Ziada Dina Hazem, El Saadany Sherif, Enaba Mohamed, Ghazy Medhat, Hasan Azza
Department of Tropical Medicine, Tanta University, Tanta, Egypt.
Can J Gastroenterol. 2012 Jun;26(6):325-9. doi: 10.1155/2012/291457.
Hepatitis C virus (HCV) infection may induce insulin resistance (IR) irrespective of the severity of liver disease, and there is evidence of a central role for IR in failure to achieve sustained virological response (SVR) in HCV patients.
To assess IR as a predictor of the severity of hepatic fibrosis in Egyptian HCV patients, and its effect on early viral kinetics and virological response to HCV therapy.
A total of 140 chronic HCV patients were divided into two groups according to the homeostasis model assessment-IR (HOMA-IR). Group 1 consisted of 48 chronic HCV patients with HOMA-IR >=2, and group 2 consisted of 92 chronic HVC patients without IR (HOMA IR <2). All patients were treated with combination therapy (pegylated interferon-alpha 2a plus ribavirin) for 48 weeks and studied for viral kinetics throughout the period of therapy.
The study revealed that older age, higher body mass index and HOMA-IR >=2 were significantly associated with advanced fibrosis. Rapid virological response, complete early virological response and SVR were significantly lower in the IR-HCV group compared with the non-IR-HCV group. Univariate and multivariate analyses revealed that older age, fibrosis (F>=3), high viral load (>600,000 IU⁄mL) and HOMA-IR >=2 were significantly associated with a lack of viral kinetics as well as SVR. However, HOMA-IR >=2 was the main independent variable associated with lack of SVR. On the other hand, body mass index, plasma insulin level and HOMA-IR decreased significantly compared with starting levels in patients who achieved SVR. This suggests a cause and effect relationship between HCV infection and IR.
IR in chronic HCV patients is associated with progressive fibrosis and slow viral kinetics, and could be a predictor for lack of rapid and early virological response. Therefore, HOMA-IR levels should be measured and improved before starting antiviral treatment.
丙型肝炎病毒(HCV)感染可能会引发胰岛素抵抗(IR),而与肝脏疾病的严重程度无关,并且有证据表明IR在丙型肝炎患者未能实现持续病毒学应答(SVR)中起核心作用。
评估IR作为埃及丙型肝炎患者肝纤维化严重程度的预测指标,及其对早期病毒动力学和丙型肝炎治疗病毒学应答的影响。
根据稳态模型评估-IR(HOMA-IR)将140例慢性丙型肝炎患者分为两组。第1组由48例HOMA-IR≥2的慢性丙型肝炎患者组成,第2组由92例无IR(HOMA IR<2)的慢性丙型肝炎患者组成。所有患者接受联合治疗(聚乙二醇化干扰素-α2a加利巴韦林)48周,并在整个治疗期间研究病毒动力学。
研究表明,年龄较大、体重指数较高和HOMA-IR≥2与晚期纤维化显著相关。与非IR-HCV组相比,IR-HCV组的快速病毒学应答、完全早期病毒学应答和SVR显著更低。单因素和多因素分析显示,年龄较大、纤维化(F≥3)、高病毒载量(>600,000 IU/mL)和HOMA-IR≥2与缺乏病毒动力学以及SVR显著相关。然而,HOMA-IR≥2是与缺乏SVR相关的主要独立变量。另一方面,与实现SVR的患者的起始水平相比,体重指数、血浆胰岛素水平和HOMA-IR显著降低。这表明丙型肝炎病毒感染与IR之间存在因果关系。
慢性丙型肝炎患者的IR与进行性纤维化和缓慢的病毒动力学相关,并且可能是缺乏快速和早期病毒学应答的预测指标。因此,在开始抗病毒治疗前应测量并改善HOMA-IR水平。