5. |
- Georgiadis, S, et al.
(författare)
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CAN SINGLE IMPUTATION TECHNIQUES FOR BASDAI COMPONENTS RELIABLY CALCULATE THE COMPOSITE SCORE IN AXIAL SPONDYLOARTHRITIS PATIENTS?
- 2022
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Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 81, s. 212-213
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- In axial spondyloarthritis (axSpA), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) is a key patient-reported outcome. However, one or more of its components may be missing when recorded in clinical practice.ObjectivesTo determine whether an individual patient’s BASDAI at a given timepoint can be reliably calculated with different single imputation techniques and to explore the impact of the number of missing components and/or differences between missingness of individual components.MethodsReal-life data from axSpA patients receiving tumour necrosis factor inhibitors (TNFi) from 13 countries in the European Spondyloarthritis (EuroSpA) Research Collaboration Network were utilized [1]. We studied missingness in BASDAI components based on simulations in a complete dataset, where we applied and expanded the approach of Ramiro et al. [2]. After introducing one or more missing components completely at random, BASDAI was calculated from the available components and with three different single imputation techniques: possible middle value (i.e. 50) of the component and mean and median of the available components. Differences between the observed (original) and calculated scores were assessed and correct classification of patients as having BASDAI<40 mm was additionally evaluated. For the setting with one missing component, differences arising between missing one of components 1-4 versus 5-6 were explored. Finally, the performance of imputations in relation to the values of the original score was investigated.ResultsA total of 19,894 axSpA patients with at least one complete BASDAI registration at any timepoint were included. 59,126 complete BASDAI registrations were utilized for the analyses with a mean BASDAI of 38.5 (standard deviation 25.9). Calculating BASDAI from the available components and imputing with mean or median showed similar levels of agreement (Table 1). When allowing one missing component, >90% had a difference of ≤6.9 mm between the original and calculated scores and >95% were correctly classified as BASDAI<40 (Table 1). However, separate analyses of components 1-4 and 5-6 as a function of the BASDAI score suggested that imputing any one of the first four BASDAI components resulted in a level of agreement <90% for specific BASDAI values while imputing one of the stiffness components 5-6 always reached a level of agreement >90% (Figure 1, upper panels). As expected, it was observed that regardless of the BASDAI component set to missing and the imputation technique used, correct classification of patients as BASDAI<40 was less than 95% for values around the cutoff (Figure 1, lower panels).Table 1.Level of agreement between the original and calculated BASDAI and correct classification for BASDAI<40 mmLevel of agreement with Dif≤6.9 mm* (%)Correct classification for BASDAI<40 mm** (%)1 missing componentAvailable93.996.9Value 5073.996.3Mean94.296.8Median93.196.82 missing componentsAvailable83.794.8Value 5040.792.8Mean83.594.8Median82.894.73 missing componentsAvailable71.992.6Value 5028.187.3Mean72.292.6Median69.792.2* The levels of agreement with a difference (Dif) of ≤6.9 mm between the original and calculated scores were based on the half of the smallest detectable change. Agreement of >90% was considered as acceptable. ** Correct classification of >95% was considered as acceptable.Figure 1.Level of agreement between the original and calculated BASDAI and correct classification for BASDAI<40 mm as a function of the original scoreConclusionBASDAI calculation with available components gave similar results to single imputation of missing components with mean or median. Only when missing one of BASDAI components 5 or 6, single imputation techniques can reliably calculate individual BASDAI scores. However, missing any single component value results in misclassification of patients with original BASDAI scores close to 40.References[1]Ørnbjerg et al. (2019). Ann Rheum Dis, 78(11), 1536-1544.