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| 2. |
- Di Giuseppe, D, et al.
(författare)
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BIOLOGIC REFRACTORY DISEASE IN AXIAL SPONDYLOARTHRITIS - DEFINITION, PREVALENCE AND PATIENT CHARACTERISTICS. A COLLABORATION BETWEEN FIVE NORDIC BIOLOGIC REGISTRIES
- 2021
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Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 80, s. 82-83
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- In clinical practice, some patients with axial spondyloarthritis (axSpA) fail several consecutive biological treatments (bDMARDs). How this group of ”refractory” patients should best be defined, how common they are, and what their characteristics are, is poorly understood.Objectives:To explore the point prevalence of bDMARD refractory disease in axSpA over time, according to different definitions, and to describe the characteristics of refractory vs. not-refractory patients upon start of their first bDMARD.Methods:Observational prospective cohort study. Patients with axSpA (ankylosing spondylitis/non-radiographic axial SpA) starting a first bDMARD 2009-2018 were identified in biologic registries in Denmark, Sweden, Finland, Norway and Iceland. Clinical characteristics and treatments were retrieved, and data were pooled for analysis.Refractory disease was defined based on the number of different bDMARD treatments started in individual patients: mild (≥3 bDMARDs), moderate (≥4), and strict (5 or more). Restart of same bDMARD with another bDMARD in between counted as separate courses whereas switch from originator to corresponding biosimilar was ignored.Proportions of patients fulfilling each definition of refractory disease at 2 and 5 years after the start of 1st bDMARD were calculated.Point-prevalence per calendar-year was calculated as the number of patients with refractory disease at the end of each year, divided by the total number of patients ever having starting a first bDMARD before that time-point, and who were still alive and resident in the country.Results:The point prevalence of refractory axSpA increased with calendar-time (Figure). Among 12,037 included axSpA patients (64% male), the point-prevalence of bDMARD refractory disease in 2018 was 16%/7%/3% according to mild/moderate/strict definitions (Table).Table 1.Biologic refractory axSpA according to three definitionsA.Baseline characteristics upon start 1st bDMARDRefractory definitionOverall cohortMILDMODERATESTRICTN120371969832351Age, years42 (13)41 (12)41 (12)41 (12)Male, %64%57%54%56%Disease duration, years7 (10)6 (9)6 (8)5 (8)BASDAI, 0-10053 (28)60 (29)63 (27)66 (35)ASDAS3.3 (1.1)3.5 (1.2)3.6 (1.0)3.7 (1.1)CRP, mg/L16 (23)18 (26)21 (28)23 (32)Patient global, VAS, 0-10059 (25)65 (22)66 (22)67 (23)Patient Pain, VAS, 0-10057 (24)62 (22)63 (22)63 (22)Fatigue, VAS, 0-10059 (27)66 (26)66 (26)68 (25)B.Proportions of patients having refractory disease 2 and 5 years after start of their first bDMARD2 years, %5%1%0%5 years, %13%4%1%Numbers are means (SD) unless otherwise statedUpon start of their 1st bDMARD, patients later fulfilling the definitions for refractory axSpA were more frequently women, had shorter disease duration, higher C-reactive protein and higher patient reported outcomes.Overall, 5%/1%/0% had mild/moderate/strict refractory disease 2 years after start of first bDMARD, after 5 years it was 13%/4%/1% (Table).Conclusion:In this large Nordic observational cohort of axSpA patients treated in routine care, we could demonstrate that a substantial proportion of all patients had used multiple bDMARDs. In 2018, one in six patients had received ≥3 bDMARDs, indicating a bDMARD refractory disease. Multiple switching was more frequent during later years, probably due to more bDMARDs becoming available. The characteristics of refractory axSpA, including sex and disease activity, will have to be further explored, as will the impact of refractory disease on long-term outcomes.Acknowledgements:the DANBIO, SRQ, ICEBIO, ROB-FIN and NOR-DMARD registries.Partly sponsored by Nordforsk and Foreum.Disclosure of Interests:Daniela Di Giuseppe: None declared, Ulf Lindström: None declared, Kalle Aaltonen: None declared, Heikki Relas Speakers bureau: Abbvie, Celgene, MSD, Roche, Sella Aarrestad Provan: None declared, Björn Gudbjornsson Speakers bureau: Amgen and Novartis, Merete L. Hetland Grant/research support from: AbbVie, Biogen, BMS, Celtrion, Eli Lilly Denmark A/S, Janssen Biologics B.V, Lundbeck Fonden, MSD, Pfizer, Roche, Samsung Biopis, Sandoz. MLH chairs the steering committee of the Danish Rheumatology Quality Registry (DANBIO), which receives public funding from the hospital owners and funding from pharmaceutical companies. MLH co-chairs the EuroSpA research collaboration, which generates real-world evidence of treatment of psoriatic arthritis and axial spondyloarthritis based on secondary use of quality data and is partly funded by Novartis., Johan Askling: None declared, Tanja Schjødt Jørgensen: None declared, Lene Dreyer Speakers bureau: Eli-Lilly and Galderma, Grant/research support from: BMS, Dan Nordström: None declared, Brigitte Michelsen: None declared, Arni Jon Geirsson: None declared, Lennart T.H. Jacobsson: None declared, Bente Glintborg Grant/research support from: Abbvie, BMS, Pfizer, Lundbeck foundation
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| 3. |
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| 4. |
- 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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| 5. |
- Lindstrom, U, et al.
