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
10.3760/cma.j.issn.1003-9279.2009.04.013
- VernacularTitle:慢性丙型肝炎患者血清ANA、anti-LKM1的检测及其产生机制探讨
- Author:
Li BAI
1
;
Hai-Ying LU
;
Zhen-Ru FENG
;
Min YU
;
Wen-Gang LI
;
Wei-Bo GONG
;
Xiao-Yuan XU
Author Information
1. 首都医科大学附属北京佑安医院
- Keywords:
Hepatitis C;
Hepacivirus;
Autoantibodies
- From:
Chinese Journal of Experimental and Clinical Virology
2009;23(4):278-281
- CountryChina
- Language:Chinese
-
Abstract:
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.
