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1. Biological use influences the impact of inflammation on risk of major adverse cardiovascular events in rheumatoid arthritis.

Author

Karpouzas, George, Ormseth, Sarah, van Riel, Piet, Gonzalez-Gay, Miguel, Corrales, Alfonso, Rantapää-Dahlqvist, Solbritt, Sfikakis, Petros, Dessein, Patrick, Tsang, Linda, Hitchon, Carol, El-Gabalawy, Hani, Pascual-Ramos, Virginia, Contreras-Yáñez, Irazú, Colunga-Pedraza, Iris, Galarza-Delgado, Dionicio, Azpiri-Lopez, Jose, Semb, Anne, Misra, Durga, Hauge, Ellen-Margrethe, and Kitas, George

Subjects
Arthritis, Rheumatoid, Biological Therapy, Cardiovascular Diseases, Inflammation, Humans, Arthritis, Rheumatoid, Male, Female, Middle Aged, Antirheumatic Agents, Cardiovascular Diseases, Inflammation, Aged, Biomarkers, C-Reactive Protein, Risk Factors, Severity of Illness Index
Abstract

OBJECTIVES: Chronic inflammation promotes cardiovascular risk in rheumatoid arthritis (RA). Biological disease-modifying antirheumatic drugs (bDMARDs) improve disease activity and cardiovascular disease outcomes. We explored whether bDMARDs influence the impact of disease activity and inflammatory markers on long-term cardiovascular risk in RA. METHODS: We studied 4370 participants without cardiovascular disease in a 10-country observational cohort of patients with RA. Endpoints were (1) major adverse cardiovascular events (MACE) encompassing myocardial infarction, stroke and cardiovascular death; and (2) any ischaemic cardiovascular events (iCVE) including MACE plus revascularisation, angina, transient ischaemic attack and peripheral arterial disease. RESULTS: Over 26 534 patient-years, 239 MACE and 362 iCVE occurred. The interaction between 28-joint Disease Activity Score with C-reactive protein (DAS28-CRP) and bDMARD use was significant for MACE (p=0.017), suggesting the effect of DAS28-CRP on MACE risk differed among bDMARD users (n=515) and non-users (n=3855). DAS28-CRP (per unit increase) is associated with MACE risk in bDMARD non-users (HR 1.21 (95% CI 1.07 to 1.37)) but not users (HR 0.69 (95% CI 0.40 to 1.20)). The interaction between CRP (per log unit increase) and bDMARD use was also significant for MACE (p=0.011). CRP associated with MACE risk in bDMARD non-users (HR 1.16 (95% CI 1.04 to 1.30)), but not users (HR 0.65 (95% CI 0.36 to 1.17)). No interaction was observed between bDMARD use and DAS28-CRP (p=0.167) or CRP (p=0.237) for iCVE risk. CONCLUSIONS: RA activity and inflammatory markers associated with risk of MACE in bDMARD non-users but not users suggesting the possibility of biological-specific benefits locally on arterial wall independently of effects on systemic inflammation.

Published
2024

2. Diabetes mellitus and cardiovascular risk management in patients with rheumatoid arthritis: an international audit

Author

Semb, Anne Grete, Rollefstad, Silvia, Ikdahl, Eirik, Wibetoe, Grunde, Sexton, Joseph, Crowson, Cindy, van Riel, Piet, Kitas, George, Graham, Ian, Rantapää-Dahlqvist, Solbritt, Karpouzas, George Athanasios, Myasoedova, Elena, Gonzalez-Gay, Miguel A, Sfikakis, Petros P, Tektonidou, Maria G, Lazarini, Argyro, Vassilopoulos, Dimitrios, Kuriya, Bindee, Hitchon, Carol, Stoenoiu, Maria Simona, Durez, Patrick, Pascual-Ramos, Virginia, Galarza-Delgado, Dionicio Angel, Faggiano, Pompilio, Misra, Durga Prasanna, Borg, Andrew A, Mu, Rong, Mirrakhimov, Erkin M, Gheta, Diane, Douglas, Karen, Agarwal, Vikas, Myasoedova, Svetlana, Krougly, Lev, Popkova, Tatiana Valentinovna, Tuchyňová, Alena, Tomcik, Michal, Vrablik, Michal, Lastuvka, Jiri, Horak, Pavel, Medkova, Helena Kaspar, and Kerola, Anne M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Heart Disease, Prevention, Arthritis, Clinical Research, Cardiovascular, Hypertension, Diabetes, Autoimmune Disease, Rheumatoid Arthritis, Inflammatory and immune system, Good Health and Well Being, Arthritis, Rheumatoid, Cardiovascular Diseases, Diabetes Mellitus, Heart Disease Risk Factors, Humans, Risk Factors, arthritis, rheumatoid, hypertension, lipids, cardiovascular diseases, atherosclerosis, SURF-RA collaborators, Clinical sciences
Abstract

The objective was to examine the prevalence of atherosclerotic cardiovascular disease (ASCVD) and its risk factors among patients with RA with diabetes mellitus (RA-DM) and patients with RA without diabetes mellitus (RAwoDM), and to evaluate lipid and blood pressure (BP) goal attainment in RA-DM and RAwoDM in primary and secondary prevention. The cohort was derived from the Survey of Cardiovascular Disease Risk Factors in Patients with Rheumatoid Arthritis from 53 centres/19 countries/3 continents during 2014-2019. We evaluated the prevalence of cardiovascular disease (CVD) among RA-DM and RAwoDM. The study population was divided into those with and without ASCVD, and within these groups we compared risk factors and CVD preventive treatment between RA-DM and RAwoDM. The study population comprised of 10 543 patients with RA, of whom 1381 (13%) had DM. ASCVD was present in 26.7% in RA-DM compared with 11.6% RAwoDM (p

