Review
Atherosclerosis in Sjögren’s syndrome: evidence, possible mechanisms and knowledge gaps
V. Valim1, E. Gerdts2, R. Jonsson3, G.A. Ferreira4, K.A. Brokstad5, J.G. Brun6, H.B. Midtbø7, P.M. Mydel8
- Department of Medicine, Federal University of Espírito Santo, Vitória, Brazil; and Broegelmann Research Laboratory, University of Bergen, Norway. val.valim@gmail.com
- Department of Clinical Science, University of Bergen, Norway.
- Broegelmann Research Laboratory, and Department of Clinical Science, University of Bergen, Norway.
- Department of Locomotor Systems, Federal University of Minas Gerais, Belo Horizonte, Brazil.
- Broegelmann Research Laboratory, University of Bergen, Norway.
- Department of Clinical Science, University of Bergen; and Department of Rheumatology, Haukeland University Hospital, Bergen, Norway.
- Department of Clinical Science, University of Bergen; and Department of Heart Disease, Haukeland University Hospital, Bergen, Norway.
- Broegelmann Research Laboratory, University of Bergen, Norway.
CER8610
2016 Vol.34, N°1
PI 0133, PF 0142
Review
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PMID: 26812164 [PubMed]
Received: 15/05/2015
Accepted : 04/09/2015
In Press: 20/01/2016
Published: 10/02/2016
Abstract
Inflammation has been associated with higher cardiovascular risk in rheumatic autoimmune diseases like rheumatoid arthritis (RA) and systemic lupus erythematosus. More recently, primary Sjögren’s syndrome (pSS) was also demonstrated as an independent risk factor for cardiovascular disease, emerging as a new interesting model to study atherosclerosis in autoimmune diseases. Patients with pSS have a higher prevalence of developing traditional cardiovascular risk factors like hypertension and dyslipidaemia predisposing for endothelial dysfunction and premature atherosclerosis. However, the disease-specific mechanisms for premature atherosclerosis in pSS are not fully understood. The aim of this review was to critically analyse the current literature on cardiovascular risks in pSS and to discuss the traditional and disease-associated risk factors. We also suggest possible new mechanisms that should be explored in future research to close the current knowledge gaps on the association of pSS, premature atherosclerosis, and clinical cardiovascular disease.
