Antibodies Against Mutated Citrullinated Vimentin Are a Better Predictor of Disease Activity at 24 Months in Early Rheumatoid Arthritis Than Antibodies Against Cyclic Citrullinated Peptides
LENA INNALA, HEIDI KOKKONEN, CATHARINA ERIKSSON, ERIK JIDELL, EWA BERGLIN, and SOLBRITT RANTAPÄÄ DAHLQVST
Methods. The ACPA, e.g., antibodies against mutated citrullinated vimentin (MCV), cyclic citrullinated peptides (CCP) type 2 and 3 (both of IgG isotype) and 3.1 (of both IgG and IgA isotypes), were analyzed at baseline in patients with early RA (n = 210) and in population controls (n = 102) using an enzyme immunoassay. A receiver-operating characteristic curve was constructed for each antibody. Disease activity [swollen and tender joints, visual analog scale for global health, and erythrocyte sedimentation rate (ESR)] was evaluated at baseline and regularly for 24 months. Radiographs of hands and feet were graded using the Larsen score.
Results. Patients with anti-MCV antibodies had significantly less reduction in Disease Activity Score (DAS28) over time (p < 0.01), and significantly increased area under the curve (AUC) for DAS28 (p < 0.05), ESR (p < 0.01), C-reactive protein (p < 0.01), and swollen joint count (p = 0.057) compared to those without. Corresponding differences were not found in patients with anti-CCP2, CCP3, and CCP3.1 antibodies. Radiological progression (p < 0.0001-0.01) and radiological outcome (p < 0.0001-0.01) at 24 months were significantly predicted by all ACPA after baseline adjustments. PTPN22 T variant and HLA-DRB1 alleles were not related to radiological progression or inflammatory activity over time.
Conclusion. Anti-MCV antibodies are associated with a more severe RA disease, as measured by DAS28, ESR, and swollen joint count over time, compared with anti-CCP2, CCP3, and CCP3.1 antibodies. Radiological progression was predicted equally by all 4 autoantibodies. (J Rheumatol First Release April 1 2008)
Key Indexing Terms:
ANTI-CYCLIC CITRULLINATED PEPTIDE 2 ANTIBODIES
From the Department of Rheumatology, Department of Clinical Immunology, and Department of Transfusion Medicine, University Hospital, Umeå, Sweden.
Supported by grants from the Swedish Research Council (K2003-74XD-14705-01), King Gustaf V's 80-Year Fund, and the Swedish Rheumatism Association.
L. Innala, MD; H. Kokkonen, MSc, Department of Rheumatology; C. Eriksson, MD, Department of Clinical Immunology; E. Jidell, MD, Department of Transfusion Medicine; E. Berglin, MD, PhD; S. Rantapää Dahlqvist, MD, PhD, Department of Rheumatology, University Hospital.
Address reprint requests to Dr. S. Rantapää-Dahlqvist, Department of Public Health and Clinical Medicine, Rheumatology, University Hospital, 901 85 Umeå, Sweden. E-mail: firstname.lastname@example.org.
Accepted for publication January 10, 2008.