慢性丙型病毒性肝炎患者抗病毒期间血清肝纤维化指标的变化

Alteration of the serum fibrosis markers in chronic hepatitis C patients with antiviral therapy

目的观察慢性丙型病毒性肝炎(CHC)患者抗病毒治疗期间血清肝纤维化指标的变化情况。方法 52例慢性丙型病毒性肝炎患者均接受聚乙二醇干扰素联合利巴韦林治疗,根据治疗效果分为试验组(持续病毒学应答组)39例和对照组(非持续病毒学应答组)13例,观察2组治疗前、治疗24周、治疗结束时以及结束后24周血清透明质酸、层粘连蛋白、Ⅲ型前胶原肽、Ⅳ型胶原蛋白的水平。结果试验组治疗结束时,层粘连蛋白为102.00(92.00,108.00)ng·m L^(-1),Ⅲ型前胶原肽为62.00(14.00,92.00)ng·m L^(-1),Ⅳ型胶原蛋为白63.00(57.00,70.00)ng·m L^(-1);停药后24周,透明质酸为62.00(59.00,81.00)ng·m L^(-1),层粘连蛋白为92.00(81.00,98.00)ng·m L^(-1),Ⅲ型前胶原肽为56.00(15.00,80.00)ng·m L^(-1),Ⅳ型胶原蛋白为55.00(50.00,62.00)ng·m L^(-1),与治疗前相比,差异有统计学意义(P<0.05)。结论聚乙二醇干扰素联合利巴韦林治疗丙型病毒性肝炎,随着病毒的抑制,血清肝纤维化指标明显下降,表明干扰素联合利巴韦林对慢性丙型肝炎肝纤维化的发生和发展有改善作用。

Objective To analyze the alteration of the serum fibrosis markers in chronic hepatitis C （CHC） patients with antiviral therapy. Methods Serum hyaluronic acid （ HA）, laminin （ LN）, Ⅲ procollagen protein （ PC Ⅲ） and Ⅳ collagen （ Ⅳ - C ） were detected in 52 patients with chronic hepatitis C treated with peginterferon plus ribavirin. According to the virological response, the patients were divided into treatment group（ sustained virological response group, 39 patients） and control group（ non sustained virological response group, 13 patients）. The serum fibrosis markers of the two groups were recorded before treatment, 24 weeks, the end of treatment and 24 weeks after the end of treatment. Results After treatment, the levels of LN, PC Ⅲ and Ⅳ - C in treatment group were 102.00 （ 92. 00,108.00 ） , 62. 00 （ 14.00,92. 00 ） , 63.00 （57.00,70. 00 ） ng · mL^- 1, respectively. At 24 weeks after treat- ment, the levels of HA, LN, PC2 and 3- C in treatment group were 62.00（59.00, 81.03）, 92.00 （81.00,98.03）, 56.00 （ 15.03, 80. 03）, 55.00（50. 03,62. 03） ng · mL^-1 , respectively, had significant difference with before treatment （P 〈 0. 05 ）. Conclusion The levels of serumfibrosis markers decreased significantly in CHC patients achieving sustained virological response, which demonstrated that pegylated interferon and ribavirin could slow down the development and progression of liver fibrosis in hepatitis C.