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Effectiveness of TNF-inhibitors, abatacept, IL6-inhibitors and JAK-inhibitors in 31 846 patients with rheumatoid arthritis in 19 registers from the 'JAK-pot' collaboration

dc.contributor.authorİNANÇ, GÜZİDE NEVSUN
dc.contributor.authorsLauper K., Ludici M., Mongin D., Bergstra S. A., Choquette D., Codreanu C., Cordtz R., De Cock D., Dreyer L., Elkayam O., et al.
dc.date.accessioned2023-07-05T06:26:57Z
dc.date.available2023-07-05T06:26:57Z
dc.date.issued2022-06-15
dc.description.abstractBackground JAK-inhibitors (JAKi), recently approved in rheumatoid arthritis (RA), have changed the landscape of treatment choices. We aimed to compare the effectiveness of four current second-line therapies of RA with different modes of action, since JAKi approval, in an international collaboration of 19 registers. Methods In this observational cohort study, patients initiating tumour necrosis factor inhibitors (TNFi), interleukin-6 inhibitors (IL-6i), abatacept (ABA) or JAKi were included. We compared the effectiveness of these treatments in terms of drug discontinuation and Clinical Disease Activity Index (CDAI) response rates at 1 year. Analyses were adjusted for patient, disease and treatment characteristics, including lines of therapy and accounted for competing risk. Results We included 31 846 treatment courses: 17 522 TNFi, 2775 ABA, 3863 IL-6i and 7686 JAKi. Adjusted analyses of overall discontinuation were similar across all treatments. The main single reason of stopping treatment was ineffectiveness. Compared with TNFi, JAKi were less often discontinued for ineffectiveness (adjusted HR (aHR) 0.75, 95% CI 0.67 to 0.83), as was IL-6i (aHR 0.76, 95% CI 0.67 to 0.85) and more often for adverse events (aHR 1.16, 95% CI 1.03 to 1.33). Adjusted CDAI response rates at 1 year were similar between TNFi, JAKi and IL-6i and slightly lower for ABA. Conclusion The adjusted overall drug discontinuation and 1 year response rates of JAKi and IL-6i were similar to those observed with TNFi. Compared with TNFi, JAKi were more often discontinued for adverse events and less for ineffectiveness, as were IL-6i.
dc.identifier.citationLauper K., Ludici M., Mongin D., Bergstra S. A., Choquette D., Codreanu C., Cordtz R., De Cock D., Dreyer L., Elkayam O., et al., "Effectiveness of TNF-inhibitors, abatacept, IL6-inhibitors and JAK-inhibitors in 31 846 patients with rheumatoid arthritis in 19 registers from the 'JAK-pot' collaboration", ANNALS OF THE RHEUMATIC DISEASES, cilt.81, sa.10, ss.1358-1366, 2022
dc.identifier.doi10.1136/annrheumdis-2022-222586
dc.identifier.endpage1366
dc.identifier.issn0003-4967
dc.identifier.issue10
dc.identifier.startpage1358
dc.identifier.urihttps://avesis.marmara.edu.tr/api/publication/8a0672e8-d0cf-402d-8896-5a828d43d53e/file
dc.identifier.urihttps://hdl.handle.net/11424/290746
dc.identifier.volume81
dc.language.isoeng
dc.relation.ispartofANNALS OF THE RHEUMATIC DISEASES
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectTıp
dc.subjectSağlık Bilimleri
dc.subjectDahili Tıp Bilimleri
dc.subjectİç Hastalıkları
dc.subjectİmmünoloji ve Romatoloji
dc.subjectMedicine
dc.subjectHealth Sciences
dc.subjectInternal Medicine Sciences
dc.subjectInternal Diseases
dc.subjectImmunology and Rheumatology
dc.subjectROMATOLOJİ
dc.subjectKlinik Tıp
dc.subjectKlinik Tıp (MED)
dc.subjectRHEUMATOLOGY
dc.subjectCLINICAL MEDICINE
dc.subjectClinical Medicine (MED)
dc.subjectRomatoloji
dc.subjectRheumatology
dc.subjectEpidemiology
dc.subjectBiological Therapy
dc.subjectTumor Necrosis Factor Inhibitors
dc.subjectArthritis
dc.subjectRheumatoid
dc.subjectTherapeutics
dc.subjectNECROSIS-FACTOR-ALPHA
dc.subjectDOUBLE-BLIND
dc.subjectPLUS METHOTREXATE
dc.subjectPHASE-III
dc.subjectADALIMUMAB
dc.subjectPLACEBO
dc.subjectTOFACITINIB
dc.subjectMONOTHERAPY
dc.subjectMULTICENTER
dc.subjectINFLIXIMAB
dc.subjectArthritis, Rheumatoid
dc.titleEffectiveness of TNF-inhibitors, abatacept, IL6-inhibitors and JAK-inhibitors in 31 846 patients with rheumatoid arthritis in 19 registers from the 'JAK-pot' collaboration
dc.typearticle
dspace.entity.typePublication
local.avesis.id8a0672e8-d0cf-402d-8896-5a828d43d53e
local.indexed.atWOS
local.indexed.atPUBMED
local.indexed.atSCOPUS
relation.isAuthorOfPublicationc963a17b-4775-4dd7-8db7-ea072cc49ef1
relation.isAuthorOfPublication.latestForDiscoveryc963a17b-4775-4dd7-8db7-ea072cc49ef1

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