TY - JOUR
T1 - Atorvastatin reduced soluble receptors of TNF-alpha in systemic lupus erythematosus
AU - Ferreira, Gilda Aparecida
AU - Teixeira, Antonio Lúcio
AU - Calderaro, Debora Cerqueira
AU - Sato, Emília Inoue
N1 - Publisher Copyright:
© Copyright Clinical and Experimental Rheumatology 2016.
PY - 2016
Y1 - 2016
N2 - Objective: The aim of this study was to evaluate the efficacy of atorvastatin to reduce the plasma levels of TNF system molecules (TNF-a, 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-a, 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-a 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-a 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-a. The plasma levels of TNF-a, sTNFR1 and sTNFR2 may play a role in SLE activity and atherosclerosis, and might be evaluated as targets for new therapies.
AB - Objective: The aim of this study was to evaluate the efficacy of atorvastatin to reduce the plasma levels of TNF system molecules (TNF-a, 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-a, 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-a 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-a 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-a. The plasma levels of TNF-a, sTNFR1 and sTNFR2 may play a role in SLE activity and atherosclerosis, and might be evaluated as targets for new therapies.
KW - Atherosclerosis
KW - Atorvastatin
KW - Receptors
KW - Systemic lupus erythematosus
KW - Tumour necrosis factor
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M3 - Article
C2 - 26574625
AN - SCOPUS:84958757805
SN - 0392-856X
VL - 34
SP - 42
EP - 48
JO - Clinical and Experimental Rheumatology
JF - Clinical and Experimental Rheumatology
IS - 1
ER -