Mazzella G, Accogli E, Sottili S, Festi D, Orsini M, Salzetta A, Novelli V, Cipolla A, Fabbri C, Pezzoli A, Roda E
Cattedra di Gastroenterologia, University of Bologna, Chieti, Italy.
J Hepatol. 1996 Feb;24(2):141-7. doi: 10.1016/s0168-8278(96)80022-5.
BACKGROUND/AIMS: The aims of alpha-interferon treatment for chronic viral liver infections are clearance of the virus and healing of the disease. Hepatocellular carcinoma is a complication of viral cirrhosis; but it is not yet known whether treatment of viral cirrhosis with alpha-interferon prevents this complication.
The incidence and the risk (Cox regression analysis) of developing hepatocellular carcinoma were calculated in 347 patients with hepatic cirrhosis; 227 (34 hepatitis B virus and 193 hepatitis C virus related) were treated with alpha-interferon and 120 (28 hepatitis B virus and 92 hepatitis C virus) did not receive this treatment, in order to evaluate the efficacy of alpha-interferon in the prevention of hepatocellular carcinoma. In all patients, the cirrhosis was well compensated (Child A).
Over mean follow-up periods of 49 months for hepatitis B virus and 32 months for hepatitis C virus, 20/347 patients (6/62 hepatitis B virus and 14/285 hepatitis C virus) developed hepatocellular carcinoma. The risk of developing this tumor was significantly greater in males (p < 0.007) and in patients not treated with alpha-interferon (p < 0.01). The Relative Risk of developing hepatocellular carcinoma increased significantly (p < 0.0002) with each passing year. In patients with hepatic cirrhosis secondary to hepatitis B virus infections, the risk did not seem to be modified by alpha-interferon treatment, even though a greater, but not significant risk (Relative Risk = 4.9; p = 0.3) was calculated for untreated patients; in contrast, in hepatitis C virus-related cirrhosis, this risk was reduced by a factor of 4.0 (p = 0.04). The tumor developed only in non-responder patients regardless of virus type. After adjustment for confounding factors (sex, age, alcohol consumption, cigarette smoking), a statistically significant (p < 0.025) effect of interferon treatment in preventing hepatocellular carcinoma was still demonstrated when responders were matched with controls, but not when responders were compared with non-responders.
These results show that, in addition to its ability to halt the progression of viral-induced liver disease, alpha-interferon is also of benefit in patients with hepatitis C virus cirrhosis who respond to this treatment by lowering their risk of developing hepatocellular carcinoma.
背景/目的:α-干扰素治疗慢性病毒性肝感染的目的是清除病毒和治愈疾病。肝细胞癌是病毒性肝硬化的一种并发症;但尚不清楚用α-干扰素治疗病毒性肝硬化是否能预防这种并发症。
计算347例肝硬化患者发生肝细胞癌的发生率和风险(Cox回归分析);227例(34例乙型肝炎病毒相关和193例丙型肝炎病毒相关)接受α-干扰素治疗,120例(28例乙型肝炎病毒相关和92例丙型肝炎病毒相关)未接受该治疗,以评估α-干扰素预防肝细胞癌的疗效。所有患者的肝硬化均为代偿良好(Child A级)。
乙型肝炎病毒感染患者的平均随访期为49个月,丙型肝炎病毒感染患者为32个月,347例患者中有20例(乙型肝炎病毒感染62例中的6例,丙型肝炎病毒感染285例中的14例)发生肝细胞癌。男性(p < 0.007)和未接受α-干扰素治疗的患者(p < 0.01)发生这种肿瘤的风险显著更高。每年发生肝细胞癌的相对风险显著增加(p < 0.0002)。在乙型肝炎病毒感染继发的肝硬化患者中,α-干扰素治疗似乎并未改变风险,尽管未治疗患者的风险更高但不显著(相对风险 = 4.9;p = 0.3);相反,在丙型肝炎病毒相关的肝硬化中,这种风险降低了4.0倍(p = 0.04)。无论病毒类型如何,肿瘤仅在无应答患者中发生。在对混杂因素(性别、年龄、饮酒、吸烟)进行调整后,当将应答者与对照组匹配时,仍显示干扰素治疗在预防肝细胞癌方面具有统计学显著(p < 0.025)的效果,但当应答者与无应答者进行比较时则不然。
这些结果表明,除了能够阻止病毒诱导的肝病进展外,α-干扰素对丙型肝炎病毒肝硬化且对该治疗有应答的患者也有益处,可降低其发生肝细胞癌的风险。