title: Atorvastatin reduced soluble receptors of TNF-alpha in systemic lupus erythematosus.
abstract: OBJECTIVE
  The aim of this study was to evaluate the efficacy of atorvastatin to reduce the plasma levels of TNF system molecules (TNF-α, 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-α, 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-α and sTNFR 1 levels and SLICC score. Patients with current nephritis and patients with anti-ds-DNA 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-α and sTNFR2 plasma levels. The SLEDAI and SLICC scores were independent determinants of the plasma levels of sRTNF1.
  
  
  CONCLUSIONS
  Atorvastatin reduced soluble receptors of TNF-α. The plasma levels of TNF-α, sTNFR1 and sTNFR2 may play a role in SLE activity and atherosclerosis, and might be evaluated as targets for new therapies.
authors.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. gildaferreira9@gmail.com.
authors.forename: Gilda Aparecida
authors.initials: GA
authors.lastname: Ferreira
authors.affiliation: Department of Internal Medicine, Medical School, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
authors.forename: Antonio Lúcio
authors.initials: AL
authors.lastname: Teixeira
authors.affiliation: Rheumatology Service, Hospital das Clínicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
authors.forename: Debora Cerqueira
authors.initials: DC
authors.lastname: Calderaro
authors.affiliation: Rheumatology Division, Universidade Federal de São Paulo/Escola Paulista de Medicina (UNIFESP/EPM), São Paulo, Brazil.
authors.forename: Emília Inoue
authors.initials: EI
authors.lastname: Sato
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000097:blood / Q000175:diagnosis / Q000276:immunology / Q000517:prevention & control*; D000069059:Atorvastatin / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D001938:Brazil; D015536:Down-Regulation; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood*; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood*; D012307:Risk Factors; D012720:Severity of Illness Index; D013997:Time Factors; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D055815:Young Adult
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; C506235:TNFRSF1A protein, human; C415902:TNFRSF1B protein, human; D014409:Tumor Necrosis Factor-alpha; D000069059:Atorvastatin