Table 1.
Baseline characteristics of treatment courses before and after propensity score matching.
Fig 1.
The flow chart shows the selection of treatment courses and patients included in the analysis. Of the initial 3,378 treatment courses from 1,747 patients in the ANSWER cohort, 675 courses (295 patients) were excluded due to missing Clinical Disease Activity Index (CDAI) data, lack of follow-up, or discontinuation before treatment initiation. The eligible dataset before propensity score matching included 2,703 courses from 1,452 patients. After propensity score matching, the matched analysis dataset comprised 1,521 courses from 883 patients. Abbreviations: CDAI, Clinical Disease Activity Index.
Fig 2.
Kaplan–Meier curves of overall b/tsDMARD retention in RA patients with or without anti-SS-A antibodies.
Kaplan–Meier curves show the overall retention of biologic and targeted synthetic disease-modifying antirheumatic drug (b/tsDMARD) over 24 months in rheumatoid arthritis (RA) patients according to anti-SS-A antibody status. Overall retention rates were similar between antibody-positive and -negative patients. Analyses were performed after propensity score matching. The number at risk is shown below the plot. The curves are shown for one representative imputed matched dataset (imputation 1). Abbreviations: Ab, antibody; b/tsDMARD, biologic and targeted synthetic disease-modifying antirheumatic drug; CI, confidence interval; HR, hazard ratio; RA, rheumatoid arthritis.
Table 2.
Hazard ratios (HRs) and subdistribution hazard ratios (sHRs) for b/tsDMARD discontinuation in rheumatoid arthritis patients with or without anti-SS-A antibodies.
Fig 3.
Kaplan–Meier and cumulative incidence curves of b/tsDMARD retention and discontinuation in RA patients with or without anti-SS-A antibodies.
(A) Kaplan–Meier curves of biologic and targeted synthetic disease-modifying antirheumatic drug (b/tsDMARD) retention by mode of action (MOA: TNF inhibitors [TNFi], IL-6 receptor inhibitors [IL6i], CTLA4-Ig, and JAK inhibitors [JAKi]) in rheumatoid arthritis (RA) patients with or without anti-SS-A antibodies. Anti-SS-A antibody-positive patients tended to show lower retention with IL6i and CTLA4-Ig, while retention appeared similar with TNFi or JAKi. (B) Cumulative incidence function curves of b/tsDMARD discontinuation due to adverse events, ineffectiveness, or remission in RA patients with or without anti-SS-A antibodies. Anti-SS-A antibody-positive patients showed a higher cumulative incidence of discontinuation due to adverse events, while no clear differences were observed for ineffectiveness or remission. (C) Cumulative incidence function curves of b/tsDMARD discontinuation due to adverse events by MOA (TNFi, IL6i, CTLA4-Ig, JAKi) according to anti-SS-A antibody status. Anti-SS-A antibody positivity was associated with a higher risk of discontinuation due to adverse events with IL6i and TNFi, while no clear differences were observed with CTLA4-Ig or JAKi. The number at risk and the number of events are shown below each plot. The curves are shown for one representative imputed matched dataset (imputation 1). Cumulative incidence functions were estimated in the presence of competing risks. Abbreviations: Ab, antibody; b/tsDMARD, biologic and targeted synthetic disease-modifying antirheumatic drug; CI, confidence interval; CTLA4-Ig, cytotoxic T lymphocyte-associated antigen 4-immunoglobulin; IL6i, interleukin-6 receptor inhibitors; JAKi, Janus kinase inhibitors; MOA, mode of action; RA, rheumatoid arthritis; TNFi, tumor necrosis factor inhibitors.