Published
2021

3. Prediction of cardiovascular events in rheumatoid arthritis using risk age calculations: evaluation of concordance across risk age models

Author

Wibetoe, Grunde, Sexton, Joseph, Ikdahl, Eirik, Rollefstad, Silvia, Kitas, George D, van Riel, Piet, Gabriel, Sherine, Kvien, Tore K, Douglas, Karen, Sandoo, Aamer, Arts, Elke E, Wållberg-Jonsson, Solveig, Dahlqvist, Solbritt Rantapää, Karpouzas, George, Dessein, Patrick H, Tsang, Linda, El-Gabalawy, Hani, Hitchon, Carol A, Pascual-Ramos, Virginia, Contreas-Yañes, Irazu, Sfikakis, Petros P, González-Gay, Miguel A, Colunga-Pedraz, Iris J, Galarza-Delgado, Dionicio A, Azpiri-Lopez, Jose Ramon, Crowson, Cynthia S, and Semb, Anne Grete

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Cardiovascular, Rheumatoid Arthritis, Heart Disease, Autoimmune Disease, Prevention, Arthritis, Aging, Inflammatory and immune system, Good Health and Well Being, Adult, Age Factors, Aged, Arthritis, Rheumatoid, Cardiovascular Diseases, Female, Humans, Male, Middle Aged, Risk Assessment, Risk Factors, Cardiovascular risk age, Vascular age, Cardiovascular disease, Risk factors, Rheumatoid arthritis, Immunology, Public Health and Health Services, Arthritis & Rheumatology, Clinical sciences
Abstract

BackgroundIn younger individuals, low absolute risk of cardiovascular disease (CVD) may conceal an increased risk age and relative risk of CVD. Calculation of risk age is proposed as an adjuvant to absolute CVD risk estimation in European guidelines. We aimed to compare the discriminative ability of available risk age models in prediction of CVD in rheumatoid arthritis (RA). Secondly, we also evaluated the performance of risk age models in subgroups based on RA disease characteristics.MethodsRA patients aged 30-70 years were included from an international consortium named A Trans-Atlantic Cardiovascular Consortium for Rheumatoid Arthritis (ATACC-RA). Prior CVD and diabetes mellitus were exclusion criteria. The discriminatory ability of specific risk age models was evaluated using c-statistics and their standard errors after calculating time until fatal or non-fatal CVD or last follow-up.ResultsA total of 1974 patients were included in the main analyses, and 144 events were observed during follow-up, the median follow-up being 5.0 years. The risk age models gave highly correlated results, demonstrating R2 values ranging from 0.87 to 0.97. However, risk age estimations differed > 5 years in 15-32% of patients. C-statistics ranged 0.68-0.72 with standard errors of approximately 0.03. Despite certain RA characteristics being associated with low c-indices, standard errors were high. Restricting analysis to European RA patients yielded similar results.ConclusionsThe cardiovascular risk age and vascular age models have comparable performance in predicting CVD in RA patients. The influence of RA disease characteristics on the predictive ability of these prediction models remains inconclusive.

Published
2020

4. Smoking cessation is associated with lower disease activity and predicts cardiovascular risk reduction in rheumatoid arthritis patients

Author

Roelsgaard, Ida K, Ikdahl, Eirik, Rollefstad, Silvia, Wibetoe, Grunde, Esbensen, Bente A, Kitas, George D, van Riel, Piet, Gabriel, Sherine, Kvien, Tore K, Douglas, Karen, Wållberg-Jonsson, Solveig, Dahlqvist, Solbritt Rantapää, Karpouzas, George, Dessein, Patrick H, Tsang, Linda, El-Gabalawy, Hani, Hitchon, Carol A, Pascual-Ramos, Virginia, Contreras-Yáñez, Irazú, Sfikakis, Petros P, González-Gay, Miguel A, Crowson, Cynthia S, and Semb, Anne Grete

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Tobacco Smoke and Health, Arthritis, Prevention, Cardiovascular, Heart Disease, Tobacco, Clinical Research, Good Health and Well Being, Adult, Aged, Arthritis, Rheumatoid, Blood Pressure, Cardiovascular Diseases, Female, Humans, Lipoproteins, Male, Middle Aged, Risk Factors, Risk Reduction Behavior, Severity of Illness Index, Smoking, Smoking Cessation, rheumatoid arthritis, epidemiology, behaviour, quality of life, outcome measures, Immunology, Public Health and Health Services, Arthritis & Rheumatology, Clinical sciences
Abstract

ObjectivesSmoking is a major risk factor for the development of both cardiovascular disease (CVD) and RA and may cause attenuated responses to anti-rheumatic treatments. Our aim was to compare disease activity, CVD risk factors and CVD event rates across smoking status in RA patients.MethodsDisease characteristics, CVD risk factors and relevant medications were recorded in RA patients without prior CVD from 10 countries (Norway, UK, Netherlands, USA, Sweden, Greece, South Africa, Spain, Canada and Mexico). Information on CVD events was collected. Adjusted analysis of variance, logistic regression and Cox models were applied to compare RA disease activity (DAS28), CVD risk factors and event rates across categories of smoking status.ResultsOf the 3311 RA patients (1012 former, 887 current and 1412 never smokers), 235 experienced CVD events during a median follow-up of 3.5 years (interquartile range 2.5-6.1). At enrolment, current smokers were more likely to have moderate or high disease activity compared with former and never smokers (P

