Anticarcinogenic impact of interferon on patients with chronic hepatitis C: a large-scale long-term study in a single center.

Anticarcinogenic impact of interferon on patients with chronic hepatitis C: a large-scale long-term study in a single center.
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DOI:
10.1159/000087268
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发表时间:
2006-01-01
期刊:
影响因子:
4.6
通讯作者:
Kumada, Hiromitsu
Kumada, Hiromitsu
中科院分区:
医学4区
文献类型:
--
作者:
Ikeda, Kenji;Arase, Yasuji;Kumada, Hiromitsu

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背景:干扰素(IFN)的抗癌能力在一组日本慢性丙型肝炎患者中进行了评估。患者和方法:对2166例慢性丙型肝炎患者的肝癌发生率进行了分析,其中1654例接受了IFN治疗,512例未接受IFN治疗。结果:在第5年末,治疗组和未治疗组的粗肝癌发生率分别为2.6和4.6%,第10年时为5.8和12.7%,第15年时为13.9和23.9%(治疗组完成IFN治疗后)(p < 0.001)。在多变量分析中,IFN将癌变风险比降低至0.42 (p < 0.001),校正了纤维化分期、γ -谷氨酰转肽酶水平、性别、血小板计数和年龄等重要协变量。在接受IFN治疗的1,654名患者中,606名(36.6%)丙型肝炎病毒(HCV) RNA持续丢失,另外266名(16.1%)丙氨酸转氨酶在完成IFN治疗后6个月或更长时间内没有HCV RNA丢失,达到正常水平。在第5年末,持续病毒学应答者和生化应答者的累积肝癌发生率分别为1.4和2.0%,第10年末为1.9和3.6%,第15年末为1.9和7.5%。持续病毒学反应的风险比为0.10 (p < 0.001),生化反应的风险比为0.12 (p < 0.001)。IFN治疗后,血清HCV RNA不减少的情况下,转氨酶水平的正常化降低了肝癌的发生。结论:IFN在日本整体上显著降低了慢性丙型肝炎患者的肝癌发生率,即使是那些不能从血清中清除HCV RNA的患者。
BACKGROUND: The anticarcinogenic capacity of interferon (IFN) was assessed in a cohort of Japanese patients with chronic hepatitis C en masse.PATIENTS AND METHODS: The rate of hepatocarcinogenesis was analyzed in 2,166 patients with chronic hepatitis C, of whom 1,654 had received IFN therapy while 512 had not.RESULTS: Crude rates of hepatocarcinogenesis in treated and untreated patients were 2.6 and 4.6% at the end of the 5th year, 5.8 and 12.7% at the 10th year and 13.9 and 23.9% at the 15th year (after completion of IFN therapy for those treated) (p < 0.001). IFN decreased the hazard ratio of carcinogenesis to 0.42 (p < 0.001) in multivariate analysis with adjustments for significant covariates including fibrotic stage, gamma-glutamyl transpeptidase level, gender, platelet count and age. Among the 1,654 patients treated with IFN, 606 (36.6%) achieved persistent loss of hepatitis C virus (HCV) RNA and an additional 266 (16.1%) gained normal levels of alanine aminotransferase without loss of HCV RNA for 6 months or longer after the completion of IFN therapy. Cumulative rates of hepatocarcinogenesis in sustained virological responders and biochemical responders were 1.4 and 2.0% at the end of the 5th year, 1.9 and 3.6% at the 10th year and 1.9 and 7.5% at the 15th year, respectively. The hazard ratio of sustained virological response was 0.10 (p < 0.001), and that of biochemical response was 0.12 (p < 0.001). Normalization of aminotransferase levels after IFN therapy without loss of serum HCV RNA decreased hepatocarcinogenesis.CONCLUSION: IFN significantly decreased the rate of hepatocarcinogenesis in patients with chronic hepatitis C as a whole in Japan, even in those who fail to clear HCV RNA from serum.