Infectious Diseases Unit, Hospital General Universitario de Elche, Elche, Alicante, Spain.
J Antimicrob Chemother. 2011 Aug;66(8):1861-8. doi: 10.1093/jac/dkr202. Epub 2011 May 28.
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.
In a longitudinal study, biomarkers of inflammation, coagulation and oxidative stress were measured during and after therapy.
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.
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.
通过连续测量 HCV 单感染和 HCV/HIV 共感染患者的几种实验室标志物,研究聚乙二醇干扰素-α联合利巴韦林治疗丙型肝炎病毒 (HCV) 对心血管疾病风险的影响。
在一项纵向研究中,在治疗期间和治疗后测量了炎症、凝血和氧化应激的生物标志物。
共纳入 56 例患者;32 例(57.1%)为 HCV/HIV 共感染,24 例(42.9%)为 HCV 单感染。与基线相比,在 HCV 治疗期间,基质金属蛋白酶-9(MMP-9)(P<0.001)、细胞间黏附分子-1(ICAM-1)(P≤0.01)和氧化型低密度脂蛋白(oxLDL)(P=0.002)的浓度显著降低。相反,在治疗期间血管细胞黏附分子-1(VCAM-1)、单核细胞趋化蛋白-1 和纤维蛋白原的水平增加。治疗停止后,与基线相比,ICAM-1、VCAM-1 和肿瘤坏死因子-α的水平显著降低,这种变化仅限于持续病毒学应答的患者。治疗结束时转氨酶和 HCV-RNA 从基线的下降与治疗结束后 6 个月时 ICAM-1 浓度的下降呈正相关。在 HIV 感染和未感染患者中,生物标志物的变化相似。
治疗 HCV 会引起几种心血管风险生物标志物的不同变化,大多数是抗动脉粥样硬化作用,尽管只有持续病毒学应答患者在治疗停止后仍保持抗动脉粥样硬化作用。