Published
2020

6. Impact of risk factors associated with cardiovascular outcomes in patients with rheumatoid arthritis

Author

Crowson, Cynthia S, Rollefstad, Silvia, Ikdahl, Eirik, Kitas, George D, van Riel, Piet LCM, Gabriel, Sherine E, Matteson, Eric L, Kvien, Tore K, Douglas, Karen, Sandoo, Aamer, Arts, Elke, Wållberg-Jonsson, Solveig, Innala, Lena, Karpouzas, George, Dessein, Patrick H, Tsang, Linda, El-Gabalawy, Hani, Hitchon, Carol, Ramos, Virginia Pascual, Yáñez, Irazú Contreras, Sfikakis, Petros P, Zampeli, Evangelia, Gonzalez-Gay, Miguel A, Corrales, Alfonso, Laar, Mart van de, Vonkeman, Harald E, Meek, Inger, and Semb, Anne Grete

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Cardiovascular, Aging, Prevention, Rheumatoid Arthritis, Clinical Research, Heart Disease, Arthritis, Autoimmune Disease, 2.4 Surveillance and distribution, 2.3 Psychological, social and economic factors, Aetiology, Inflammatory and immune system, Good Health and Well Being, Adult, Aged, Arthritis, Rheumatoid, Cardiovascular Diseases, Cholesterol, Cohort Studies, Female, Follow-Up Studies, Humans, Hypertension, Incidence, Male, Middle Aged, Risk Factors, Severity of Illness Index, Sex Factors, Smoking, A Trans-Atlantic Cardiovascular Consortium for Rheumatoid Arthritis, Cardiovascular disease, population attributable risk, rheumatoid arthritis, risk factor, Public Health and Health Services, Arthritis & Rheumatology, Clinical sciences
Abstract

ObjectivesPatients with rheumatoid arthritis (RA) have an excess risk of cardiovascular disease (CVD). We aimed to assess the impact of CVD risk factors, including potential sex differences, and RA-specific variables on CVD outcome in a large, international cohort of patients with RA.MethodsIn 13 rheumatology centres, data on CVD risk factors and RA characteristics were collected at baseline. CVD outcomes (myocardial infarction, angina, revascularisation, stroke, peripheral vascular disease and CVD death) were collected using standardised definitions.Results5638 patients with RA and no prior CVD were included (mean age: 55.3 (SD: 14.0) years, 76% women). During mean follow-up of 5.8 (SD: 4.4) years, 148 men and 241 women developed a CVD event (10-year cumulative incidence 20.9% and 11.1%, respectively). Men had a higher burden of CVD risk factors, including increased blood pressure, higher total cholesterol and smoking prevalence than women (all p

Published
2018

7. Rheumatoid arthritis-specific cardiovascular risk scores are not superior to general risk scores: a validation analysis of patients from seven countries.

Author

Crowson, Cynthia S, Gabriel, Sherine E, Semb, Anne Grete, van Riel, Piet LCM, Karpouzas, George, Dessein, Patrick H, Hitchon, Carol, Pascual-Ramos, Virginia, Kitas, George D, Douglas, Karen, Sandoo, Aamer, Rollefstad, Silvia, Ikdahl, Eirik, Kvien, Tore K, Arts, Elke, Fransen, Jaap, Tsang, Linda, El-Gabalawy, Hani, Yáñez, Irazú Contreras, Matteson, Eric L, Rantapää-Dahlqvist, Solbritt, Wållberg-Jonsson, Solveig, Innala, Lena, Sfikakis, Petros P, Zampeli, Evi, Gonzalez-Gay, Miguel A, Corrales, Alfonso, van de Laar, Mart, Vonkeman, Harald, Meek, Inger, Husni, Elaine, Overman, Robert, Colunga, Iris, and Galarza, Dionicio

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Cardiovascular, Heart Disease, Prevention, Arthritis, Clinical Research, Adult, Age Distribution, Aged, Algorithms, Arthritis, Rheumatoid, Canada, Cardiovascular Diseases, Cohort Studies, Comorbidity, Female, Humans, Incidence, Internationality, Male, Mexico, Middle Aged, Netherlands, Norway, Predictive Value of Tests, Prognosis, Risk Assessment, Severity of Illness Index, Sex Distribution, South Africa, United Kingdom, United States, rheumatoid arthritis, cardiovascular disease, risk prediction, risk assessment, Trans-Atlantic Cardiovascular Consortium for Rheumatoid Arthritis, Public Health and Health Services, Arthritis & Rheumatology, Clinical sciences
Abstract

ObjectivesCardiovascular disease (CVD) risk calculators developed for the general population do not accurately predict CVD events in patients with RA. We sought to externally validate risk calculators recommended for use in patients with RA including the EULAR 1.5 multiplier, the Expanded Cardiovascular Risk Prediction Score for RA (ERS-RA) and QRISK2.MethodsSeven RA cohorts from UK, Norway, Netherlands, USA, South Africa, Canada and Mexico were combined. Data on baseline CVD risk factors, RA characteristics and CVD outcomes (including myocardial infarction, ischaemic stroke and cardiovascular death) were collected using standardized definitions. Performance of QRISK2, EULAR multiplier and ERS-RA was compared with other risk calculators [American College of Cardiology/American Heart Association (ACC/AHA), Framingham Adult Treatment Panel III Framingham risk score-Adult Treatment Panel (FRS-ATP) and Reynolds Risk Score] using c-statistics and net reclassification index.ResultsAmong 1796 RA patients without prior CVD [mean ( s . d .) age: 54.0 (14.0) years, 74% female], 100 developed CVD events during a mean follow-up of 6.9 years (12430 person-years). Estimated CVD risk by ERS-RA [mean ( s . d .) 8.8% (9.8%)] was comparable to FRS-ATP [mean ( s . d .) 9.1% (8.3%)] and Reynolds [mean ( s . d .) 9.2% (12.2%)], but lower than ACC/AHA [mean ( s . d .) 9.8% (12.1%)]. QRISK2 substantially overestimated risk [mean ( s . d .) 15.5% (13.9%)]. Discrimination was not improved for ERS-RA (c-statistic = 0.69), QRISK2 or EULAR multiplier applied to ACC/AHA compared with ACC/AHA (c-statistic = 0.72 for all) or for FRS-ATP (c-statistic = 0.75). The net reclassification index for ERS-RA was low (-0.8% vs ACC/AHA and 2.3% vs FRS-ATP).ConclusionThe QRISK2, EULAR multiplier and ERS-RA algorithms did not predict CVD risk more accurately in patients with RA than CVD risk calculators developed for the general population.

