CAJ | 학술논문

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.
목적 관찰만성병형간염(CHC)환자중항핵항체(ANA)、항간신미립체항체(anti-LKM1)적검출정황,병심입탐토기산생궤제.방법 통과다인소분석탐토자신항체산생여년령、성별、HCV RNA함량、HCV기인형、생화지표급림상특정등지표적관계.결과 360례CHC환자중,ANA양성솔위12.5%(451360),anti-LKMi적양성솔위2.5%(91360).CHC환자적자신항체검출솔고우만성을형간염(CHB)환자(15%vs2.9%,P=0.006)이저우자신면역성간염(AIH)환자(15%vs47.9%,P<0.001);녀성환자적자신항체검출솔고우남성(P<0.05);자신항체양성조HCV RNA함량저우자신항체음성조(1.23×107 vs 7.2× 107고패/L,P<0.05).자신항체양성조화음성조환자적년령、HCV기인형、생화지표、간경화발생솔적차이균무통계학의의.접수간우소치료조화미접수간우문치료조환자적자신항체검출솔차이무통계학의의(P>0.05).결론 CHC환자혈청중가검측출AIH상관자신항체;자신항체가능병비유간우소치료소유발;흔가능시HCV인발자신면역,도치자신항체적출현.
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.