ABSENCE OF LKM-1 ANTIBODY REACTIVITY IN AUTOIMMUNE AND HEPATITIS-C-RELATED CHRONIC LIVER-DISEASE IN SWEDEN

Citation
S. Lindgren et al., ABSENCE OF LKM-1 ANTIBODY REACTIVITY IN AUTOIMMUNE AND HEPATITIS-C-RELATED CHRONIC LIVER-DISEASE IN SWEDEN, Scandinavian journal of gastroenterology, 32(2), 1997, pp. 175-178
Citations number
27
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
0036-5521
Volume
32
Issue
2
Year of publication
1997
Pages
175 - 178
Database
ISI
SICI code
0036-5521(1997)32:2<175:AOLARI>2.0.ZU;2-1
Abstract
Background: Type-2 autoimmune hepatitis is a subgroup of chronic hepat itis characterized by the presence of liver/kidney microsomal autoanti bodies type 1 (LKM-1). A frequent association with chronic hepatitis C suggests that hepatitis virus might trigger autoimmune reactivity. LK M-1-positive chronic hepatitis is not uncommon in southern Europe but is rarely seen in the USA and the UK. The prevalence in Scandinavia is hitherto unknown. Methods: We used an automated prototype LKM-1 immun ometry-based assay (IMx) to detect LKM-1 antibodies in sera from 350 S wedish patients with chronic liver diseases (100 with primary biliary cirrhosis, 80 with primary sclerosing cholangitis, 100 with hepatitis C, and 70 patients with various forms of chronic hepatitis, including 36 autoimmune cases), and from 17 children with autoimmune hepatitis. Sera reactive in the IMx assay were subjected to immunofluorescence te sting. Results: No clearly LKM-reactive sera were detected. Serum samp les from 29 patients were borderline reactive in the IMx assay but tes ted negative in the confirmatory immunofluorescence test. Positive tes ts in the former assay were likely caused by reactivity against micros omal antigens other than LKM-1/cytochrome P450IID6. Conclusions: LKM-1 -positive type-2 autoimmune hepatitis is very rare in Sweden. Furtherm ore, chronic hepatitis C did nor trigger this type of autoimmune react ivity in our patients, probably owing to genetic insusceptibility.