Published
2017

8. Biological use influences the impact of inflammation on risk of major adverse cardiovascular events in rheumatoid arthritis

Author

Karpouzas, George Athanasios, Ormseth, Sarah R., van Riel, Piet Leonardus Cornelis Maria, Gonzalez-Gay, Miguel A., Corrales, Alfonso, Rantapää-Dahlqvist, Solbritt, Sfikakis, Petros P., Dessein, Patrick, Tsang, Linda, Hitchon, Carol, El-Gabalawy, Hani, Pascual-Ramos, Virginia, Contreras-Yáñez, Irazú, Colunga-Pedraza, Iris J., Galarza-Delgado, Dionicio Angel, Azpiri-Lopez, Jose Ramon, Semb, Anne Grete, Misra, Durga Prasanna, Hauge, Ellen-Margrethe, Kitas, George, Karpouzas, George Athanasios, Ormseth, Sarah R., van Riel, Piet Leonardus Cornelis Maria, Gonzalez-Gay, Miguel A., Corrales, Alfonso, Rantapää-Dahlqvist, Solbritt, Sfikakis, Petros P., Dessein, Patrick, Tsang, Linda, Hitchon, Carol, El-Gabalawy, Hani, Pascual-Ramos, Virginia, Contreras-Yáñez, Irazú, Colunga-Pedraza, Iris J., Galarza-Delgado, Dionicio Angel, Azpiri-Lopez, Jose Ramon, Semb, Anne Grete, Misra, Durga Prasanna, Hauge, Ellen-Margrethe, and Kitas, George

Abstract

Objectives: Chronic inflammation promotes cardiovascular risk in rheumatoid arthritis (RA). Biological disease-modifying antirheumatic drugs (bDMARDs) improve disease activity and cardiovascular disease outcomes. We explored whether bDMARDs influence the impact of disease activity and inflammatory markers on long-term cardiovascular risk in RA. Methods: We studied 4370 participants without cardiovascular disease in a 10-country observational cohort of patients with RA. Endpoints were (1) major adverse cardiovascular events (MACE) encompassing myocardial infarction, stroke and cardiovascular death; and (2) any ischaemic cardiovascular events (iCVE) including MACE plus revascularisation, angina, transient ischaemic attack and peripheral arterial disease. Results: Over 26 534 patient-years, 239 MACE and 362 iCVE occurred. The interaction between 28-joint Disease Activity Score with C-reactive protein (DAS28-CRP) and bDMARD use was significant for MACE (p=0.017), suggesting the effect of DAS28-CRP on MACE risk differed among bDMARD users (n=515) and non-users (n=3855). DAS28-CRP (per unit increase) is associated with MACE risk in bDMARD non-users (HR 1.21 (95% CI 1.07 to 1.37)) but not users (HR 0.69 (95% CI 0.40 to 1.20)). The interaction between CRP (per log unit increase) and bDMARD use was also significant for MACE (p=0.011). CRP associated with MACE risk in bDMARD non-users (HR 1.16 (95% CI 1.04 to 1.30)), but not users (HR 0.65 (95% CI 0.36 to 1.17)). No interaction was observed between bDMARD use and DAS28-CRP (p=0.167) or CRP (p=0.237) for iCVE risk. Conclusions: RA activity and inflammatory markers associated with risk of MACE in bDMARD non-users but not users suggesting the possibility of biological-specific benefits locally on arterial wall independently of effects on systemic inflammation.

Published
2024
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10. Gegevensverwerking

Author

Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., van Riel, Piet L. C. M., Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., and van Riel, Piet L. C. M.

Published
2016
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11. Het onderzoeksvoorstel

Author

Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., van Riel, Piet L. C. M., Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., and van Riel, Piet L. C. M.

Published
2016
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12. Publiceren

Author

Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., van Riel, Piet L. C. M., Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., and van Riel, Piet L. C. M.

Published
2016
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13. Meetinstrumenten

Author

Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., van Riel, Piet L. C. M., Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., and van Riel, Piet L. C. M.

Published
2016
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15. Vormen van onderzoek

Author

Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., van Riel, Piet L. C. M., Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., and van Riel, Piet L. C. M.

Published
2016
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16. Steekproefomvang en powerberekening

Author

Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., van Riel, Piet L. C. M., Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., and van Riel, Piet L. C. M.

Published
2016
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17. Literatuur en literatuuronderzoek

Author

Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., van Riel, Piet L. C. M., Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., and van Riel, Piet L. C. M.

Published
2016
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18. Fasen van onderzoek – stappenplan

Author

Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., van Riel, Piet L. C. M., Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., and van Riel, Piet L. C. M.

