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Anti-Cyclic Citrullinated Peptide versus Anti-Sa Antibodies in Diagnosis of Rheumatoid Arthritis in an Outpatient Clinic for Connective Tissue Disease and Spondyloarthritis
FRANCISCO-JAVIER LÓPEZ-LONGO, MARGARITA RODRÍGUEZ-MAHOU, SILVIA SÁNCHEZ-RAMÓN, ANA ESTECHA, MÓNICA BALSERA, ROSA PLAZA, EDUARDO FERNÁNDEZ-CRUZ, and LUIS CARREÑO PÉREZ ABSTRACT. Objective. To compare the diagnostic value of anti-cyclic citrullinated peptide (anti-CCP) and anti-Sa antibodies in serum for prediction of rheumatoid arthritis (RA) in an outpatient clinic for connective tissue diseases and spondyloarthritides. Methods. A cross-sectional study was carried out to analyze the presence or absence of anti-CCP and anti-Sa antibodies in the sera of 250 randomly selected patients. The disease distribution in the study was as follows: 87 patients had RA (34.8%); 90 (36%) had other connective tissue diseases (CTD); 50 (20%) spondyloarthritis; 19 (7.6%) polymyalgia rheumatica; and 4 (1.6%) juvenile idiopathic arthritis. Results. Anti-CCP antibodies were detected in 63 patients with RA and in 9 patients with other illnesses [sensitivity 72.4%, specificity 94.4%, positive predictive value (PPV) 87.5%]. Anti-Sa antibodies were detected in 38 patients with RA and in 6 patients with other illnesses (sensitivity 43.6%, specificity 96.3%, PPV 86.3%). Anti-CCP and anti-Sa results were discordant in up to 47 of 87 RA patients. No relation between the presence of anti-Sa and higher or lower titers of anti-CCP antibodies was observed. Conclusion. The diagnostic value in RA is similar for both antibodies. However, the sensitivity of anti-CCP detection is higher than that of anti-Sa. Our results suggest that presence of anti-Sa antibodies in serum may be useful as a complementary assay when anti-CCP antibodies are negative and RA is suspected. (J Rheumatol 2006;33:1476–81) Key Indexing Terms:
ANTI-CYCLIC CITRULLINATED PEPTIDE ANTIBODIES From the Departments of Rheumatology, Immunology, and Experimental Medicine, Hospital General Universitario Gregorio Marañón, Madrid, Spain. Supported by grants from the FIS (PI021026 and PI021079), Red de investigación G03/152, and FER/Abbott. F-J. López-Longo, MD, PhD, Department of Rheumatology; M. Rodríguez-Mahou, PhD; S. Sánchez-Ramón, MD, PhD, Department of Immunology; A. Estecha, BSc; M. Balsera, PhD; R. Plaza, PhD, Department of Experimental Medicine; E. Fernández-Cruz, MD, PhD, Department of Immunology; L. Carreño Pérez, MD, PhD, Department of Rheumatology. Address reprint requests to Dra. M. Rodríguez-Mahou, Servicio de Inmunología, Hospital General Universitario Gregorio Marañón, C/ Dr. Esquerdo 46, 28007 Madrid, Spain. E-mail: mrodriguezma.hgugm@salud.madrid.org Accepted for publicaton March 28, 2006.
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