(författare)
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COMPARISON OF TREATMENT RETENTION OF SECUKINUMAB AND TNF-INHIBITORS IN PSORIATIC ARTHRITIS. OBSERVATIONAL DATA FROM A NORDIC COLLABORATION.
- 2020
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Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 79, s. 427-428
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- A head-to-head trial (EXCEED) has indicated similar effectiveness of secukinumab (SEC) and the tumor necrosis factor inhibitor (TNFi) adalimumab (ADA) in psoriatic arthritis (PsA). In the clinical setting, treatment retention serves as a combined measure of overall effectiveness and tolerability.Objectives:To explore baseline patient characteristics, and compare treatment retention rates for SEC and each of etanercept (ETN), infliximab (IFX), golimumab (GOL), certolizimab (CZP) and ADA in PsA.Methods:Patients starting SEC or any TNFi in 2015-2018, in the 5 Nordic countries, were identified in clinical rheumatology registers. Data were pooled for analysis and stratified by 1st, 2ndand ≥3rdline of treatment. One year treatment retention was compared by crude Kaplan-Meier curves and a proportional hazard model for risk of discontinuation, censored at 1 year and adjusted for sex, age, country and baseline CRP, patient global and use of csDMARD, with ADA as reference.Results:In total, 6062 patients with PsA were included, contributing 8172 treatment starts (table 1). SEC was mainly used as 2ndor ≥3rdline treatment. The survival curves and 1-year treatment retention rates, stratified by line of treatment, were similar for SEC compared to the TNFis, with some differences between the different TNFi (fig 1, table 2). Adjusted hazard ratios (HR) also indicated similar risk of SEC withdrawal compared to ADA (table 2).Table 1.Patient characteristics at treatment start1stline2ndline≥3rdlineSECN=164TNFiN=3808SECN=273TNFiN=1767SECN=767TNFiN=1393Females48%47%44%42%36%39%Age, years52 (13)49 (13)50 (12)50 (13)52 (12)51 (12)Disease duration, years12 (10)10 (10)13 (10)13 (10)16 (10)16 (10)Swollen joint count 283 (4)2 (3)2 (3)2 (3)3 (4)2 (3)CRP, mg/L10 (18)10 (17)7 (11)9 (17)13 (22)11 (20)Patient global score57 (24)58 (24)60 (25)59 (26)68 (23)65 (24)Concomitant therapycsDMARD30%60%41%57%49%53% Methotrexate24%49%31%48%40%44% Sulphasalazine2%9%5%5%4%6%Numbers are mean (SD) unless noted otherwiseTable 2.One year treatment retention and hazard of discontinuation for SEC and TNFiLine of treatmentDrugN1 year treatment retention % (95% CI)Adjusted HR (95% CI) for discontinuation1stlineADA56973 (69-76)RefCZP27366 (60-72)1.2 (0.9-1.6)ETN174773 (71-75)0.9 (0.7-1.1)GOL21267 (60-73)1.2 (0.9-1.7)IFX100762 (59-65)1.4 (1.1-1.7)SEC16472 (63-78)1.0 (0.7-1.4)2ndlineADA41569 (63-73)RefCZP17651 (43-58)1.6 (1.2-2.2)ETN70163 (59-66)1.2 (0.9-1.5)GOL15169 (61-76)0.9 (0.6-1.2)IFX32465 (59-70)1.0 (0.8-1.4)SEC27369 (62-74)0.9 (0.7-1.2)≥3rdlineADA34667 (62-72)RefCZP22149 (42-56)1.5 (1.2-2.0)ETN37262 (57-67)1.1 (0.9-1.5)GOL20656 (49-63)1.3 (1.0-1.8)IFX24857 (50-63)1.3 (1.0-1.8)SEC76763 (59-67)1.0 (0.8-1.3)Conclusion:In this large study of bDMARD treatment of PsA in clinical practice, SEC was most often used as 2ndor ≥3rdline treatment, and the treatment retention of SEC was comparable with that of TNFi. Further analyses, taking into account other comorbidities, channeling and effectiveness will be presented.Acknowledgments:UL and BG are shared first, and LJ and LEK shared last authors.Partly funded by Nordforsk and FOREUM.Disclosure of Interests:Ulf Lindström: None declared, Bente Glintborg Grant/research support from: Grants from Pfizer, Biogen and Abbvie, Daniela Di Giuseppe: None declared, Tanja