Published
2016
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19. Bescherming van onderzoeksdeelnemers

Author

Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., van Riel, Piet L. C. M., Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., and van Riel, Piet L. C. M.

Published
2016
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20. Organisatie en financiering

Author

Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., van Riel, Piet L. C. M., Zielhuis, Gerhard A., Heydendael, Paul H. J. M., Maltha, Jaap C., and van Riel, Piet L. C. M.

Published
2016
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21. Genetics of rheumatoid arthritis contributes to biology and drug discovery.

Author

Okada, Yukinori, Wu, Di, Trynka, Gosia, Raj, Towfique, Terao, Chikashi, Ikari, Katsunori, Kochi, Yuta, Ohmura, Koichiro, Suzuki, Akari, Yoshida, Shinji, Graham, Robert, Manoharan, Arun, Ortmann, Ward, Bhangale, Tushar, Denny, Joshua, Carroll, Robert, Eyler, Anne, Greenberg, Jeffrey, Kremer, Joel, Pappas, Dimitrios, Jiang, Lei, Yin, Jian, Ye, Lingying, Su, Ding-Feng, Yang, Jian, Xie, Gang, Keystone, Ed, Westra, Harm-Jan, Esko, Tõnu, Metspalu, Andres, Zhou, Xuezhong, Gupta, Namrata, Mirel, Daniel, Stahl, Eli, Diogo, Dorothée, Cui, Jing, Liao, Katherine, Guo, Michael, Myouzen, Keiko, Kawaguchi, Takahisa, Coenen, Marieke, van Riel, Piet, van de Laar, Mart, Guchelaar, Henk-Jan, Huizinga, Tom, Dieudé, Philippe, Mariette, Xavier, Bridges, S, Zhernakova, Alexandra, Toes, Rene, Tak, Paul, Miceli-Richard, Corinne, Bang, So-Young, Lee, Hye-Soon, Martin, Javier, Gonzalez-Gay, Miguel, Rodriguez-Rodriguez, Luis, Rantapää-Dahlqvist, Solbritt, Arlestig, Lisbeth, Choi, Hyon, Kamatani, Yoichiro, Galan, Pilar, Lathrop, Mark, Eyre, Steve, Bowes, John, Barton, Anne, de Vries, Niek, Moreland, Larry, Karlson, Elizabeth, Taniguchi, Atsuo, Yamada, Ryo, Kubo, Michiaki, Liu, Jun, Bae, Sang-Cheol, Worthington, Jane, Padyukov, Leonid, Klareskog, Lars, Gregersen, Peter, Raychaudhuri, Soumya, Stranger, Barbara, De Jager, Philip, Franke, Lude, Visscher, Peter, Brown, Matthew, Yamanaka, Hisashi, Mimori, Tsuneyo, Takahashi, Atsushi, Xu, Huji, Behrens, Timothy, Siminovitch, Katherine, Momohara, Shigeki, Matsuda, Fumihiko, Yamamoto, Kazuhiko, Plenge, Robert, and Criswell, Lindsey

Subjects
Alleles, Animals, Arthritis, Rheumatoid, Asian People, Case-Control Studies, Computational Biology, Drug Discovery, Drug Repositioning, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Hematologic Neoplasms, Humans, Male, Mice, Mice, Knockout, Molecular Targeted Therapy, Polymorphism, Single Nucleotide, White People
Abstract

A major challenge in human genetics is to devise a systematic strategy to integrate disease-associated variants with diverse genomic and biological data sets to provide insight into disease pathogenesis and guide drug discovery for complex traits such as rheumatoid arthritis (RA). Here we performed a genome-wide association study meta-analysis in a total of >100,000 subjects of European and Asian ancestries (29,880 RA cases and 73,758 controls), by evaluating ∼10 million single-nucleotide polymorphisms. We discovered 42 novel RA risk loci at a genome-wide level of significance, bringing the total to 101 (refs 2 - 4). We devised an in silico pipeline using established bioinformatics methods based on functional annotation, cis-acting expression quantitative trait loci and pathway analyses--as well as novel methods based on genetic overlap with human primary immunodeficiency, haematological cancer somatic mutations and knockout mouse phenotypes--to identify 98 biological candidate genes at these 101 risk loci. We demonstrate that these genes are the targets of approved therapies for RA, and further suggest that drugs approved for other indications may be repurposed for the treatment of RA. Together, this comprehensive genetic study sheds light on fundamental genes, pathways and cell types that contribute to RA pathogenesis, and provides empirical evidence that the genetics of RA can provide important information for drug discovery.

Published
2014

24. Genome-wide association analysis of anti-TNF drug response in patients with rheumatoid arthritis

Author

Mirkov, Maša Umiċeviċ, Cui, Jing, Vermeulen, Sita H, Stahl, Eli A, Toonen, Erik JM, Makkinje, Remco R, Lee, Annette T, Huizinga, Tom WJ, Allaart, Renee, Barton, Anne, Mariette, Xavier, Miceli, Corinne Richard, Criswell, Lindsey A, Tak, Paul P, de Vries, Niek, Saevarsdottir, Saedis, Padyukov, Leonid, Bridges, S Louis, van Schaardenburg, Dirk-Jan, Jansen, Tim L, Dutmer, Ellen AJ, van de Laar, Mart AFJ, Barrera, Pilar, Radstake, Timothy RDJ, van Riel, Piet LCM, Scheffer, Hans, Franke, Barbara, Brunner, Han G, Plenge, Robert M, Gregersen, Peter K, Guchelaar, Henk-Jan, and Coenen, Marieke JH

