Racial differences in systemic sclerosis disease presentation: a European Scleroderma Trials and Research group study.
- Jaeger VK Department of Rheumatology, University Hospital Basel, Basel, Switzerland.
- Tikly M Division of Rheumatology, Chris Hani Baragwanath Academic Hospital, University of the Witwatersrand, Johannesburg, South Africa.
- Xu D Department of Rheumatology, Peking Union Medical College Hospital, Beijing, China.
- Siegert E Department of Rheumatology and Immunology, University Hospital Charité, Berlin, Germany.
- Hachulla E Département de Médecine Interne et Immunologie Clinique, Centre de Référence des Maladies Systémiques et Auto-Immunes Rares du Nord et Nord-Ouest (CERAINO), LIRIC, INSERM, Univ. Lille, CHU Lille, Lille, France.
- Airò P UO Reumatologia ed Immunologia Clinica, Spedali Civili, Brescia, Italy.
- Valentini G Rheumatology Department, Second University of Naples, Naples, Italy.
- Matucci Cerinic M Department of Experimental and Clinical Rheumatology, Division of Rheumatology AOUC, University of Florence, Florence, Italy.
- Distler O Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland.
- Cozzi F Rheumatology Unit, Department of Medicine, University of Padova, Padova, Italy.
- Carreira P Servicio de Reumatologia, Hospital Universitario 12 de Octubre, Madrid, Spain.
- Allanore Y Department of Rheumatology A, Paris Descartes University, Cochin Hospital, Paris, France.
- Müller-Ladner U Justus-Liebig-University of Giessen, Kerckhoff-Klinik, Germany, Bad Nauheim.
- Ananieva LP VA Nasonova Institute of Rheumatology, Moscow, Russian Federation.
- Balbir-Gurman A B. Shine Rheumatology Institute, Rambam Health Care Campus, Rappaport Faculty of Medicine, Technion - Institute of Technology, Haifa, Israel.
- Distler JHW Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.
- Czirják L Department of Rheumatology and Immunology, University of Pécs, Pécs, Hungary.
- Li M Department of Rheumatology, Peking Union Medical College Hospital, Beijing, China.
- Henes J Department of Internal Medicine II, Eberhard-Karls-University Tübingen, Tübingen, Germany.
- Jimenez SA Scleroderma Centre, Thomas Jefferson University, Philadelphia, PA, USA.
- Smith V Faculty of Internal Medicine, Ghent University, Ghent, Belgium.
- Damjanov N Institute of Rheumatology, University of Belgrade Medical School, Belgrade, Serbia.
- Denton CP Department of Rheumatology, University College London, Royal Free Hospital, London, UK.
- DelGaldo F Leeds Musculoskeletal Biomedical Research Unit (LMBRU), University of Leeds, Leeds, UK.
- Saketkoo LA Tulane University Lung Centre, University Medical Centre Scleroderma and Sarcoidosis Patient Care and Research Centre, New Orleans, LA, USA.
- Walker UA Department of Rheumatology, University Hospital Basel, Basel, Switzerland.
- 2019-11-05
Published in:
- Rheumatology (Oxford, England). - 2020
organ manifestations
races
systemic sclerosis
Adult
African Continental Ancestry Group
Aged
Asian Continental Ancestry Group
Autoantibodies
DNA Topoisomerases, Type I
European Continental Ancestry Group
Female
Humans
Hypertension, Pulmonary
Lung
Male
Middle Aged
Scleroderma, Systemic
English
OBJECTIVES
Racial factors play a significant role in SSc. We evaluated differences in SSc presentations between white patients (WP), Asian patients (AP) and black patients (BP) and analysed the effects of geographical locations.
METHODS
SSc characteristics of patients from the EUSTAR cohort were cross-sectionally compared across racial groups using survival and multiple logistic regression analyses.
RESULTS
The study included 9162 WP, 341 AP and 181 BP. AP developed the first non-RP feature faster than WP but slower than BP. AP were less frequently anti-centromere (ACA; odds ratio (OR) = 0.4, P < 0.001) and more frequently anti-topoisomerase-I autoantibodies (ATA) positive (OR = 1.2, P = 0.068), while BP were less likely to be ACA and ATA positive than were WP [OR(ACA) = 0.3, P < 0.001; OR(ATA) = 0.5, P = 0.020]. AP had less often (OR = 0.7, P = 0.06) and BP more often (OR = 2.7, P < 0.001) diffuse skin involvement than had WP. AP and BP were more likely to have pulmonary hypertension [OR(AP) = 2.6, P < 0.001; OR(BP) = 2.7, P = 0.03 vs WP] and a reduced forced vital capacity [OR(AP) = 2.5, P < 0.001; OR(BP) = 2.4, P < 0.004] than were WP. AP more often had an impaired diffusing capacity of the lung than had BP and WP [OR(AP vs BP) = 1.9, P = 0.038; OR(AP vs WP) = 2.4, P < 0.001]. After RP onset, AP and BP had a higher hazard to die than had WP [hazard ratio (HR) (AP) = 1.6, P = 0.011; HR(BP) = 2.1, P < 0.001].
CONCLUSION
Compared with WP, and mostly independent of geographical location, AP have a faster and earlier disease onset with high prevalences of ATA, pulmonary hypertension and forced vital capacity impairment and higher mortality. BP had the fastest disease onset, a high prevalence of diffuse skin involvement and nominally the highest mortality.
Racial factors play a significant role in SSc. We evaluated differences in SSc presentations between white patients (WP), Asian patients (AP) and black patients (BP) and analysed the effects of geographical locations.
METHODS
SSc characteristics of patients from the EUSTAR cohort were cross-sectionally compared across racial groups using survival and multiple logistic regression analyses.
RESULTS
The study included 9162 WP, 341 AP and 181 BP. AP developed the first non-RP feature faster than WP but slower than BP. AP were less frequently anti-centromere (ACA; odds ratio (OR) = 0.4, P < 0.001) and more frequently anti-topoisomerase-I autoantibodies (ATA) positive (OR = 1.2, P = 0.068), while BP were less likely to be ACA and ATA positive than were WP [OR(ACA) = 0.3, P < 0.001; OR(ATA) = 0.5, P = 0.020]. AP had less often (OR = 0.7, P = 0.06) and BP more often (OR = 2.7, P < 0.001) diffuse skin involvement than had WP. AP and BP were more likely to have pulmonary hypertension [OR(AP) = 2.6, P < 0.001; OR(BP) = 2.7, P = 0.03 vs WP] and a reduced forced vital capacity [OR(AP) = 2.5, P < 0.001; OR(BP) = 2.4, P < 0.004] than were WP. AP more often had an impaired diffusing capacity of the lung than had BP and WP [OR(AP vs BP) = 1.9, P = 0.038; OR(AP vs WP) = 2.4, P < 0.001]. After RP onset, AP and BP had a higher hazard to die than had WP [hazard ratio (HR) (AP) = 1.6, P = 0.011; HR(BP) = 2.1, P < 0.001].
CONCLUSION
Compared with WP, and mostly independent of geographical location, AP have a faster and earlier disease onset with high prevalences of ATA, pulmonary hypertension and forced vital capacity impairment and higher mortality. BP had the fastest disease onset, a high prevalence of diffuse skin involvement and nominally the highest mortality.
- Language
-
- English
- Open access status
- green
- Identifiers
-
- DOI 10.1093/rheumatology/kez486
- PMID 31680161
- Persistent URL
- https://sonar.ch/global/documents/82146
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