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Evolution of Antinuclear Antibodies and Clinical Patterns in Patients with Active Rheumatoid Arthritis with Longterm Infliximab Therapy
ELISABETH COMBY, PASCALE TANAFF, DELPHINE MARIOTTE, VALERIE COSTENTIN-PIGNOL, CHRISTIAN MARCELLI, and JEAN JACQUES BALLET
ABSTRACT. Methods. Sera from 58 RA patients, treated for one to 3 years with infliximab, were retrospectively analyzed. Matched control groups were RA patients treated with corticosteroids or methotrexate. FANA were tested using HEp-2 cells, and anti-dsDNA and anti-ssDNA IgG by ELISA. After 28 months of infliximab therapy, clinical status was evaluated in 43/58 patients with uninterrupted therapy and associations with autoantibody levels were investigated. Data were documented for patients who discontinued infliximab. Results. Over the 3 year period, significant increases in FANA and anti-ssDNA IgG levels were observed in infliximab treated patients (p < 0.001 and p < 0.01, respectively). In 43 patients with an uninterrupted infliximab regimen, association was found between high FANA (≥ 1/1280) and lower age (p = 0.048) and patient's assessment of infliximab's efficacy (p = 0.014). Three patients developed anti-dsDNA IgG, preceded by high anti-ssDNA IgG levels, and one of them developed a lupus-like syndrome. Neither the initial presence of high FANA levels nor their increase ≥ 1/1280 was significantly associated with discontinuation of infliximab. In contrast, at baseline (p = 0.0012) and at the time of infliximab discontinuation (p = 0.0078), anti-ssDNA IgG (≥ 500 arbitrary units) were more frequent in 7 patients who stopped infliximab due to skin or systemic anaphylactoid reactions. Conclusion. Monitoring of serum FANA, anti-dsDNA, and anti-ssDNA IgG antibodies provided predictors of lupus-like symptoms and/or anaphylactoid reactions in patients with RA. (J Rheumatol 2006;33:24-30) Key Indexing Terms:
TUMOR NECROSIS FACTOR-a
From the Laboratoire d'Immunologie et Immunopathologie, UPRES-EA 2128, and Service de Rhumatologie, CHU, Caen, France. Supported by grants from Conseil Régional de Basse-Normandie and CHU de Caen. E. Comby, MD, Clinical Immunologist; D. Mariotte, PharmD, Assistant Hospitalo-Universitaire; J.J. Ballet, MD, Professor of Immunology, Laboratoire d'Immunologie et Immunopathologie and UPRES-EA 2128, CHU Caen; P. Tanaff, MD; V. Costentin-Pignol, MD; C. Marcelli, MD, Professor of Rheumatology, Service de Rhumatologie, CHU Caen. Address reprint requests to Dr. E. Comby, Laboratoire d'Immunologie et Immunopathologie, Hôpital Clemenceau, CHU, Caen, France. E-mail: comby-e@chu-caen.fr Accepted for publication August 8, 2005. |