Schjødt Jørgensen Speakers bureau: Abbvie, Pfizer, Roche, Novartis, UCB, Biogen, and Eli Lilly, Björn Gudbjornsson Speakers bureau: Novartis and Amgen, Kathrine L. Grøn Grant/research support from: BMS, Sella Aarrestad Provan Consultant of: Novartis, Brigitte Michelsen: None declared, Merete L. Hetland Grant/research support from: BMS, MSD, AbbVie, Roche, Novartis, Biogen and Pfizer, Consultant of: Eli Lilly, Speakers bureau: Orion Pharma, Biogen, Pfizer, CellTrion, Merck and Samsung Bioepis, Johan K Wallman Consultant of: AbbVie, Celgene, Eli Lilly, Novartis and UCB Pharma, Dan Nordström Consultant of: Abbvie, Celgene, Lilly, Novartis, Pfizer, Roche and UCB., Speakers bureau: Abbvie, Celgene, Lilly, Novartis, Pfizer, Roche and UCB., Nina Trokovic: None declared, Thorvardur Love: None declared, Niels Steen Krogh: None declared, Johan Askling Grant/research support from: JA acts or has acted as PI for agreements between Karolinska Institutet and the following entities, mainly in the context of the ARTIS national safety monitoring programme of immunomodulators in rheumatology: Abbvie, BMS, Eli Lilly, Merck, MSD, Pfizer, Roche, Samsung Bioepis, Sanofi, and UCB Pharma, Lennart T.H. Jacobsson Consultant of: AbbVie, Eli Lilly, Janssen, Novartis and Pfizer, Lars Erik Kristensen Consultant of: UCB Pharma (Advisory Board), Sannofi (Advisory Board), Abbvie (Advisory Board), Biogen (Advisory Board), Speakers bureau: AbbVie, Amgen, Biogen, Bristol-Myers Squibb,Celgene, Eli Lilly, Gilead, Forward Pharma, Janssen Pharmaceuticals, MSD, Novartis, Pfizer, and UCB Pharma
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| 6. |
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| 7. |
- Ornbjerg, LM, et al.
(författare)
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SECULAR TRENDS IN BASELINE CHARACTERISTICS, TREATMENT RETENTION AND RESPONSE RATES IN 27189 BIO-NAIVE AXIAL SPONDYLOARTHRITIS PATIENTS INITIATING TNFI - RESULTS FROM THE EUROSPA COLLABORATION
- 2021
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Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 80, s. 217-218
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Knowledge of changes over time in baseline characteristics and tumor necrosis factor inhibitor (TNFi) response in bio-naïve axial spondyloarthritis (axSpA) patients treated in routine care is limited.Objectives:To investigate secular trends in baseline characteristics and retention, remission and response rates in axSpA patients initiating a first TNFi.Methods:Prospectively collected data on bio-naïve axSpA patients starting TNFi in routine care from 15 European countries were pooled. According to year of TNFi initiation, three groups were defined a priori based on bDMARD availability: Group A (1999–2008), Group B (2009–2014) and Group C (2015–2018). Retention rates (Kaplan-Meier), crude and LUNDEX adjusted1 remission (Ankylosing Spondylitis Disease Activity Score (ASDAS) <1.3, Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) <20) and response (ASDAS Major and Clinically Important Improvement (MI/CII), BASDAI 50) rates were assessed at 6, 12 and 24 months. No statistical comparisons were made.Results:In total, 27189 axSpA patients were included (5945, 11255 and 9989 in groups A, B and C).At baseline, patients in group A were older, had longer disease duration and a larger proportion of male and HLA-B27 positive patients compared to B and C, whereas disease activity was similar across groups.Retention rates at 6, 12 and 24 months were highest in group A (88%/81%/71%) but differed little between B (84%/74%/64%) and C (85%/76%/67%).In all groups, median ASDAS and BASDAI had decreased markedly at 6 months (Table 1). The ASDAS values at 12 and 24 months and BASDAI at 24 months were higher in group A compared with groups B and C. Similarly, crude remission and response rates were lowest in group A. After adjustments for drug retention (LUNDEX), remission and response rates showed less pronounced between-group differences regarding ASDAS measures and no relevant differences regarding BASDAI measures.Conclusion:Nowadays, axSpA patients initiating TNFi are younger with shorter disease duration and more frequently female and HLA-B27 negative than previously, while baseline disease activity is unchanged. Drug retention rates have decreased, whereas crude remission and response rates have increased. This may indicate expanded indication but also a stable disease activity threshold for TNFi initiation over time, an increased focus on targeting disease remission and more available treatment options.References:[1]Arthritis Rheum 2006; 54: 600-6.Table 1.Secular trends in baseline characteristics, treatment retention, remission and response rates in European axSpA patients initiating a 1st TNFiBaseline characteristicsGroup A(1999–2008)Group B(2009–2014)Group C(2015–2018)Age, years, median (IQR)57 (49–66)51 (42–60)46 (37–56)Male, %666057HLA-B27, %877772Years since diagnosis, median (IQR)5 (1–12)2 (0–8)2 (0–7)Smokers, %232425ASDAS, median (IQR)3.5 (2.8–4.1)3.4 (2.8–4.1)3.5 (2.8–4.1)BASDAI, median, (IQR)57 (42–71)59 (43–72)57 (41–71)TNFi drug, % (Adalimumab /Etanercept / Infliximab /Certolizumab / Golimumab)22 / 35 / 43 / 0 / 037 / 21 / 20 / 4 / 1827 / 28 / 24 / 8 / 13Follow up6 months12 months24 monthsGr AGr BGr CGr AGr BGr CGr AGr BGr CRetention rates, %, (95% CI)88 (88–89)84 (83–85)85 (84–86)81 (80–82)74 (74–75)76 (75–76)71 (70–72)64 (63–65)67 (66–68)ASDAS, median, (IQR)1.8 (1.2–2.8)1.9 (1.2–2.8)1.8 (1.2–2.6)1.9 (1.3–2.6)1.7 (1.2–2.5)1.6 (1.1–2.4)1.9 (1.4–2.6)1.7 (1.1–2.4)1.5 (1.1–2.2)ASDAS inactive disease, %, c/L28 / 2528 / 2430 / 2624 / 1932 / 2434 / 2623 / 1634 / 2039 / 23ASDAS CII, %, c/L57 / 5159 / 5063 / 5461 / 5063 / 4767 / 5159 / 4168 / 4074 / 45ASDAS MI, %, c/L31 / 2732 / 2737 / 3232 / 2637 / 2741 / 3130 / 2042 / 2546 / 28BASDAI, median, (IQR)23 (10–40)26 (11–48)24 (10–44)21 (10–38)23 (10–42)20 (8–39)22 (9–40)20 (8–39)16 (6–35)BASDAI remission, %, c/L44 / 4040 / 3443 / 3645 / 3645 / 3450 / 3844 / 3048 / 2956 / 34BASDAI 50 response, %, c/L53 / 4750 / 4253 / 4557 / 4656 / 4258 / 4457 / 3960 / 3563 / 38Gr, Group; c/L, crude/LUNDEX adjusted.Acknowledgements:Novartis Pharma AG and IQVIA for supporting the EuroSpA Research Collaboration Network.Disclosure of Interests:Lykke Midtbøll Ørnbjerg Grant/research support from: Novartis, Sara Nysom Christiansen Speakers bureau: BMS and GE, Grant/research support from: Novartis, Simon Horskjær Rasmussen: None declared, Anne Gitte Loft Speakers bureau: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Consultant of: AbbVie, Janssen, Lilly, MSD, Novartis, Pfizer, UCB, Grant/research support from: Novartis, Ulf Lindström: None declared, Jakub Zavada: None declared, Florenzo Iannone: None declared, Fatos Onen: None declared, Michael J. Nissen Speakers bureau: Novartis, Eli Lilly, Celgene, and Pfizer, Consultant of: Novartis, Eli Lilly, Celgene, and Pfizer, Brigitte Michelsen Consultant of: Novartis, Grant/research support from: Novartis, Maria Jose Santos Speakers bureau: AbbVie, Novartis, Pfizer, Gary Macfarlane Grant/research support from: GlaxoSmithKline, Dan Nordström Consultant of: Abbvie, BMS, MSD, Novartis, Pfizer, Roche, UCB, Manuel Pombo-Suarez: None declared, Catalin Codreanu Speakers bureau: AbbVie, Amgen, Egis, Novartis, Pfizer, UCB, Grant/research support from: AbbVie, Amgen, Egis, Novartis, Pfizer, UCB, Matija