背景：胰岛素抵抗与丙型肝炎病毒感染相关，是一个已知的对肝纤维化进展及PEG干扰素/利巴韦林治疗后应答的影响条件。目的：本研究旨在评估抗病毒治疗后持续性病毒学应答能否从长远上预防胰岛素抵抗形成。患者及方法：患者是Milan安全耐受研究队列的成员，接受了PEG干扰素α2a/利巴韦林或PEG干扰素α2b/利巴韦林治疗，在基线和治疗结束后24月进行了动态平衡模型评估(HOMA) 。对全部患者（n=431）的肝活检样本进行了分期、分级和脂肪变评估。结果：在基线存在胰岛素抵抗（ HOMA 值大于2）的患者有48位（12%），并发现胰岛素抵抗与体重(P = 0.03)、HCV病毒载量< 0.6 × 10⁶ IU/L (P = 0.006)、纤维化分级≥ 4 (P = 0.01) 及中重度脂肪变相关(P = 0.03)。未发现胰岛素抵抗对治疗结束时应答率(75% versus 69%, P = 0.4) 、持续病毒学应答率 (63% versus 60%, P = 0.8)及复发率(19% versus 24%, P = 0.5)产生影响。治疗后，354位非糖尿病患者中有49（14%）位形成了胰岛素抵抗。SVR患者基线和治疗后HOMA平均值相似(1.11 ± 0.8 versus 1.18 ± 1.1, P = 0.25), 而治疗失败的患者后期随访HOMA平均值显著增加(1.20 ± 0.85 versus 1.49 ± 1.3, P = 0.007)，并且未获得SVR患者新生胰岛素抵抗率高于SVR患者(17% versus 7%, P = 0.007)。 进行logistic 回归分析，发现治疗失败(OR = 2.81, 95% CI = 1.39-5.67, P = 0.004)和体重指数增加10% (OR = 6.42, 95% CI = 1.69-24.3, P = 0.006) 与新发胰岛素抵抗相关。结论：慢丙肝非糖尿病患者经PEG干扰素联合利巴韦林治疗后获得SVR预防新发胰岛素抵抗

吉林大学第一医院肝胆胰内科 吴瑞红 摘译

本文首次发表于[Hepatology, 2012, 56(5):1681-1687]

            Sustained Virological Response Prevents the Development of Insulin Resistance in Patients With Chronic Hepatitis C

Backgrounds：Hepatitis C virus (HCV) infection is associated with insulin resistance (IR), which is a condition known to influence the progression of liver fibrosis and the response to pegylated interferon (PEG-IFN)/ribavirin (RBV) therapy. Aims：We aimed to assess whether a sustained virological response (SVR) after antiviral therapy prevents the development of IR in the long term. Patients and Methods：Members of the Milan Safety Tolerability study cohort, who received PEG-IFNα 2a/RBV or PEG-IFNα2b/RBV, underwent a homeostasis model assessment (HOMA) at the baseline and 24 months after treatment completion. For all patients (n = 431), a liver biopsy sample was scored for grading, staging (Ishak), and steatosis. Results：At the baseline, IR (HOMA value > 2) was detected in 48 patients (12%), and it was associated with body weight (P = 0.03), an HCV load < 0.6 × 10⁶ IU/L (P = 0.006), fibrosis staging ≥ 4 (P = 0.01), and moderate to severe steatosis (P = 0.03). IR did not influence the rates of end-of-treatment response (75% versus 69%, P = 0.4), SVR (63% versus 60%, P = 0.8), or relapse (19% versus 24%, P = 0.5). Results：After treatment, IR developed in 49 of the 354 nondiabetic patients (14%). Although the mean baseline and posttreatment HOMA values were similar in SVR patients (1.11 ± 0.8 versus 1.18 ± 1.1, P = 0.25), patients experiencing treatment failure showed a significant increase in the mean HOMA value at the follow-up visit (1.20 ± 0.85 versus 1.49 ± 1.3, P = 0.007), and there was an increased rate of de novo IR in non-SVR patients versus SVR patients (17% versus 7%, P = 0.007). According to a logistic regression analysis, treatment failure (odds ratio = 2.81, 95% confidence interval = 1.39-5.67, P = 0.004) and a 10% body mass index increase (odds ratio = 6.42, 95% confidence interval = 1.69-24.3, P = 0.006) were significantly associated with the development of de novo IR. Conclusion: In nondiabetic patients with chronic HCV, the achievement of SVR with PEG-IFN and RBV prevents the development of de novo IR. 点击下载此文件