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Arthritis, Rheumatoid Arthritis, Genetics, Autoimmune Disease, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Adalimumab, Antibodies, Monoclonal, Antibodies, Monoclonal, Humanized, Antirheumatic Agents, Arthritis, Rheumatoid, DNA Mutational Analysis, Drug Resistance, Etanercept, Female, Gene Expression Regulation, Genetic Markers, Genome-Wide Association Study, Humans, Immunoglobulin G, Infliximab, Male, Polymorphism, Single Nucleotide, Receptors, Tumor Necrosis Factor, Registries, Tumor Necrosis Factor-alpha, Anti-TNF, Gene Polymorphism, Pharmacogenetics, Public Health and Health Services, Arthritis & Rheumatology, Clinical sciences
Abstract

BackgroundTreatment strategies blocking tumour necrosis factor (anti-TNF) have proven very successful in patients with rheumatoid arthritis (RA). However, a significant subset of patients does not respond for unknown reasons. Currently, there are no means of identifying these patients before treatment. This study was aimed at identifying genetic factors predicting anti-TNF treatment outcome in patients with RA using a genome-wide association approach.MethodsWe conducted a multistage, genome-wide association study with a primary analysis of 2 557 253 single-nucleotide polymorphisms (SNPs) in 882 patients with RA receiving anti-TNF therapy included through the Dutch Rheumatoid Arthritis Monitoring (DREAM) registry and the database of Apotheekzorg. Linear regression analysis of changes in the Disease Activity Score in 28 joints after 14 weeks of treatment was performed using an additive model. Markers with p

Published
2013

27. Identification of novel genetic markers associated with clinical phenotypes of systemic sclerosis through a genome-wide association strategy.

Author

Gorlova, Olga, Martin, Jose-Ezequiel, Rueda, Blanca, Koeleman, Bobby PC, Ying, Jun, Teruel, Maria, Diaz-Gallo, Lina-Marcela, Broen, Jasper C, Vonk, Madelon C, Simeon, Carmen P, Alizadeh, Behrooz Z, Coenen, Marieke JH, Voskuyl, Alexandre E, Schuerwegh, Annemie J, van Riel, Piet LCM, Vanthuyne, Marie, van 't Slot, Ruben, Italiaander, Annet, Ophoff, Roel A, Hunzelmann, Nicolas, Fonollosa, Vicente, Ortego-Centeno, Norberto, González-Gay, Miguel A, García-Hernández, Francisco J, González-Escribano, María F, Airo, Paolo, van Laar, Jacob, Worthington, Jane, Hesselstrand, Roger, Smith, Vanessa, de Keyser, Filip, Houssiau, Fredric, Chee, Meng May, Madhok, Rajan, Shiels, Paul G, Westhovens, Rene, Kreuter, Alexander, de Baere, Elfride, Witte, Torsten, Padyukov, Leonid, Nordin, Annika, Scorza, Raffaella, Lunardi, Claudio, Lie, Benedicte A, Hoffmann-Vold, Anna-Maria, Palm, Oyvind, García de la Peña, Paloma, Carreira, Patricia, Spanish Scleroderma Group, Varga, John, Hinchcliff, Monique, Lee, Annette T, Gourh, Pravitt, Amos, Christopher I, Wigley, Frederick M, Hummers, Laura K, Nelson, J Lee, Riemekasten, Gabriella, Herrick, Ariane, Beretta, Lorenzo, Fonseca, Carmen, Denton, Christopher P, Gregersen, Peter K, Agarwal, Sandeep, Assassi, Shervin, Tan, Filemon K, Arnett, Frank C, Radstake, Timothy RDJ, Mayes, Maureen D, and Martin, Javier

Subjects
Spanish Scleroderma Group, Humans, Scleroderma, Systemic, Genetic Predisposition to Disease, Genetic Markers, Autoantibodies, HLA Antigens, Phenotype, Polymorphism, Single Nucleotide, Alleles, Middle Aged, Female, Male, Genome-Wide Association Study, Genetic Loci, Polymorphism, Single Nucleotide, Scleroderma, Systemic, Genetics, Developmental Biology
Abstract

The aim of this study was to determine, through a genome-wide association study (GWAS), the genetic components contributing to different clinical sub-phenotypes of systemic sclerosis (SSc). We considered limited (lcSSc) and diffuse (dcSSc) cutaneous involvement, and the relationships with presence of the SSc-specific auto-antibodies, anti-centromere (ACA), and anti-topoisomerase I (ATA). Four GWAS cohorts, comprising 2,296 SSc patients and 5,171 healthy controls, were meta-analyzed looking for associations in the selected subgroups. Eighteen polymorphisms were further tested in nine independent cohorts comprising an additional 3,175 SSc patients and 4,971 controls. Conditional analysis for associated SNPs in the HLA region was performed to explore their independent association in antibody subgroups. Overall analysis showed that non-HLA polymorphism rs11642873 in IRF8 gene to be associated at GWAS level with lcSSc (P = 2.32×10(-12), OR = 0.75). Also, rs12540874 in GRB10 gene (P = 1.27 × 10(-6), OR = 1.15) and rs11047102 in SOX5 gene (P = 1.39×10(-7), OR = 1.36) showed a suggestive association with lcSSc and ACA subgroups respectively. In the HLA region, we observed highly associated allelic combinations in the HLA-DQB1 locus with ACA (P = 1.79×10(-61), OR = 2.48), in the HLA-DPA1/B1 loci with ATA (P = 4.57×10(-76), OR = 8.84), and in NOTCH4 with ACA P = 8.84×10(-21), OR = 0.55) and ATA (P = 1.14×10(-8), OR = 0.54). We have identified three new non-HLA genes (IRF8, GRB10, and SOX5) associated with SSc clinical and auto-antibody subgroups. Within the HLA region, HLA-DQB1, HLA-DPA1/B1, and NOTCH4 associations with SSc are likely confined to specific auto-antibodies. These data emphasize the differential genetic components of subphenotypes of SSc.

