Rheumatology Advance Access originally published online on January 7, 2008
Rheumatology 2008 47(3):382-383; doi:10.1093/rheumatology/kem346
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Comment on: Atorvastatin therapy improves endothelial-dependent vasodilation in patients with systemic lupus erythematosus: an 8 weeks controlled trial: reply
1Universidade Federal de Minas Gerais, Belo Horizonte and 2Universidade Federal de São Paulo, São Paulo, Brazil
Correspondence to: E. I. Sato, Rua Botucatu 740, CEP 040 23-900, São Paulo, Brazil. E-mail: emiliasato{at}reumato.epm.br
SIR, We would like to thank Dr Kotyla [1] for their interest in our study. We agree that statins have a significant role in the modulation of the cytokines and are an important therapeutic option for patients with systemic lupus erythematosus (SLE).
SLE patients, independently of the clinical features, present a higher level of cytokines than controls. Chun and colleagues [2] reported that SLE patients had higher interleukin (IL)-6, IL-10, IL-12 and interferon-
(IFN-) serum levels than controls. In addition, IL-6 and IL-10 serum levels were significantly elevated in active SLE patients and correlated with the SLE disease activity index (SLEDAI), erythrocyte sedimentation rate and C-reactive protein [2].
ILs are involved in several phases of atherogenesis, mainly promoting the inflammation related to the atherosclerosis and interfering in the lipid metabolism [3]. Additionally, it has been shown that cytokines are important non-traditional risk factors (disease-related risk factors) for accelerated and premature atherosclerosis in SLE patients [4]. Asanuma and colleagues [5] demonstrated that IL-6 and MCP-1 serum levels were higher in SLE patients than in controls and were related with disease activity. After adjusting for confounding variables, increased IL-6 levels were positively correlated with the extent of coronary calcification [5].
The interesting result found by Kotyla and colleagues [6] showing a significant suppression of tumour necrosis factor-
(TNF-) concentration in SLE patients’ sera after 4 weeks of simvastatin is in agreement with the previous demonstration by Yokota and colleagues [7] that simvastatin inhibits the synthesis of IL-6, IL-8 as well as the proliferation of fibroblast-like synoviocytes induced by TNF- in rheumatoid arthritis patients. In our study [8], atorvastatin use was associated with reduced disease activity (SLEDAI scores) and improvement in the endothelial cell function, as also observed by Kotyla et al. [6] using simvastatin.
Therefore, we agree that statins may play an important role in the treatment of SLE patients regarding the prevention of cardiovascular disease as well as the immunomodulation over the chronic inflammatory activity of the disease. These preliminary finding must be confirmed by multicentre and long-term studies to define whether statin treatment in SLE patients is indeed associated with a relevant reduction of cardiovascular morbidity and mortality as well as with an amelioration of the inflammatory status and if this drug category should be broadly indicated for SLE patients.
Disclosure statement: The authors have declared no conflicts of interest.
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- Kotyla PJ. Comment on: Atorvastatin therapy improves endothelial-dependent vasodilation in patients with systemic lupus erythematosus: an 8 weeks controlled trial. Rheumatology (2008) (in press).
- Chun HY, Chung JW, Kim HA, et al. Cytokine IL-6 and IL-10 as biomarkers in systemic lupus erythematosus. J Clin Immunol (2007) 27:461–6.[CrossRef][Web of Science][Medline]
- Mol MJ, Demacker PN, Stalenhoef AF. The role of modification of lipoproteins and of the immune system in early atherogenesis. Neth J Med (1993) 43:83–90.[Web of Science][Medline]
- Shovman O, Gilburd B, Shoenfeld Y. The role of inflammatory cytokines in the pathogenesis of systemic lupus erythematosus-related atherosclerosis: a novel target for treatment? J Rheumatol (2006) 33:445–7.
[Free Full Text] - Asanuma Y, Chung CP, Oeser A, et al. Increased concentration of proatherogenic inflammatory cytokines in systemic lupus erythematosus: relationship to cardiovascular risk factors. J Rheumatol (2006) 33:539–45.
[Abstract/Free Full Text] - Kotyla PJ, Sliwinska-Kotyla B, Kucharz EJ. TNF alpha as a potential target in the treatment of SLE: a role of HMG-Coa reductase inhibitor simvastatin. J Rheumatol (2006) 33:2361.
[Free Full Text] - Yokota K, Miyazaki T, Hirano M, Akiyama Y, Mitura T. Simvastatin inhibits production of interleukin 6 (IL-6) and IL-8 and cell proliferation induced by tumor necrosis factor alpha in fibroblast-like synoviocytes from patients with rheumatoid arthritis. J Rheumatol (2006) 33:463–71.
[Abstract/Free Full Text] - Ferreira GA, Navarro TP, Telles RW, Andrade LEC, Sato EI. Atorvastatin therapy improves endothelial-dependent vasodilation in patients with systemic lupus erythematosus: an 8 weeks controlled trial. Rheumatology (2007) 46:1560–5.
[Abstract/Free Full Text]
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