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Rheumatology 2003; 42: 353-356
© 2003 British Society for Rheumatology

Novel autoantibodies to pituitary gland specific factor 1a in patients with rheumatoid arthritis

S. Tanaka, K. Tatsumi, T. Tomita1, M. Kimura, T. Takano, H. Yoshikawa1 and N. Amino

Department of Laboratory Medicine (D2) and
1 Department of Orthopaedic Surgery, Osaka University Graduate School of Medicine, Osaka, Japan

Objective. We recently identified a new protein, pituitary gland specific factor 1a (PGSF1a), that is specifically transcribed in the pituitary gland. In our investigation of anti-PGSF1a antibody for pituitary diseases, we examined it in patients with RA and other autoimmune diseases. We unexpectedly discovered the frequent existence of anti-PGSF1a antibody in patients with RA. We therefore examined the prevalence of this antibody to understand its clinical significance in RA.

Methods. Anti-PGSF1a antibody was detected by radioligand assay using recombinant 35S-labelled PGSF1a protein. Antibody activity is expressed as an index that was obtained by comparison with normal pooled serum.

Results. RA patients had a significantly higher mean anti-PGSF1a antibody index (n=46, 1.28±0.38, P < 0.001) than healthy controls (n=36, 1.04±0.13). Indices greater than the cut-off value (mean+2 S.D. of healthy controls) were found in 43.5% (20/46) and 10.0% (2/20) of patients with RA and osteoarthritis, respectively. There was no correlation between the activities of anti-PGSF1a antibodies and titres of rheumatoid factor (RF) or serum C-reactive protein concentrations, but RA patients with more erosive disease had a higher mean anti-PGSF1a antibody index. Four of eight sera samples obtained from RF-negative RA patients were positive for anti-PGSF1a antibodies.

Conclusion. Anti-PGSF1a antibody is a useful new marker for the diagnosis of RA, especially for RF-negative RA, and may relate to clinical manifestations of RA.

KEY WORDS: Rheumatoid arthritis, Osteoarthritis, Rheumatoid factor, Autoantibody, PGSF1a, Pituitary, RF-negative RA, Seronegative RA.

Correspondence to: K. Tatsumi, Department of Laboratory Medicine, Osaka University Graduate School of Medicine (D2), Suita-shi Yamada-oka 2–2, Osaka 565-0871, Japan. E-mail: tatsumi{at}labo.med.osaka-u.ac.jp


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