Published
2011

28. Cardiovascular magnetic resonance in rheumatology: Current status and recommendations for use

Author

Mavrogeni, Sophie I., Kitas, George D., Dimitroulas, Theodoros, Sfikakis, Petros P., Seo, Philip, Gabriel, Sherine, Patel, Amit R., Gargani, Luna, Bombardieri, Stefano, Matucci-Cerinic, Marco, Lombardi, Massimo, Pepe, Alessia, Aletras, Anthony H., Kolovou, Genovefa, Miszalski, Tomasz, van Riel, Piet, Semb, AnneGrete, Gonzalez-Gay, Miguel Angel, Dessein, Patrick, Karpouzas, George, Puntmann, Valentina, Nagel, Eike, Bratis, Konstantinos, Karabela, Georgia, Stavropoulos, Efthymios, Katsifis, Gikas, Koutsogeorgopoulou, Loukia, van Rossum, Albert, Rademakers, Frank, Pohost, Gerald, and Lima, Joao A.C.

Published
2016
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29. Measuring the Therapeutic Relationship in Internet-Based Interventions

Author

Ferwerda, Maaike, van Beugen, Sylvia, van Riel, Piet C.L.M., van de Kerkhof, Peter C.M., de Jong, Elke M.G.J., Smit, Jurgen V., Zeeuwen-Franssen, Manon E.J., Kroft, Elisabeth B.M., Visser, Henk, Vonkeman, Harald E., Creemers, Marjonne C.W., van Middendorp, Henriet, and Evers, Andrea W.M.

Published
2016

30. Predictors of biologic-free disease control in patients with rheumatoid arthritis after stopping tumor necrosis factor inhibitor treatment

Author

Ghiti Moghadam, Marjan, Lamers-Karnebeek, Femke B. G., Vonkeman, Harald E., ten Klooster, Peter M., Tekstra, Janneke, van Schaeybroeck, Barbara, Klaasen, Ruth, van Onna, Marieke, Bernelot Moens, Hein J., Visser, Henk, Schilder, Annemarie M., Kok, Marc R., Landewé, Robert B. M., van Riel, Piet L. C. M., van de Laar, Mart A. F. J., Jansen, Tim L., and on behalf of the Dutch National POET Collaboration

Published
2019
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31. Latitude gradient influences the age of onset of rheumatoid arthritis: a worldwide survey

Author

Ramos-Remus, Cesar, Ramirez-Gomez, Andrea, Brambila-Barba, Victor, Barajas-Ochoa, Aldo, Castillo-Ortiz, Jose D., Adebajo, Adewale O., Espinoza, Luis R., Aceves-Avila, Francisco J., Sánchez-González, Jorge M., Boudersa, Nadia, Slimani, Samy, Ladjouze-Rezig, Aicha, Diaz, Mónica P., Kirmayr, Karin I., Asnal, Cecilia A., Catoggio, Luis J., Citera, Gustavo, Casado, Gustavo C., Alvarez, Analia P., Pisoni, Cecilia N., Benavente, Emilio, Lopez-Cabanillas, Adriana, Baez, Roberto M., Pons-Estel, Bernardo A., Sacnún, Mónica P., Cavallasca, Javier A., Paniego, Raúl H., Proudman, Susanna M., Thomas, Ranjeny, Major, Gabor, Mathers, David M., Schrieber, Leslie, Haq, Syed A., Islam, Nazrul, Dessein, Patrick H., von Muhlen, Carlos A., Bianchi, Washington A., da R. Castelar-Pinheiro, Geraldo, Feldman-Pollak, Daniel, Cossermelli, Waldenise, Bonfiglioli, Karina R., Giorgi, Rina D., Zabsonre-Tiendrebeogo, Wendlassida J., Russell, Anthony S., Olaru, Lilia, Karsh, Jacob, Fuentealba, Carlos, Aguilera, Sergio, Castro-Esparza, Irene H., Burgos, Paula I., Neira, Oscar, Li, Zhan-guo, Tam, Lai-Shan, Mok, Mo Y., Medina, Yimy F., Moreno-Alvarez, Mario J., Zúñiga-Vera, Andrés E., Vera, Claudia, Quezada, Ivonne, Moreno, Iván M., Calapaqui, Wendy, El-Mardenly, Ghada, Salama, M. Salah, Ragab, Gaafar, Hadidi, Tahsin, Gado, Kamel, Leirisalo-Repo, Marjatta, Tuompo, Riitta, Koivuniemi, Riitta, Berenbaum, Francis, Allanore, Yannick, Constantin, Arnaud, Buttgereit, Frank, Schulze-Koops, Hendrik, Liz, Myriam, Dey, Dzifa, Alonzo-Borjas, Hugo D., Santiago-Pastelín, Carlos B., Cuéllar-Cruz, Víctor, Dharmanand, Balebail G., Yathish, G. C., Akerkar, Shashank M., Malaviya, Anand N., Ahmadzadeh, Arman, Hasunuma, Tomoko, Owino, Benard O., Pacheco-Tena, César, Frausto-Arenas, Aaron, De la Madrid-Cernas, Adrián A., Cardona-Cabrera, Román, Centeno-Valadez, Juan D., Rodríguez-Torres, Isaura M., Vaidya, Binit, Gupta, Arun K., Harrison, Andrew A., Grainger, Rebecca, Nwankwo, Henry M., Diamantopoulos, Andreas P., Mæland, Elisabeth, Besada, Emilio, Gorriz, Luis, Duarte, Margarita, Albrecht, Maria T. Romero-de, Cabrera-Villalba, Sonia, Segami, María I., García-Poma, Augusto, Pérez-Medina, Wilkerson, Ramos, María P., Navarra, Sandra V., Racaza, Geraldine Z., Penserga, Ester G., Manapat-Reyes, Bernadette H., Dianongco, Maria L., Lichauco, Juan J., Torralba, Tito P., Al-Emadi, Samar, Hammoudeh, Mohammed, Botchkova, Anna G., AlSaeedi, Sabri H., Almoallim, Hani, Al-Arfaj, Hussein F., Koh, Wei H., Leung, Ying Y., Whitelaw, David A., Hodkinson, Bridget, García-Miguel, Javier, Duro, Juan C., Andreu, José L., Martin-Mola, Emilio, Ahijón-Lana, María, Finckh, Axel, Alpízar-Rodríguez, Deshiré, Osiri, Manathip, Kasitanon, Nuntana, Louthrenoo, Worawit, de Vries, Niek, van Denderen, Christiaan, Gerritsen, Martjin, van Vollenhoven, Ronald F., Jansen, Tim L., van Riel, Piet, Núñez-Sotelo, Concepción M., Villegas-Morales, Sol, and GEO-RA Group

