慢性丙型肝炎患者血清ANA、anti-LKM1的检测及其产生机制探讨

目的 观察慢性丙型肝炎(CHC)患者中抗核抗体(ANA)、抗肝肾微粒体抗体(anti-LKM1)的检出情况,并深入探讨其产生机制.方法 通过多因素分析探讨自身抗体产生与年龄、性别、HCV RNA含量、HCV基因型、生化指标及临床特征等指标的关系.结果 360例CHC患者中,ANA阳性率为12.5%(451360),anti-LKMi的阳性率为2.5%(91360).CHC患者的自身抗体检出率高于慢性乙型肝炎(CHB)患者(15%vs2.9%,P=0.006)而低于自身免疫性肝炎(AIH)患者(15%vs47.9%,P<0.001);女性患者的自身抗体检出率高于男性(P<0.05);自身抗体阳性组HCV RNA含量低于自身抗体阴性组(1.23×107 vs 7.2× 107拷贝/L,P<0.05).自身抗体阳性组和阴性组患者的年龄、HCV基因型、生化指标、肝硬化发生率的差异均无统计学意义.接受干扰素治疗组和未接受干扰紊治疗组患者的自身抗体检出率差异无统计学意义(P>0.05).结论 CHC患者血清中可检测出AIH相关自身抗体;自身抗体可能并非由干扰素治疗所诱发;很可能是HCV引发自身免疫,导致自身抗体的出现.

Detection anti the production mechanism of antinuclear antibodies(ANA) and anti-liver/kidney microsomal type 1 antibodies(anti-LKM1) in patients with chronic hepatitis C

Objective To investigate the prevalence of anfinaclear antibodies (ANA) and anti-liver/ kidney microsomal type 1 antibodies (anti-LKM1) in patients with chronic hepatitis C (CHC)and to explore the mechanism of production of these autoantibodies. Methods Serum samples were collected from 360 patients with CHC (case group), 69 patients with chronic hepatitis B (CHB) and 69 patients with autoimmune hepatitis (AIH) (control group). Senun ANA and anti-LKM1 were detected by indirect immunofluorescence (IIF) technique and enzyme-linked iramunosorbent assay (ELISA), respectively. Multi-factor analysis w.aa performed to explore the correlations of the production of autoanfibodies with some factors such eta age, sex, viral loads, HCV genotype, biochemical parameters and clinical characteristics. Results Fifty-four (15%) of 360 patients infected with HCV were positive in autoantibedies. The prevalence of ANA and anti-LKMl were 12.5% (45/360) and 2.5% (9/360), respectively. The positive rote of autoantibodies in patients with CHC was significantly higher than that in patients with CHB (15% vs 2.9%, P = 0.006), but significantly lower than that in patients with AIH (15% vs 47.9%, P < 0.001). Twenty-one (11.35%) of 185 male patients and 33 (18.86%) of 175 female patients were positive in autoantibodies, the difference in positive rate was significant (P < 0.05). HCV virus loads in the autoantibedies negative group were higher than that in the autoantibodies positive group (7.2× 107 copies/L vs 1.23×107 copies/L, P < 0.05). There were not significant differences in age and genotype between the autoantibedy positive group and the autoantibody negative group. The serum biochemical parameters of the autoantibedy positive group were similar ta those of the autoantibody negative group. The differences were not significant for the course of disease, clinical symptom, the incidence of cirrhosis between the autoantibedy positive group and the autoantibody negative group. The prevalence of autoantibodies was not different for patients with or without interferon treatment (P > 0.05). Conclusion Autoantibodies related to AIH can be detected in CHC patients; interferon may not induce the production of autoantibodies; it is very likely that HCV infection induces the autoimmune reaction and the production of autoantibodios.