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目的 观察合并庚型肝炎病毒 (HGV)感染在慢性乙型肝炎 (CHB)患者肝脏病变中的远期作用 ,并探讨HGV致病性。方法 选择 5年前后根据自愿原则以Menghini法行两次肝穿刺活体组织学检查的CHB患者 45例 ,其中应用免疫组织化学过氧化物酶与抗过氧化物酶复合物 (PAP)法检测肝组织中HGVNS5抗原 (HGV Ag)两次均阳性的患者 (合并HGV感染组 ) 2 1例、两次均阴性的患者 (未合并HGV感染组 ) 2 4例。两组患者 5年前年龄、性别、病程、血清HBV DNA含量、肝脏损害等方面的差异均无显著意义 ,治疗方法亦相同 ,但均未能产生持续疗效 ,具有可比性。回顾性对比分析两组患者 5年后肝脏病理学变化。结果 合并与未合并HGV感染组 5年前肝脏损害的基本病变、炎症活动度 (G1、G2、G3、G4例数分布分别为 3、7、7、4;5、8、7、4)及纤维化程度 (S1、S2、S3、S4分别为 4、7、7、3;6、8、6、4)差异无显著意义 (P >0 .0 5 ) ,5年后 (G1、G2、G3、G4分别为 3、5、7、6 ;4、6、8、6 ;S1、S2、S3、S4分别为 3、6、5、7;4、7、5、8)差异仍无显著意义 (P >0 .0 5 )。结论 合并HGV感染并未导致CHB肝脏病变激活、加速纤维化进展。HGV感染对CHB肝脏远期病变无明显作用。HGV的肝脏致病性至多是微弱的。
Objective To investigate the long-term effects of hepatocellular carcinoma (HGV) infection on liver lesions in patients with chronic hepatitis B (CHB) and to investigate the pathogenicity of HGV. Methods Fifty-five patients with CHB who underwent liver biopsy twice a year by Menghini method were selected according to the voluntary principle five years later. The liver tissues were detected by immunohistochemistry and anti-peroxidase complex (PAP) 21 patients with positive HGVNS5 antigen (HGV Ag) two times (with HGV infection) and 24 patients with negative HGV infection (without HGV infection). There was no significant difference between the two groups in their age, sex, course of disease, serum HBV DNA content and liver damage 5 years ago. The treatment methods were also the same, but they failed to produce sustained effect and were comparable. Retrospective analysis of two groups of patients after 5 years of liver pathology. Results The basic lesion, inflammatory activity (the number distribution of G1, G2, G3 and G4 were 3, 7, 7, 4; 5, 8, 7 and 4 respectively) The degree of fibrosis (S1, S2, S3, S4 were 4,7,7,3; 6,8,6,4 respectively) had no significant difference (P> 0.05) G3, G4 were 3, 5, 7, 6; 4, 6, 8, 6 respectively; there was still no significant difference between S1, S2, S3 and S4 Significance (P> 0.05). Conclusions HGV infection did not result in activation of CHB liver lesions and accelerated the progression of fibrosis. HGV infection has no significant effect on long-term lesions of CHB liver. HGV liver pathogenicity is weak at best.