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This article is part of the supplement: 25th European Workshop for Rheumatology Research

Poster presentation

Elevated titers of anti-ribosomal-P antibodies in systemic lupus erythematosus

G Zandman-Goddard1, B Gilburd1, S Bardechevski1, L Stojanovich1, P Langevitz2 and Y Shoenfeld1

Author Affiliations

1 Center for Autoimmune Diseases and Department of Medicine 'B', Sheba Medical Center, Tel-Hashomer, Israel

2 Rheumatology Unit, Sackler Faculty of Medicine, Tel-Aviv University, Israel

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Arthritis Research & Therapy 2005, 7(Suppl 1):P13  doi:10.1186/ar1534


The electronic version of this article is the complete one and can be found online at:


Received:11 January 2005
Published:17 February 2005

© 2005 BioMed Central Ltd

Objective

Ribosomal P is located in the cytoplasm. The detection of antibodies is to the 60 kda fraction. Anti-ribosomal P antibodies are highly specific for systemic lupus erythematosus (SLE), and are detected at a 15–20% frequency according to the literature. Elevated anti-ribosomal P titers correlate with disease activity and are specifically associated with neuropsychiatric disease such as psychosis/depression. and coexist with anti-dsDNA antibodies. The aim of our study was to evaluate the frequency of anti-ribosomal P antibody titers and the correlation with manifestations in SLE patients.

Methods

Sera samples from 174 individuals were evaluated for titers of anti-ribosomal P antibodies: 77 samples from SLE patients, 22 patients with antiphospholipid syndrome (APS), 20 patients with familial Mediterranean fever, 12 patients with infections, and 43 healthy controls. Anti-ribosomal P antibody titers were tested by ELISA. Manifestations of SLE at the time of serum sampling were determined by the SLEDAI score.

Results

Six SLE patients (11%) harbored elevated anti-ribosomal P antibody titers. Five SLE patients were females, mean age 44.3 years (range, 18–73 years old), and the mean SLEDAI mean score was 7 (range, 3–10) indicating moderate disease. Elevated titers of anti-dsDNA were detected in 50% of SLE patients with elevated anti-ribosomal P antibodies. One patient had secondary APS. One patient with elevated titers of anti-ribosomal had renal disease and psychosis. Three patients had a rash, while none of the patients had arthritis or leukopenia. Anti-ribosomal P titers were not elevated in patients with primary APS, familial Mediterranean fever, infections, or in healthy controls.

Conclusion

The prevalence of elevated titers of anti-ribosomal P antibodies was restricted to SLE patients. No correlation with a specific manifestation was found.