV-infected and -uninfected patients. CONCLUSIONS: Treatment for HCV induces different changes in several cardiovascular risk biomarkers, most being anti-atherogenic effects, although only the anti-atherogenic effects remain after treatment discontinuation in patients with sustained virological response.
Authors: Kara W Chew; Lei Hua; Debika Bhattacharya; Adeel A Butt; Lorelei Bornfleth; Raymond T Chung; Janet W Andersen; Judith S Currier Journal: Open Forum Infect Dis Date: 2014-12-03 Impact factor: 3.835
Authors: Carlo Torti; Vincenzo Scaglione; Bruno Mario Cesana; Chiara Costa; Nadia Marascio; Elisabetta Schiaroli; Chiara Busti; Sabrina Bastianelli; Maria Mazzitelli; Enrico Maria Trecarichi; Daniela Francisci Journal: Health Sci Rep Date: 2021-05-02
Authors: Lauren E Kushner; Aaron M Wendelboe; Laura C Lazzeroni; Aarthi Chary; Mark A Winters; Anu Osinusi; Shyam Kottilil; Michael A Polis; Mark Holodniy Journal: PLoS One Date: 2013-04-04 Impact factor: 3.240