Histological benefits of virological response to peginterferon alfa-2a monotherapy in patients with hepatitis C and advanced fibrosis or compensated cirrhosis

Histological benefits of virological response to peginterferon alfa-2a monotherapy in patients with hepatitis C and advanced fibrosis or compensated cirrhosis
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DOI:
10.1111/j.1365-2036.2008.03620.x
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发表时间:
2008-04-01
影响因子:
7.6
通讯作者:
Heathcote, E. J.
Heathcote, E. J.
中科院分区:
医学1区
文献类型:
--
作者:
Everson, G. T.;Balart, L.;Heathcote, E. J.

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慢性丙型肝炎病毒合并晚期纤维化或肝硬化的患者有疾病进展和肝脏失代偿的危险。目的探讨聚乙二醇干扰素α -2a(90或180 μ g/周)或干扰素α -2a(300万单位,每周3次)治疗48周对配对活检患者肝脏组织学的影响。方法分别于治疗前和治疗结束后6个月行肝活检。比较组织学和病毒学反应。结果获得持续病毒学应答的患者(n = 40)在纤维化(-1.0,P < 0.0001)和炎症(-0.65,P < 0.0001)方面表现出最大的改善。在治疗期间清除丙型肝炎病毒,但后来复发的患者(n = 59),在纤维化(-0.04,P < 0.0001)和炎症(-0.14,P = 0.0768)方面的改善较少。无应答者(n = 85)炎症或纤维化无明显改善。多元回归分析显示,促进纤维化改善的唯一因素是持续的病毒学反应(vs.无反应,P = 0.0005; vs.复发,P = 0.7525)和体重指数
Background Patients with chronic hepatitis C virus and advanced fibrosis or cirrhosis are at risk for disease progression and hepatic decompensation.Aim To determine the effects on hepatic histology of treatment with peginterferon alfa-2a (90 or 180 mu g/week) or interferon alfa-2a (3 million units three times weekly) for 48 weeks in patients with paired biopsies.Methods Liver biopsies were obtained at baseline and 6 months after end of treatment. Histological and virological responses were compared.Results Patients attaining sustained virological response (n = 40) demonstrated the greatest improvements in fibrosis (-1.0, P < 0.0001) and inflammation (-0.65, P < 0.0001). Patients who cleared hepatitis C virus during treatment, but later relapsed (n = 59), experienced less improvement in fibrosis (-0.04, P < 0.0001) and inflammation (-0.14, P = 0.0768). Nonresponders (n = 85) showed no significant improvement in inflammation or fibrosis. Multiple regression analysis showed that the only factors contributing to improvement in fibrosis were sustained virological response (vs. nonresponder, P = 0.0005; vs. relapse, P = 0.7525) and body mass index