Published
2017
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36. EULAR points to consider for the management of difficult-to-treat rheumatoid arthritis

Author

Unit Opleiding Aios, Infection & Immunity, Lab Reumatologie/Klinische Immunologie, Regenerative Medicine and Stem Cells, JC onderzoeksprogramma Methodologie, VS-REU, MS Reumatologie/Immunologie/Infectie, Nagy, György, Roodenrijs, Nadia M T, Welsing, Paco M J, Kedves, Melinda, Hamar, Attila, van der Goes, Marlies C, Kent, Alison, Bakkers, Margot, Pchelnikova, Polina, Blaas, Etienne, Senolt, Ladislav, Szekanecz, Zoltan, Choy, Ernest H, Dougados, Maxime, Jacobs, Johannes Wg, Geenen, Rinie, Bijlsma, Johannes Wj, Zink, Angela, Aletaha, Daniel, Schoneveld, Leonard, van Riel, Piet, Dumas, Sophie, Prior, Yeliz, Nikiphorou, Elena, Ferraccioli, Gianfranco, Schett, Georg, Hyrich, Kimme L, Mueller-Ladner, Ulf, Buch, Maya H, McInnes, Iain B, van der Heijde, Désirée, van Laar, Jacob M, Unit Opleiding Aios, Infection & Immunity, Lab Reumatologie/Klinische Immunologie, Regenerative Medicine and Stem Cells, JC onderzoeksprogramma Methodologie, VS-REU, MS Reumatologie/Immunologie/Infectie, Nagy, György, Roodenrijs, Nadia M T, Welsing, Paco M J, Kedves, Melinda, Hamar, Attila, van der Goes, Marlies C, Kent, Alison, Bakkers, Margot, Pchelnikova, Polina, Blaas, Etienne, Senolt, Ladislav, Szekanecz, Zoltan, Choy, Ernest H, Dougados, Maxime, Jacobs, Johannes Wg, Geenen, Rinie, Bijlsma, Johannes Wj, Zink, Angela, Aletaha, Daniel, Schoneveld, Leonard, van Riel, Piet, Dumas, Sophie, Prior, Yeliz, Nikiphorou, Elena, Ferraccioli, Gianfranco, Schett, Georg, Hyrich, Kimme L, Mueller-Ladner, Ulf, Buch, Maya H, McInnes, Iain B, van der Heijde, Désirée, and van Laar, Jacob M

Published
2022

39. Limited value for ultrasonography in predicting flare in rheumatoid arthritis patients with low disease activity stopping TNF inhibitors

Author

Lamers-Karnebeek, Femke B., Luime, Jolanda J., Ten Cate, David F., Teerenstra, Steven, Swen, Nanno W. A. A., Gerards, Andreas H., Hendrikx, Jos, van Rooyen, Emma M., Voorneman, Ramon, Haagsma, Cees, Basoski, Natalja, de Jager, Mike, Ghiti Moghadam, Marjan, Efde, Monique N., Goekoop-Ruiterman, Yvonne P. M., van Riel, Piet L. C. M., Jacobs, Johannes W. G., and Jansen, Tim L.

Published
2017
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44. Linkage Proof for PTPN22, a Rheumatoid Arthritis Susceptibility Gene and a Human Autoimmunity Gene

Author

Michou, Laëtitia, Lasbleiz, Sandra, Rat, Anne-Christine, Migliorini, Paola, Balsa, Alejandro, Westhovens, René, Barrera, Pilar, Alves, Helena, Pierlot, Céline, Glikmans, Elodie, Garnier, Sophie, Dausset, Jean, Vaz, Carlos, Fernandes, Manuela, Petit-Teixeira, Elisabeth, Lemaire, Isabelle, Pascual-Salcedo, Dora, Bombardieri, Stefano, Dequeker, Jan, Radstake, Timothy R., Van Riel, Piet, van de Putte, Leo, Lopes-Vaz, Antonio, Prum, Bernard, Bardin, Thomas, Dieudé, Philippe, and Cornélis, François

Published
2007
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