Association of autoantibodies to glucose‐6‐phosphate isomerase with extraarticular complications in rheumatoid arthritis

Objective In the K/BxN mouse model, autoantibodies against glucose‐6‐phosphate isomerase (GPI) cause arthritis. The relevance of this model for human disease remains a subject of controversy. We set out to determine whether GPI autoantibodies occur in patients with rheumatoid arthritis (RA) and, if...

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Bibliographic Details
Published in:Arthritis and rheumatism 2004-02, Vol.50 (2), p.395-399
Main Authors: van Gaalen, Floris A., Toes, Rene E. M., Ditzel, Henrik J., Schaller, Monica, Breedveld, Ferdinand C., Verweij, Cor L., Huizinga, Tom W. J.
Format: Article
Language:English
Subjects:
Adult
Aged
Aged, 80 and over
Arthritis, Rheumatoid - complications
Arthritis, Rheumatoid - immunology
Arthritis, Rheumatoid - pathology
Autoantibodies - blood
Biological and medical sciences
Diseases of the osteoarticular system
Enzyme-Linked Immunosorbent Assay
Felty Syndrome - etiology
Felty Syndrome - immunology
Felty Syndrome - pathology
Female
Glucose-6-Phosphate Isomerase - immunology
Humans
Inflammatory joint diseases
Male
Medical sciences
Middle Aged
Rheumatoid Nodule - etiology
Rheumatoid Nodule - immunology
Rheumatoid Nodule - pathology
Vasculitis - etiology
Vasculitis - immunology
Vasculitis - pathology
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Summary:Objective In the K/BxN mouse model, autoantibodies against glucose‐6‐phosphate isomerase (GPI) cause arthritis. The relevance of this model for human disease remains a subject of controversy. We set out to determine whether GPI autoantibodies occur in patients with rheumatoid arthritis (RA) and, if so, at what stage of the RA. Methods Using an enzyme‐linked immunosorbent assay, serum from 131 RA patients and 28 healthy controls was tested for autoantibodies against recombinant human GPI. Patients were grouped according to disease duration and presence of rheumatoid nodules, rheumatoid vasculitis, and Felty's syndrome, which are extraarticular complications of RA. Results Elevated levels of autoantibodies against GPI were present in 5% of patients with uncomplicated RA and 4% of controls. In RA complicated by extraarticular manifestations, anti‐GPI antibodies were observed in 18% of patients with rheumatoid nodules, 45% of patients with rheumatoid vasculitis, and 92% of patients with Felty's syndrome. Conclusion In patients with RA, autoantibodies to GPI are associated with the occurrence of extraarticular complications.
ISSN:0004-3591
1529-0131
DOI:10.1002/art.20028