| 3. |
- Van Bentum, R, et al.
(författare)
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MICROVASCULAR CHANGES OF THE RETINA IN ANKYLOSING SPONDYLITIS, AND THE ASSOCIATION WITH CARDIOVASCULAR DISEASE - THE EYE FOR A HEART STUDY.
- 2020
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Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 79, s. 1654-1654
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Patients with ankylosing spondylitis (AS) have an increased risk at cardiovascular disease (CVD). Microvasculature changes might precede overt CVD, but have been poorly studied in AS. The small vessels of the retina are accessible for non-invasive visualization, and microvascular changes (retinal arteriolar narrowing, venular widening, loss of tortuosity) are described in association with CVD in other diseases.Objectives:The aim of this study was to compare the retinal microvasculature of AS patients with healthy controls, and to assess gender differences.Methods:A cross-sectional, case-control study comparing AS patients (fulfilling the modified New York criteria, Rheumatology outpatient clinic of Reade and Amsterdam UMC) with healthy controls (EMIF-AD PreClinAD cohort of the Dutch Twins Register(1)), men:women=1:1. Most important inclusion criteria were: age 50-75 years, diabetes mellitus was excluded. All subjects underwent Optical Coherence Tomography Angiography and fundus photography (≥1 eye), analyzed with Singapore I Vessel Assessment software (Table 2). Differences between AS and controls were evaluated with generalised estimating equations (GEE), adjusted for demographics and cardiovascular risk, and stratified for gender.Results:In total, 59 AS patients (mean disease duration 36 years) and 105 controls were included. Controls were significantly older than patients, but did not differ in cardiovascular profile (Table 1). Patients had a significantly lower retinal arteriolar tortuosity (β-0.1;p=0.02), and higher vessel density (β 0.5,p=0.02), than controls (Table 2). Also, male AS patients showed a lower arteriovenular ratio compared to male controls (β -0.03,p=0.04). There were no differences between women with and without AS. In AS, a high disease activity was associated with a wider (unfavorable) venular diameter (p=0.05), whereas biologic use showed a wider (more favorable) arteriolar diameter (p<0.01).Conclusion:This study detected several retinal microvascular changes, in AS patients compared to controls, of which some are associated with CVD based on previous studies. Some changes were only observed in male-, but not in female, patients. A new finding was an increased capillary density in AS, of which the association with CVD-risk has not yet been studied before.References:[1]Konijnenberg E et al. The EMIF-AD PreclinAD study: study design and baseline cohort overview. Alzheimers Res Ther. 2018; 10:75.Table 1.Patient characteristics AS (n=57) and controls (n=105)ASControlspGender, women (%)30 (51)52 (50)nsAge, mean yrs (SD)60 (6)68 (4)<0.01Smoking currently, yes (%)11 (19)8 (8)0.06Body mass index, mean (SD)26 (4)26 (3)nsHypertension, yes (%)23 (39)39 (37)nsDyslipidemia, yes (%)9 (15)18 (17)nsCardiovascular disease history, yes (%)9 (15)15 (14)nsNSAIDS (%)24 (41)6 (6)<0.01Biological (mostly TNF inhibitor)* (%)29 (49)0 (0)<0.01AS Disease Activity Score, mean (SD)2.1 ±0.9Table 2.Retinal vascular parameters, differences AS and Control subjectsCrudeAdjusted for:Age, gender, BMI smoking, hypertension, dyslipidemiaRetinal vascular parametersβ(95%CI)pβ(95%CI)pDiameterArteriolar1.6(-2.0, 5.2)0.37-0.2(-4.8, 4.4)0.92Venular5.4(-0.66, 11.5)0.082.5(-5.4, 10.4)0.53Arteriovenular ratio-0.01(-0.03, 0.01)0.43-0.01(-0.03, 0.02)0.65TortuosityArteriolar-0.05(-0.12, 0.03)0.19-0.1(-0.2, -0.01)0.02ComplexityFractal dimension0.01(0.00, 0.03)0.040.0(-0.02, 0.02)0.88Vessel DensityInner ring0.8(0.5, 1.1)<0.0010.5(0.1, 0.9)0.02Outer ring0.7(0.4, 1.0)<0.0010.2(-0.2, 0.6)0.42Disclosure of Interests:Rianne van Bentum: None declared, Milad Baniaamam: None declared, Buket Kinaci-Tas: None declared, Jacoba van de Kreeke: None declared, Pieter Jelle Visser: None declared, Erik Serné: None declared, Michael Nurmohamed Grant/research support from: Not related to this research, Consultant of: Not related to this research, Speakers bureau: Not related to this research, Irene van der Horst-Bruinsma Grant/research support from: AbbVie, Novartis, Eli Lilly, Bristol-Myers Squibb, MSD, Pfizer, UCB Pharma, Consultant of: AbbVie, Novartis, Eli Lilly, Bristol-Myers Squibb, MSD, Pfizer, UCB Pharma
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| 10. |
- 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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