[2]Ramiro et al. (2014). Rheumatology, 53(2), 374-376.AcknowledgementsNovartis Pharma AG and IQVIA for supporting the EuroSpA collaboration.Disclosure of InterestsStylianos Georgiadis Grant/research support from: Novartis, Myriam Riek Grant/research support from: Novartis, Christos Polysopoulos Grant/research support from: Novartis, Almut Scherer Grant/research support from: Novartis, Daniela Di Giuseppe: None declared, Gareth T. Jones Speakers bureau: Janssen, Grant/research support from: AbbVie, Pfizer, UCB, Amgen, GSK, Merete Lund Hetland Grant/research support from: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Medac, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis, Mikkel Østergaard Speakers bureau: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, UCB, Consultant of: Abbvie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Hospira, Janssen, Merck, Novartis, Novo, Orion, Pfizer, Regeneron, Roche, Sandoz, Sanofi, UCB, Grant/research support from: Abbvie, BMS, Merck, Celgene, Novartis, Simon Horskjær Rasmussen Grant/research support from: Novartis, Johan K Wallman Consultant of: AbbVie, Amgen, Celgene, Eli Lilly, Novartis, Bente Glintborg Grant/research support from: Pfizer, Abbvie, BMS, Anne Gitte Loft Speakers bureau: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Consultant of: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Karel Pavelka Speakers bureau: Pfizer, MSD, BMS, UCB, Amgen, Egis, Roche, AbbVie, Consultant of: Pfizer, MSD, BMS, UCB, Amgen, Egis, Roche, AbbVie, Jakub Zavada Speakers bureau: Abbvie, Elli-Lilly, Sandoz, Novartis, Egis, UCB, Consultant of: Abbvie, Elli-Lilly, Sandoz, Novartis, Egis, UCB, Merih Birlik: None declared, Ayten Yazici Grant/research support from: Roche, Brigitte Michelsen Grant/research support from: Novartis, Eirik kristianslund: None declared, Adrian Ciurea Speakers bureau: AbbVie, Eli Lilly, Merck Sharp & Dohme, Novartis, Pfizer, Consultant of: AbbVie, Eli Lilly, Merck Sharp & Dohme, Novartis, Pfizer, Michael J. Nissen Speakers bureau: AbbVie, Eli Lilly, Janssens, Novartis, Pfizer, Consultant of: AbbVie, Eli Lilly, Janssens, Novartis, Pfizer, Ana Maria Rodrigues Speakers bureau: Abbvie, Amgen, Consultant of: Abbvie, Amgen, Grant/research support from: Novartis, Pfizer, Amgen, Maria Jose Santos Speakers bureau: Abbvie, AstraZeneca, Lilly, Novartis, Pfizer, Gary Macfarlane Grant/research support from: GSK, Anna-Mari Hokkanen Grant/research support from: MSD, Heikki Relas Speakers bureau: Abbvie, Celgene, Pfizer, UCB, Viatris, Consultant of: Abbvie, Celgene, Pfizer, UCB, Viatris, Catalin Codreanu Speakers bureau: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Consultant of: AbbVie, Amgen, Boehringer Ingelheim, Ewopharma, Lilly, Novartis, Pfizer, Corina Mogosan: None declared, Ziga Rotar Speakers bureau: Abbvie, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek, Janssen, Consultant of: Abbvie, Novartis, MSD, Medis, Biogen, Eli Lilly, Pfizer, Sanofi, Lek, Janssen, Matija Tomsic Speakers bureau: Abbvie, Amgen, Biogen, Eli Lilly, Janssen, Medis, MSD, Novartis, Pfizer, Sanofi, Sandoz-Lek, Consultant of: Abbvie, Amgen, Biogen, Eli Lilly, Janssen, Medis, MSD, Novartis, Pfizer, Sanofi, Sandoz-Lek, Björn Gudbjornsson Speakers bureau: Amgen, Novartis, Consultant of: Amgen, Novartis, Arni Jon Geirsson: None declared, Pasoon Hellamand Grant/research support from: Novartis, Marleen G.H. van de Sande Speakers bureau: Eli Lilly, Novartis, UCB, Janssen, Abbvie, Consultant of: Eli Lilly, Novartis, UCB, Janssen, Abbvie, Grant/research support from: Eli Lilly, Novartis, UCB, Janssen, Abbvie, Isabel Castrejon: None declared, Manuel Pombo-Suarez Consultant of: Abbvie, MSD, Roche, Bruno Frediani: None declared, Florenzo Iannone Speakers bureau: Abbvie, Amgen, AstraZeneca, BMS, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Consultant of: Abbvie, Amgen, AstraZeneca, BMS, Galapagos, Janssen, Lilly, MSD, Novartis, Pfizer, Roche, UCB, Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis
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9. |
- Glintborg, B, et al.
