Clinical Significance of Autoantibodies to Glucose-6-phosphate Isomerase in Serum of Patients with Rheumatoid Arthritis.
10.4078/jkra.2007.14.4.340
- Author:
Yu Mi BYEON
1
;
Sang Hyon KIM
;
Sung Hwan PARK
Author Information
1. Department of Internal Medicine, Chosun University College of Medicine, Gwanju, Korea. mdkim9111@hanmail.net
- Publication Type:Original Article
- Keywords:
Anti-GPI antibody;
Rheumatoid arthritis;
Shared epitope
- MeSH:
Animals;
Arthritis, Rheumatoid*;
Autoantibodies*;
Enzyme-Linked Immunosorbent Assay;
Glucose-6-Phosphate Isomerase*;
Glucose-6-Phosphate*;
Humans;
Mice;
Osteoarthritis;
Rheumatoid Factor
- From:The Journal of the Korean Rheumatism Association
2007;14(4):340-344
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: Anti-glucose-6-phosphate isomerase (GPI) antibody (Ab) is known to be arthritogenic in K/BxN mice. Anti-GPI Ab is present in some patients with rheumatoid arthritis (RA), but their clinical manifestations are not clearly elucidated. The purpose of this study was to evaluate whether GPI serves as a specific autoantigen in patients with RA and to investigate the relationship of anti-GPI Ab with clinical parameters of RA. METHODS: Sera were collected from 54 patients with RA, 15 patients with osteoarthritis (OA) and 28 healthy controls. The samples were tested by enzyme-linked immunosorbent assay (ELISA) using human recombinant GPI as antigen. Patients with RA were classified according to rheumatoid factor (RF) positivity, the presence of RA shared epitope (SE), the presence of extraarticular manifestations, and evidence of bony erosive changes. RESULTS: Serum levels of anti-GPI Ab were higher in patients with RA than controls (1599.46+/-1022.48 versus 344.82+/-223.16 AU, p<0.001), and the levels of patients with OA were also higher than controls (1161.47+/-917.44 versus 344.82+/-223.16 AU, p<0.01). In RA, there were no significant difference in anti-GPI Ab levels according to RF positivity, the presence of RA SE, the presence of extraarticular manifestations, and evidence of bony erosive changes. CONCLUSION: Our results suggest that anti-GPI Ab may not be RA specific Ab and not related to the severity of RA.
