Rheumatology Advance Access originally published online on October 13, 2006
Rheumatology 2006 45(12):1581-1582; doi:10.1093/rheumatology/kel350
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Re: Traditional cardiovascular risk factors in primary Sjögren's syndrome: role of dyslipidaemia
1Gene Therapy and Therapeutics Branch/National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA and 2Division of Clinical Immunology and Rheumatology, Academic Medical Center/University of Amsterdam, The Netherlands
Correspondence to: Dr Beatrijs M. Lodde, GTTB/NIDCR, National Institutes of Health, 10 Center Drive, Room 1N114, MSC 1190, Bethesda, MD 20892-1190, USA. E-mail: blodde{at}mail.nih.gov
SIR, we would like to thank Gerli et al. [1] for their reply and the post hoc analysis of their recent Sjögren's syndrome (SS) study [2] performed. This analysis confirmed our findings [3] in relation to the presence of anti-SSA/B autoantibodies and lower total and HDL cholesterol levels.
In addition, Gerli et al.'s study showed anti-SSA antibodies, but not lipid levels, to be an independent predictor of mean carotid arterial thickening [2]. As referenced in our article, in RA and SLE several possible factors, including autoantibodies, can lead through vascular damage to a dysfunctional vasculature more susceptible to traditional cardiovascular risk factors, such as cholesterol levels, than in general. In addition, decreased lipid levels tended to predict cardiovascular morbidity and mortality in RA [4]. An association between intima-media thickening and altered lipid levels in SS patients could perhaps, as Gerli and co-authors had suggested, be detected in larger population-based studies with longer follow-up.
Gerli et al. believe that the presence of anti-SSA/B autoantibodies is better for disease diagnosis than as a reflection of disease activity. As they indicate, these autoantibodies are thought to be a marker of autoimmune dysregulation characterizing an SS patient's subset with more severe disease [5, 6]. Indeed, anti-SSA autoantibodies are detected in virtually all SS patients with coexistent vasculitis and in some of these patients it may be the only detectable antibody [7]. Again, this vasculitis can subsequently result in cardiovascular morbidity [8].
Moreover, anti-SSB autoantibody proved to be a highly significant marker of organ involvement in a large cohort of primary SS patients [5]. Interestingly, during an SS outcome measures workshop, Soloman et al. showed in a meta-analysis identifying predictive biomarkers in SS clinical trials that anti-SSB autoantibody may be a promising biomarker, in addition to IgG levels [9].
We agree immune-mediated mechanisms can play a role, but the relative contribution of each of the mechanisms needs to be further elucidated. Precocious atherosclerosis, dyslipidemia and autoimmune dysregulation could all be involved in a potential atherosclerotic risk and subsequently cardiovascular events. Gerli et al.'s and our studies provide the rationale for further research.
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- Gerli R, Bocci EB, Vaudo G, Marchesi S, Vitali C, Shoenfeld Y. Traditional cardiovascular risk factors in primary Sjögren's syndrome: role of dyslipidaemia. Rheumatology.
- Vaudo G, Bocci EB, Shoenfeld Y, et al. (2005) Precocious intima-media thickening in patients with primary Sjogren's syndrome. Arthritis Rheum 52:3890–7.[CrossRef][Web of Science][Medline]
- Lodde BM, Sankar V, Kok MR, Leakan RA, Tak PP, Pillemer SR. (2006) Serum lipid levels in Sjogren's syndrome. Rheumatology 45:481–4.
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