(författare)
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UPTAKE OF NEWER BIOLOGIC AND TARGETED SYNTHETIC DMARDS IN PSORIATIC ARTHRITIS, RESULTS FROM FOUR NORDIC BIOLOGIC REGISTRIES
- 2022
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Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 81, s. 766-767
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- The treatment landscape in psoriatic arthritis (PsA) is changing, including newer biologic and targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs) with different modes of action becoming available. However, the most effective treatment strategy in routine care remains to be established.ObjectivesTo explore the uptake and treatment patterns of newer b/tsDMARDs, namely JAK-inhibitors (JAKi; baricitinib, tofacitinib, upadacitinib), IL-17-inhibitors (ixekizumab, secukinumab), abatacept, apremilast, and ustekinumab in PsA patients from the Nordic countries. Furthermore, to describe patient characteristics and extra-musculoskeletal manifestations at treatment start (=baseline).MethodsObservational cohort study, using prospectively collected routine care data from 4 Nordic rheumatology registries. Treatments (newer b/tsDMARDs with tumor-necrosis-factor inhibitors (TNFi) as the reference) initiated from January 2009 until December 2020 and corresponding baseline patient characteristics were identified. Linkage to national patient registries was used to identify previous extra-musculoskeletal manifestations (0-5 years). Country-level data were pooled for analyses. Uptake of each drug was explored as the cumulative number of treatment starts (a) overall, irrespective of previous b/tsDMARD experience, and (b) in b/tsDMARD-naïve patients. Each patient could contribute >1 treatment course.ResultsOverall, 13,364 unique patients contributing 24,325 treatment courses with either a newer b/tsDMARD (4,855, 20%) or a TNFi (19,470, 80%, whereof 10,897 were started year 2015-20) were identified. For the sub-group of 11,892 first b/tsDMARD treatment courses, 1,009 (8%) were a newer b/tsDMARD (10,883 were a TNFi, whereof 5,956 were started year 2015-20).Secukinumab dominated the newer b/tsDMARD uptake (1,848 new-starts, Figure 1). Ustekinumab-uptake increased over time both overall and in b/tsDMARD-naïve patients. In b/tsDMARD-naïve patients, apremilast had the fastest uptake (490 new-starts) (Figure 1). Use of JAKi was limited, especially in b/tsDMARD-naïve patients.Figure 1.Patients starting a newer b/tsDMARD tended to have longer disease duration and slightly higher disease activity at baseline (DAS28, patient-reported outcomes) than TNFi initiators (Table 1). Previous extra-musculoskeletal manifestations (uveitis, IBD) were rare, and with similar distributions across treatments (Table 1).Table 1.Baseline characteristics upon treatment startAbata-ceptApre-milastBari-citinibIxe-kizumabSecuki-numabTofa-citinibUpada-citinibUste-kinumabAny TNFiCumulative uptake, n3629351063421848494669119470Male gender, %334227384033333744Age54 (12)53 (12)55 (13)52 (13)51 (13)54 (13)52 (10)50 (12)49 (13)b/tsDMARD treatment number, %1952911149020562191512262518171925≥3723378746173836219Disease duration, yrs9 (8)8 (8)10 (8)10 (8)9 (9)11 (10)8 (8)8 (9)7 (8)Pain, VAS (0-100)63 (21)61 (23)64 (23)64 (25)63 (24)66 (23)75 (17)64 (23)59 (24)DAS284.73 (1.34)4.04 (1.35)3.95 (1.36)4.24 (1.19)4.13 (1.36)4.49 (1.33)4.74 (0.88)4.19 (1.32)4.07 (1.29)Uveitis, %*323123022IBD, %*113111-31Numbers are mean (SD) unless otherwise statedIBD: inflammatory bowel disease, bDMARD: biologic DMARD, ts: targeted synthetic*0-5 years previously, available all study period for Iceland, Sweden, Finland until 31Dec2018, not available for DenmarkConclusionIn this cross-country collaboration we were able to explore uptake of newer b/tsDMARDs. TNFi still dominates compared to newer b/tsDMARDs in routine care treatment of PsA. Newer b/tsDMARDs are mainly used in patients with several previous treatment failures, i.e. with longer disease duration and higher disease activity, indicating difficult to treat disease. Further studies are planned to explore real-world treatment patterns and outcomes.AcknowledgementsBG and DdiG contributed equally.Partly funded by NordForsk and Foreum grants. On behalf of the Danish DANBIO, Swedish SRQ, Norwegian NOR-DMARD, Finnish ROB-FIN and Icelandic ICEBIO registriesDisclosure of InterestsBente Glintborg Grant/research support from: Pfizer, AbbVie, BMS, Daniela Di Giuseppe: None declared, Johan K Wallman Consultant of: AbbVie, Amgen, Celgene, Eli Lilly, Novartis, Grant/research support from: AbbVie, Amgen, Eli Lilly, Novartis, Pfizer, Dan Nordström: None declared, Björn Gudbjornsson Speakers bureau: Novartis and Amgen, Merete Lund Hetland Grant/research support from: AbbVie, Biogen, BMS, Celltrion, Eli Lilly Denmark A/S, Janssen Biologics B.V, Lundbeck Fonden, MSD, Pfizer, Roche, Samsung Biopis, Sandoz, Novartis., Johan Askling Grant/research support from: Abbvie, Astra-Zeneca, BMS, Eli Lilly, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB., Gerdur Gröndal: None declared, Tuulikki Sokka-Isler Grant/research support from: Abbvie, Amgen, BMS, Celgene, Eli Lilly, GSK, Medac, MSD, Novartis, Orion Pharma, Pfizer, Roche, Sandoz, UCB, Sella Aarrestad Provan: None declared, Ulf Lindström: None declared
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