Objectives: 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.