Predicting factors for disappearance of anti-mutated citrullinated vimentin antibodies in sera of patients with rheumatoid arthritis

Abstract

Objectives: We aimed to determine the predicting factors for disappearance of anti-mutated citrullinated vimentin antibody (anti-MCV Ab) in sera from rheumatoid arthritis (RA) patients.

Methods: In 2013, 95 RA patients whose Disease Activity Score with erythrocyte sedimentation rate were moderate to severe (DAS28-ESR ≥3.2) at baseline were enrolled. Titers of anti-MCV Ab and anti-cyclic citrullinated peptide (anti-CCP) Ab for 2013 and 2014 were measured. The association of anti-MCV disappearance with disease activity, treatment, interstitial lung disease (ILD), and serum markers of ILD were retrospectively examined. Predicting factors of anti-MCV disappearance were determined by multivariable analysis.

Results: While anti-CCP positivity rate did not change during the year, anti-MCV Ab changed from positive to negative in 18 patients (=19.0%). Continuous biological disease-modifying anti-rheumatic drug use, prednisolone dose (≥5.0 mg daily), and low KL-6 level (<191 U/mL) were determined as predicting factors of anti-MCV disappearance by multivariable analysis. In our cohort, anti-MCV Ab disappearance was not linked to clinical and radiological improvement.

Conclusion: Different from anti-CCP Ab, anti-MCV Ab in sera from RA patients can disappear in a year. Some predicting factors for such negative seroconversion were found, whereas clinical significance of anti-MCV Ab disappearance was undetermined.

Keywords:

• anti-citrullinated protein antibodies
• biological disease-modifying antirheumatic drug
• interstitial lung disease
• rheumatoid arthritis

Acknowledgments

We would like to thank Akiko Yoshida for scoring mTSS.

Conflict of interest

KURAMA cohort study is supported by a grant from Daiichi Sankyo Co. Ltd. This study is conducted as investigator-initiated study. These companies had no role in the design of the study, collection, or analysis of data, the writing of the manuscript or decision to submit the manuscript for the publication. T.F. has received a research grant and/or speaker fee from Pfizer Japan Inc., Ono Pharmaceutical Co., Ltd., Daiichi Sankyo Co., Ltd., Mitsubishi-Tanabe Pharma Corporation, Eisai Co., Ltd., AbbVie GK, and Astellas Pharma Inc. M.H. and M.T. belong to a department that is financially supported by four pharmaceutical companies (Mitsubishi-Tanabe, Chugai, AYUMI, and UCB Japan). M.T. received scholarship donations from six pharmaceutical companies (Pfizer, Astellas, AbbVie GK, Taisyo Toyama, Takeda, and Eisai). M.H. received a grant from Astellas Pharma Inc., Bristol-Myers Squibb, and ONO Pharma. HI received research grant from BMS, Astellas, and Asahi-Kasei. S Morita received honoraria from four pharmaceutical companies (Pfizer, Bristol-Myers Company, ONO Pharma, Chugai). T Mimori has received research grants from Astellas, Asahi Kasei Pharma, Ayumi, Chugai, Daiichi Sankyo, Eisai, Eli Lilly, Mitsubishi-Tanabe, Nippon Kayaku, Nippon Shinyaku, Pfizer, Sanofi, and Takeda and speakers’ fee from Bristol-Myers Squibb, Chugai, and Mitsubishi-Tanabe.