TY - JOUR
T1 - Changes in Tumor Necrosis Factor Inhibitor Drug Survival in Patients With Rheumatoid Arthritis, Psoriatic Arthritis, and Ankylosing Spondylitis Over 15 Years
AU - Visman, Ingrid M.
AU - Atiqi, Sadaf
AU - Boers, Maarten
AU - Twisk, Jos W. R.
AU - Nurmohamed, Michael T.
N1 - Publisher Copyright: © 2024 The Journal of Rheumatology.
PY - 2024
Y1 - 2024
N2 - Objective. To study changes in retention of first biologic disease-modifying antirheumatic drug (DMARD) therapy over a period of 15 years in an inception cohort of patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS). Methods. We assessed patient and disease characteristics and drug survival of patients starting a biologic (tumor necrosis factor inhibitor [TNFi]) therapy between 2004 and 2019 in routine care at the Amsterdam Rheumatology and Immunology Center, Reade, the Netherlands. Starts were classified as early (2004-2008), intermediate (2009-2013), and recent (2014-2018). Kaplan-Meier plots and log-rank tests assessed the overall difference in drug survival between the 3 observation groups and between diagnoses, followed by Cox regression to estimate hazard ratios (HRs). Results. We included 1938 consecutive patients starting TNFi therapy, 63% with RA, 19% with PsA, and 19% with AS; 65% were female. Drug survival decreased significantly over time (overall P < 0.001), mostly caused by decreases in the most recent 4-year period. The HR for drug continuation was 2.04 (95% CI 1.71-2.43, P < 0.001) for the early vs the recent group and 1.92 (95% CI 1.58-2.35, P < 0.001) for the intermediate vs the recent group. Drug survival time was significantly different between diseases (overall P < 0.001), mostly caused by shorter survival in RA. The HR for drug continuation was 0.58 (95% CI 0.47-0.73, P < 0.001) for RA vs PsA and 0.63 (95% CI 0.51-0.78, P < 0.001) for RA vs AS. Conclusion. Patients with RA, PsA, and AS currently initiating biologic (TNFi) therapy discontinue the drug much sooner than those starting shortly after the drugs were introduced. This is most likely because of the availability of alternative novel biologic and targeted synthetic DMARD treatments and treat-to-target protocols enabling and necessitating earlier switching.
AB - Objective. To study changes in retention of first biologic disease-modifying antirheumatic drug (DMARD) therapy over a period of 15 years in an inception cohort of patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS). Methods. We assessed patient and disease characteristics and drug survival of patients starting a biologic (tumor necrosis factor inhibitor [TNFi]) therapy between 2004 and 2019 in routine care at the Amsterdam Rheumatology and Immunology Center, Reade, the Netherlands. Starts were classified as early (2004-2008), intermediate (2009-2013), and recent (2014-2018). Kaplan-Meier plots and log-rank tests assessed the overall difference in drug survival between the 3 observation groups and between diagnoses, followed by Cox regression to estimate hazard ratios (HRs). Results. We included 1938 consecutive patients starting TNFi therapy, 63% with RA, 19% with PsA, and 19% with AS; 65% were female. Drug survival decreased significantly over time (overall P < 0.001), mostly caused by decreases in the most recent 4-year period. The HR for drug continuation was 2.04 (95% CI 1.71-2.43, P < 0.001) for the early vs the recent group and 1.92 (95% CI 1.58-2.35, P < 0.001) for the intermediate vs the recent group. Drug survival time was significantly different between diseases (overall P < 0.001), mostly caused by shorter survival in RA. The HR for drug continuation was 0.58 (95% CI 0.47-0.73, P < 0.001) for RA vs PsA and 0.63 (95% CI 0.51-0.78, P < 0.001) for RA vs AS. Conclusion. Patients with RA, PsA, and AS currently initiating biologic (TNFi) therapy discontinue the drug much sooner than those starting shortly after the drugs were introduced. This is most likely because of the availability of alternative novel biologic and targeted synthetic DMARD treatments and treat-to-target protocols enabling and necessitating earlier switching.
KW - ankylosing spondylitis
KW - biological therapy
KW - psoriatic arthritis
KW - rheumatoid arthritis
KW - tumor necrosis factor inhibitors
UR - http://www.scopus.com/inward/record.url?scp=85181805562&partnerID=8YFLogxK
U2 - https://doi.org/10.3899/jrheum.2023-0149
DO - https://doi.org/10.3899/jrheum.2023-0149
M3 - Article
C2 - 37714543
SN - 0315-162X
VL - 51
SP - 84
EP - 87
JO - Journal of rheumatology
JF - Journal of rheumatology
IS - 1
ER -