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Associations between an expanded autoantibody profile and treatment responses to biologic therapies in patients with rheumatoid arthritis

Author

Int Immunopharmacol. 2020 Dec 23;91:107260. doi: 10.1016/j.intimp.2020.107260.Online ahead of print.

Alison D Petro 1Joseph Dougherty 2Bryant R England 3Harlan Sayles 4Michael J Duryee 5Carlos D Hunter 6Joel M Kremer 7Dimitrios A Pappas 8William H Robinson 9Jeffrey R Curtis 10Geoffrey M Thiele 11Ted R Mikuls 12

Author Information

1 University of Nebraska Medical Center & VA Nebraska-Western Iowa Health Care System, 986270 Nebraska Medical Center, Omaha, NE 68198-6270, United States. Electronic address: alison.petro@unmc.edu.

2 University of Nebraska Medical Center & VA Nebraska-Western Iowa Health Care System, 986270 Nebraska Medical Center, Omaha, NE 68198-6270, United States. Electronic address: joseph.dougherty@unmc.edu.

3 University of Nebraska Medical Center & VA Nebraska-Western Iowa Health Care System, 986270 Nebraska Medical Center, Omaha, NE 68198-6270, United States. Electronic address: bryant.england@unmc.edu.

4 University of Nebraska Medical Center & VA Nebraska-Western Iowa Health Care System, 986270 Nebraska Medical Center, Omaha, NE 68198-6270, United States. Electronic address: hsayles@unmc.edu.

5 University of Nebraska Medical Center & VA Nebraska-Western Iowa Health Care System, 986270 Nebraska Medical Center, Omaha, NE 68198-6270, United States. Electronic address: mduryee@unmc.edu.

6 University of Nebraska Medical Center & VA Nebraska-Western Iowa Health Care System, 986270 Nebraska Medical Center, Omaha, NE 68198-6270, United States. Electronic address: cdhunter@unmc.edu.

7 Albany Medical College and The Center of Rheumatology, 43 New Scotland Ave, Albany, NY 12208, United States; Corrona LLC, 1440 Main St, Waltham, MA, 02451 and Columbia University, New York, NY 10027, United States. Electronic address: jkremer@corrona.org.

8 Corrona LLC, 1440 Main St, Waltham, MA, 02451 and Columbia University, New York, NY 10027, United States. Electronic address: dpappas@corrona.org.

9 Stanford University School of Medicine, 269 Campus Dr, Stanford, CA 94305, United States; VA Palo Alto Health Care System, Palo Alto, CA 94304, United States. Electronic address: wrobins@stanford.edu.

10 University of Alabama at Birmingham, 1720 University Blvd, Birmingham, AL 35294, United States. Electronic address: jrcurtis@uabmc.edu.

11 University of Nebraska Medical Center & VA Nebraska-Western Iowa Health Care System, 986270 Nebraska Medical Center, Omaha, NE 68198-6270, United States. Electronic address: gthiele@unmc.edu.

12 University of Nebraska Medical Center & VA Nebraska-Western Iowa Health Care System, 986270 Nebraska Medical Center, Omaha, NE 68198-6270, United States. Electronic address: tmikuls@unmc.edu.

Abstract

Background: Although biologics represent a major advance in rheumatoid arthritis (RA), many patients fail to achieve adequate responses to these agents. We examined whether combined positivity to three well-characterized autoantibodies predicts treatment response among RA patients initiating biologics.

Methods: The study included biologic-naïve patients initiating anti-TNF treatment, biologic-exposed patients switching to rituximab or tocilizumab, and patients (biologic naïve or exposed) initiating abatacept. Rheumatoid factor (RF), anti-cyclic citrullinated peptide (CCP) antibody, and IgG antibodies to malondialdehyde-acetaldehyde (MAA) were measured using banked enrollment serum. The relationship between the number of autoantibodies positive (0-3) and treatment response (absolute improvement in 28-joint Disease Activity Score [DAS28-CRP] or improvement > 1.2) at 6 months was examined using multivariable linear and logistic regression.

Results: Of 1,229 patients initiating biologics, 79% were women; 89% were Caucasian. The number of baseline RA-related autoantibodies positive was associated with improved treatment response in a dose-dependent fashion. Compared to patients seronegative for all autoantibodies, adjusting for covariates, those positive for all three were more than twice (OR 2.35; 95% CI 1.57-3.51) as likely to achieve DAS28 improvement > 1.2 units. Associations of autoantibody positivity with biologic treatment response were strongest for anti-CCP antibody, persisted in analyses limited to biologic naïve patients, and did not appear to differ markedly among different agents examined.

Conclusion: An expanded autoantibody profile appears to significantly predict RA treatment response to biologic treatment in a dose-dependent fashion. Incorporating these serologic profiles with additional biomarkers or other informative patient characteristics could provide an opportunity to personalize RA management.