Atorvastatin reduced soluble receptors of tnf-alpha in systemic lupus erythematosus
dc.contributor.author | Ferreira, G. A. | |
dc.contributor.author | Teixeira, A. L. | |
dc.contributor.author | Calderaro, D. C. | |
dc.contributor.author | Sato, E. I. [UNIFESP] | |
dc.date.accessioned | 2019-01-21T10:30:07Z | |
dc.date.available | 2019-01-21T10:30:07Z | |
dc.date.issued | 2016 | |
dc.description.abstract | Objective The aim of this study was to evaluate the efficacy of atorvastatin to reduce the plasma levels of TNF system molecules (TNF-alpha, sTNFR1 and sTNFR2) and to assess their association with risk factors for accelerate atherosclerosis and clinical disease activity scores in SLE patients. Methods In a previous study, 64 female SLE patients received 20 mg/day of atorvastatin and 24 SLE patients (non-treated group) were followed for 8 weeks. Plasma levels of TNF-alpha, sTNFR 1 and sTNFR 2 were measured by ELISA, at baseline and at the end of the study. Results The plasma levels of sTNFR1 and sTNFR 2 showed a positive correlation with SLEDAI score. We also found a positive correlation between TNF-alpha and sTNFR 1 levels and SLICC score. Patients with current nephritis and patients with anti-dsDNA antibodies presented higher sTNFR1 and sTNFR2 levels. Patients with abdominal obesity and arterial hypertension also had higher plasma levels of soluble receptors. At the end of 8 weeks, we observed a significant decrease in sTNFR1 plasma levels in patients receiving atorvastatin [median (percentile), 876.5 (717-1284 pg/ml) vs. 748 (629.6-917.3 pg/ml), p=0.03], without difference regarding TNF-alpha and sTNFR2 plasma levels. The SLEDAI and SLICC scores were independent determinants of the plasma levels of sRTNF1. Conclusion Atorvastatin reduced soluble receptors of TNF-alpha. The plasma levels of TNF-alpha, sTNFR1 and sTNFR2 may play a role in SLE activity and atherosclerosis, and might be evaluated as targets for new therapies. | en |
dc.description.affiliation | Department of Locomotor System, Medical School, Universidade Federal de Minas Gerais; and Rheumatology Service, Hospital das Clínicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil | |
dc.description.affiliation | Department of Internal Medicine, Medical School, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil | |
dc.description.affiliation | Rheumatology Service, Hospital das Clínicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil | |
dc.description.affiliation | Rheumatology Division, Universidade Federal de São Paulo/Escola Paulista de Medicina (UNIFESP/EPM), São Paulo, Brazil | |
dc.description.affiliationUnifesp | Rheumatology Division, Universidade Federal de São Paulo/Escola Paulista de Medicina (UNIFESP/EPM), São Paulo, Brazil | |
dc.description.source | Web of Science | |
dc.description.sponsorship | CNPq | |
dc.description.sponsorship | Fapemig | |
dc.format.extent | 42-48 | |
dc.identifier | http://www.clinexprheumatol.org/abstract.asp?a=9060 | |
dc.identifier.citation | Clinical And Experimental Rheumatology. Pisa, v. 34, n. 1, p. 42-48, 2016. | |
dc.identifier.issn | 0392-856X | |
dc.identifier.uri | http://repositorio.unifesp.br/handle/11600/49591 | |
dc.identifier.wos | WOS:000371850400007 | |
dc.language.iso | eng | |
dc.publisher | Clinical & exper rheumatology | |
dc.relation.ispartof | Clinical And Experimental Rheumatology | |
dc.rights | info:eu-repo/semantics/restrictedAccess | |
dc.subject | Systemic Lupus Erythematosus | en |
dc.subject | Atherosclerosis | en |
dc.subject | Receptors | en |
dc.subject | Tumour Necrosis Factor | en |
dc.subject | AtorvastatinTumor-Necrosis-Factor | en |
dc.subject | Disease-Activity | en |
dc.subject | Proinflammatory Cytokines | en |
dc.subject | Insulin-Resistance | en |
dc.subject | Therapy | en |
dc.subject | Risk | en |
dc.subject | Expression | en |
dc.subject | Statins | en |
dc.subject | Markers | en |
dc.subject | Sle | en |
dc.title | Atorvastatin reduced soluble receptors of tnf-alpha in systemic lupus erythematosus | en |
dc.type | info:eu-repo/semantics/article |