Testino Gianni, Ansaldi Filippo, Andorno Enzo, Ravetti Gian Luigi, Ferro Carlo, De Iaco Fabio, Icardi Giancarlo, Valente Umberto
Unit of Hepato-Gastroenterology, S. Martino Hospital, Italy.
Hepatogastroenterology. 2002 Nov-Dec;49(48):1636-8.
BACKGROUND/AIMS: Recent experiences suggest that interferon may significantly decrease the incidence of hepatocellular carcinoma. We conducted a randomized study with interferon versus no therapy in hepatitis C virus Child A cirrhosis with abnormal alanine aminotransferase and HCV-RNA positive serum with the aim to investigate the incidence of hepatocellular carcinoma, worsening of cirrhosis's stage and death or orthotopic liver transplantation.
A cohort of 122 patients prospectively followed was analyzed retrospectively to assess the effect of interferon therapy (mean follow-up: 96 +/- 18.3 months). We only chose patients with hepatitis C virus infection who had undergone blood transfusion before 1980. Hepatitis C virus serotype was determined by hepatitis C virus serotyping 1-6 assay (Murex Biothec Limited Temple Hill, Dartford, Kent, UK). HCV-RNA level was determined by bDNA, Chiron Corporation Emeryville, CA. Diagnosis of hepatocellular carcinoma was made on the basis of the appearance of local lesions at periodic ultrasound examination of the liver and confirmed with spiral computed tomography. Fine needle biopsy under sonographic guidance was effected. Fifty-nine patients (mean age: 55.3 +/- 7) received interferon (3MU three times a week for 12 months), 8 stopped therapy for side effects, 71 did not receive interferon (mean age: 56.8 +/- 8). Baseline characteristics were similar.
It emerges how interferon does not reduce the risk of hepatocellular carcinoma in compensated cirrhosis. In interferon treated patients an improvement in relation with worsening and death/orthotopic liver transplantation has been noted.
The use of the interferon seems to be scarcely useful when structural alterations of the cirrhotic kind show up, as cirrhosis represents by itself a risk factor for hepatocellular carcinoma. Nevertheless, in relation to the worsening of cirrhosis's stage the interferon therapy can be useful in compensated cirrhosis.
背景/目的:近期经验表明,干扰素可能显著降低肝细胞癌的发病率。我们开展了一项针对丙型肝炎病毒Child A级肝硬化且丙氨酸转氨酶异常、血清HCV-RNA阳性患者的随机研究,比较干扰素治疗与不治疗的效果,旨在调查肝细胞癌的发病率、肝硬化分期恶化情况以及死亡或原位肝移植情况。
对前瞻性随访的122例患者进行回顾性分析,以评估干扰素治疗的效果(平均随访时间:96±18.3个月)。我们仅选择1980年前接受过输血的丙型肝炎病毒感染患者。丙型肝炎病毒血清型通过丙型肝炎病毒血清分型1-6检测法(英国肯特郡达特福德坦普尔山的Murex Biothec有限公司)测定。HCV-RNA水平通过加利福尼亚州埃默里维尔的Chiron公司的分支DNA检测法测定。肝细胞癌的诊断基于肝脏定期超声检查中局部病变的出现,并通过螺旋计算机断层扫描确诊。在超声引导下进行细针活检。59例患者(平均年龄:55.3±7岁)接受干扰素治疗(每周3次,每次3MU,共12个月),8例因副作用停止治疗,71例未接受干扰素治疗(平均年龄:56.8±8岁)。基线特征相似。
结果显示,干扰素并不能降低代偿期肝硬化患者患肝细胞癌的风险。在接受干扰素治疗的患者中,已注意到在病情恶化和死亡/原位肝移植方面有所改善。
当出现肝硬化类型中的结构改变时,干扰素的使用似乎几乎没有用处,因为肝硬化本身就是肝细胞癌的一个危险因素。然而,就肝硬化分期恶化而言,干扰素治疗在代偿期肝硬化中可能有用。