Tomsic Speakers bureau: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Consultant of: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Irene van der Horst-Bruinsma Speakers bureau: Abbvie, BMS, MSD, Novartis, Pfizer, Lilly, UCB, Björn Gudbjornsson Speakers bureau: Amgen and Novartis, Johan Askling: None declared, Bente Glintborg Grant/research support from: Pfizer, Biogen, AbbVie, Karel Pavelka Speakers bureau: AbbVie, Roche, MSD, UCB, Pfizer, Novartis, Egis, Gilead, Eli Lilly, Consultant of: AbbVie, Roche, MSD, UCB, Pfizer, Novartis, Egis, Gilead, Eli Lilly, Elisa Gremese: None declared, Nurullah Akkoc: None declared, Adrian Ciurea Speakers bureau: Abbvie, Eli-Lilly, MSD, Novartis, Pfizer, Eirik kristianslund: None declared, Anabela Barcelos: None declared, Gareth T. Jones Grant/research support from: Pfizer, AbbVie, UCB, Celgene, Amgen, GSK, Anna-Mari Hokkanen Grant/research support from: MSD, Carlos Sánchez-Piedra: None declared, Ruxandra Ionescu Speakers bureau: Abbvie, Amgen, Boehringer-Ingelheim Eli-Lilly,Novartis, Pfizer, Sandoz, UCB, Ziga Rotar Speakers bureau: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Consultant of: Abbvie, Amgen, Biogen, Medis, MSD, Novartis, Pfizer, Marleen G.H. van de Sande: None declared, Arni Jon Geirsson: None declared, Mikkel Østergaard Speakers bureau: AbbVie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Centocor, GSK, Hospira, Janssen, Merck, Mundipharma, Novartis, Novo, Orion, Pfizer, Regeneron, Schering-Plough, Roche, Takeda, UCB and Wyeth, Consultant of: AbbVie, BMS, Boehringer-Ingelheim, Celgene, Eli-Lilly, Centocor, GSK, Hospira, Janssen, Merck, Mundipharma, Novartis, Novo, Orion, Pfizer, Regeneron, Schering-Plough, Roche, Takeda, UCB and Wyeth, Merete L. Hetland Speakers bureau: Abbvie, Biogen, BMS, Celltrion, Eli Lilly, Janssen Biologics B.V, Lundbeck Fonden, MSD, Pfizer, Roche, Samsung Biopies, Sandoz, Novartis.
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| 8. |
- Papathoma, PE, et al.
(författare)
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A replication study, systematic review and meta-analysis of automated image-based diagnosis in parkinsonism
- 2022
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Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 12:1, s. 2763-
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Tidskriftsartikel (refereegranskat)abstract
- Differential diagnosis of parkinsonism early upon symptom onset is often challenging for clinicians and stressful for patients. Several neuroimaging methods have been previously evaluated; however specific routines remain to be established. The aim of this study was to systematically assess the diagnostic accuracy of a previously developed 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) based automated algorithm in the diagnosis of parkinsonian syndromes, including unpublished data from a prospective cohort. A series of 35 patients prospectively recruited in a movement disorder clinic in Stockholm were assessed, followed by systematic literature review and meta-analysis. In our cohort, automated image-based classification method showed excellent sensitivity and specificity for Parkinson Disease (PD) vs. atypical parkinsonian syndromes (APS), in line with the results of the meta-analysis (pooled sensitivity and specificity 0.84; 95% CI 0.79–0.88 and 0.96; 95% CI 0.91 –0.98, respectively). In conclusion, FDG-PET automated analysis has an excellent potential to distinguish between PD and APS early in the disease course and may be a valuable tool in clinical routine as well as in research applications.
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