AB0823 TREATMENT WITH ADALIMUMAB IN PATIENTS WITH CHRONIC INFLAMMATORY RHEUMATIC DISEASES: A STUDY OF TREATMENT TRAJECTORIES ON A PATIENT LEVEL IN CLINICAL PRACTICE
Authors: I. Redeker, S. Moustakis, S. Tsiami, X. Baraliakos, I. Andreica, B. Buehring, J. Braun, U. Kiltz
Journal: Annals of the Rheumatic Diseases (2021)

Background: There is evidence that drug retention rates to adalimumab (ADA) in patients (pts.) with chronic inflammatory rheumatic diseases (CIRD) are impaired by loss of efficacy and adverse events, and that about 50% of users had discontinued ADA within 5 years (1). With the introduction of ADA biosimilars in October 2018, non-medical switching from originator to ADA biosimilars is now increasingly part of daily practice in rheumatologic care. Objectives: The aim was to study treatment trajectories over two years in pts. with CIRD receiving originator ADA. Methods: Pts. with CIRD on originator ADA who switched to ADA biosimilar from October 2018 onwards were identified and followed until 2020. Disease activity (ASDAS), physical function (HAQ, BASFI), and changes in treatment were documented every 3 months. The four predefined treatment trajectories “continued ADA biosimilar therapy”, “back-switch to originator ADA therapy”, “switch to other biological (b) disease modifying anti-rheumatic drug (DMARD) therapy”, and “stopped bDMARD therapy /death /drop out” were used to compare characteristics of pts. with different trajectories. Results: A total of 111 CIRD pts. on treatment with originator ADA were switched to ADA biosimilar (Table 1). The majority of pts. 75 continued therapy with ADA biosimilar (Figure 1 next page) while 16% switched back to originator ADA, 7% switched to a different bDMARD, and 9% either stopped treatment (n=9) or died (n=1). Pts. who continued ADA biosimilar were more frequently male, older or with a longer disease duration than those who switched therapy back to originator ADA and those who switched to a different bDMARD (Table 1). The previous duration on originator ADA treatment was increased in patients who continued ADA biosimilar compared to those who switched therapy back to originator ADA and those who switched to a different bDMARD. There was more functional impairment (HAQ, BASFI) and higher disease activity (ASDAS) in pts. who switched compared to those who continued ADA biosimilar therapy (Table 1). Treatment with csDMARDs and glucocorticoids was increased in pts. who continued ADA biosimilar therapy, while pts. who switched therapy had more previous bDMARD therapies (Table 1). Table 1. Characteristics of patients at baseline for the entire group and stratified by treatment trajectory Total group N=111 (100% ) Treatment trajectory continued ADA biosimilar therapy N=75 (67.6% ) back-switch to originator ADA therapy N=18 (16.2% ) switch to different bDMARD therapy N=8 (7.2% ) no bDMARD therapy / death / drop out N=10 (9.0% ) Age, y 51.2 (14.5) 51.5 (13.6) 50.6 (16.8) 43.5 (9.5) 56.4 (19.0) Women, No. (%) 46 (41.4) 27 (36.0) 9 (50.0) 6 (75.0) 4 (40.0) RA 23 (20.7) 17 (22.7) 2 (11.1) 1 (12.5) 3 (30.0) axSpA 68 (61.3) 47 (62.7) 11 (61.1) 6 (75.0) 4 (40.0) PsA 15 (13.5) 7 (9.3) 4 (22.2) 1 (12.5) 3 (30.0) Other diagnoses 5 (4.5) 4 (5.3) 1 (5.6) 0 (0.0) 0 (0.0) Disease duration, median (IQR), y 5.0 (2.0-8.0) 5.0 (2.0-9.0) 3.5 (2.0-6.0) 2.0 (1.0-5.5) 4.5 (2.0-8.0) Duration previous originator ADA therapy 40.7 (27.7) 45.3 (27.8) 35.0 (25.2) 20.3 (24.7) 32.3 (25.1) DAS28 3.0 (1.0) 2.9 (1.0) 3.4 (1.0) - 3.3 (1.2) CRP, median (IQR), mg/L 0.2 (0.1-0.3) 0.1 (0.1-0.2) 0.2 (0.0-0.5) 0.2 (0.2-1.3) 0.3 (0.2-0.4) HAQ score 1.3 (0.8) 1.1 (0.7) 1.7 (0.8) - 1.8 (1.0) ASDAS 2.2 (1.1) 2.0 (1.0) 3.0 (1.2) 2.7 (0.9) 2.3 (0.2) BASFI 3.5 (2.6) 3.0 (2.5) 5.4 (2.4) 3.4 (1.6) 5.4 (1.6) +values are given as mean (SD) Conclusion: Two thirds of pts. who switched to ADA biosimilar remained on this therapy for 2 years. As many as 16% of pts. switched back to ADA originator. Whether or to what degree this was influenced by nocebo effects needs further study. The same is true for the effect of functional impairment – it would be interesting to know whether this was due to inflammation or structural damage. References: [1]Neovius M et al. Ann Rheum Dis 2015; 74:354-360 [2]The study was funded by Hexal Germany. Figure 1. Treatment trajectories of ADA therapy in patients with CIRD during two years ADA: adalimumab; bDMARD: biological disease modifying anti-rheumatic drug. Disclosure of Interests: None declared