PRIMARY AND SECONDARY LIVER/KIDNEY MICROSOMAL AUTOANTIBODY RESPONSE FOLLOWING INFECTION WITH HEPATITIS-C VIRUS

被引:64
作者
MACKIE, FD
PEAKMAN, M
YUN, M
SALLIE, R
SMITH, H
DAVIES, ET
MIELIVERGANI, G
VERGANI, D
机构
[1] UNIV LONDON KINGS COLL, SCH MED & DENT, DEPT IMMUNOL, LONDON SE5 9PJ, ENGLAND
[2] UNIV LONDON KINGS COLL, SCH MED & DENT, DEPT CHILD HLTH, LONDON WC2R 2LS, ENGLAND
[3] UNIV LONDON KINGS COLL, SCH MED & DENT, INST LIVER STUDIES, LONDON WC2R 2LS, ENGLAND
基金
英国惠康基金;
关键词
D O I
10.1016/0016-5085(94)90426-X
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Liver/kidney microsomal autoantibody type 1 (LKM-1), which characterizes a subtype of autoimmune hepatitis, is also found in some patients with chronic hepatitis C virus (HCV) infection. Whether HCV and LKM-1 are accidentally or causally related is unknown. This case report describes a child who became infected by HCV after liver transplantation for end-stage liver disease caused by α1-antitrypsin deficiency. LKM-1 was detected by immunofluorescence, anti-microsomal reactivity by Western blotting, anti-HCV and anti-GOR by immunoenzymatic assays, and HCV RNA by polymerase chain reaction. Two weeks after HCV infection, immunoglobulin (lg) M LKM-1 appeared, followed by lgG1 LKM-1, with titers increasing to 1/2560; antibodies to a 50-kilodalton liver microsomal protein appeared 2 months later. Sera from day 1 posttransplant became positive for HCV RNA. HCV RNA was also detected in a liver biopsy specimen obtained 3 months after surgery. The patient did not produce anti-HCV and anti-GOR antibodies throughout the study and had no histological evidence of hepatitis. The temporal relationship between HCV infection and LKM-1 production suggests that HCV may trigger a primary autoimmune response. The lack of liver damage attributable to autoimmunity or viral infection may be caused by immunosuppression. © 1994.
引用
收藏
页码:1672 / 1675
页数:4
相关论文
共 30 条
[21]   IMMUNOLOGICAL STUDIES ON TYPE-1 DIABETES IN IDENTICAL-TWINS [J].
PEAKMAN, M ;
LESLIE, RDG ;
VERGANI, D .
ARCHIVES OF DISEASE IN CHILDHOOD, 1993, 69 (01) :97-99
[22]  
PEAKMAN M, 1987, CLIN EXP IMMUNOL, V69, P543
[23]   TRANSMISSION OF HEPATITIS-C VIRUS BY ORGAN-TRANSPLANTATION [J].
PEREIRA, BJG ;
MILFORD, EL ;
KIRKMAN, RL ;
LEVEY, AS .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 325 (07) :454-460
[24]   DIAGNOSIS OF CHRONIC HEPATITIS-C AFTER LIVER-TRANSPLANTATION BY THE DETECTION OF VIRAL SEQUENCES WITH POLYMERASE CHAIN-REACTION [J].
POTERUCHA, JJ ;
RAKELA, J ;
LUMENG, L ;
LEE, CH ;
TASWELL, HF ;
WIESNER, RH .
HEPATOLOGY, 1992, 15 (01) :42-45
[25]  
Sambrook J., 1989, MOL CLONING LAB MANU
[26]   DETECTION, SEMIQUANTITATION, AND GENETIC-VARIATION IN HEPATITIS-C VIRUS SEQUENCES AMPLIFIED FROM THE PLASMA OF BLOOD-DONORS WITH ELEVATED ALANINE AMINOTRANSFERASE [J].
ULRICH, PP ;
ROMEO, JM ;
LANE, PK ;
KELLY, I ;
DANIEL, LJ ;
VYAS, GN .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 86 (05) :1609-1614
[27]  
VERGANI D, 1993, CLIN EXP IMMUNOL, V92, P367
[28]   TYPE-II AUTOIMMUNE HEPATITIS - WHAT IS THE ROLE OF THE HEPATITIS-C VIRUS [J].
VERGANI, D ;
MIELIVERGANI, G .
GASTROENTEROLOGY, 1993, 104 (06) :1870-1873
[29]   INDETERMINATE HEPATITIS-C [J].
WICKI, AN ;
JOLLERJEMELKA, H .
LANCET, 1993, 341 (8859) :1534-1534
[30]   CHARACTERIZATION OF ANTI LIVER-KIDNEY MICROSOME ANTIBODY (ANTI-LKM1) FROM HEPATITIS-C VIRUS-POSITIVE AND VIRUS NEGATIVE SERA [J].
YAMAMOTO, AM ;
CRESTEIL, D ;
HOMBERG, JC ;
ALVAREZ, F .
GASTROENTEROLOGY, 1993, 104 (06) :1762-1767