BACKGROUND: Over the past several years, numerous studies investigated the anti-inflammatory effects of statin on patients with RA. However, the findings of the individual studies were often inconsistent or conflicting. MATERIALS AND METHODS: The Pubmed, Web of Science, Embase, Cochrane Library and CNKI literature databases were searched in order to identify randomized controlled clinical trials where the association between the anti-inflammatory effect of statin and RA was investigated. Two researchers performed data extraction from eligible independently. Quality parameters and risk of bias in the included studies were assessed according to Cochrane's guidelines. The pooled Standardized Mean Difference (SMD) with a 95%CI was used to assess the anti-inflammatory effect of statin in patients with RA. RESULTS: Fifteen randomized controlled clinical, classified as "high quality" and with a relatively low risk of selection bias, were included in the meta-analysis. Of these, eight reported that there was no difference in the level of serum total lipids between the atorvastatin-treated and the conventional treatment group. However, the pooled analysis showed that atorvastatin could increase the level of serum amount of high-density lipoprotein (HDL) in RA patients by approximately x ± SD95% [HDL: SMD = 0.807, 95%CI = (0.187, 1.426), p = .011]. Meanwhile atorvastatin could reduce the level of serum low-density lipoprotein (LDL), total cholesterol (TC), and triglyceride (TG) in RA patient by x ± SD95% [LDL: SMD = -4.015, 95%CI = (-5.848, -2.183), p = .000; TC: SMD = -4.497, 95%CI = (-6.457, -2.537), p = .000; TG: SMD = -1.475, 95%CI = (-2.352, -0.599), p = .001]. Nine studies reported a change in C-Reactive Protein (CRP) after atorvastatin treatment, and the pooled analysis showed that atorvastatin decreased CRP in RA patients by x ± SD95% [SMD = -3.033, 95%CI = (-4.460, -1.606), p = .000]. Seven studies investigated the change of Erythrocyte Sedimentation Rate (ESR), and the pooled analysis showed that atorvastatin decreased ESR by x ± SD95% [SMD = -2.097, 95%CI = (-3.408, -0.786), p = .002]. Nine studies reported the improvement of disease activity score in RA patients after taking atorvastatin for 12 weeks, and the pooled analysis showed atorvastatin could decrease the DAS28 score in RA patients by x ± SD95% [SMD = -2.001, 95%CI = (-3.191, -0.811), p = .001]. CONCLUSIONS: Statins have a significant anti-inflammatory effect in RA patients. However, atorvastatin was superior to simvastatin both in terms of its anti-inflammatory and lipid-lowering activities.
BACKGROUND: Over the past several years, numerous studies investigated the anti-inflammatory effects of statin on patients with RA. However, the findings of the individual studies were often inconsistent or conflicting. MATERIALS AND METHODS: The Pubmed, Web of Science, Embase, Cochrane Library and CNKI literature databases were searched in order to identify randomized controlled clinical trials where the association between the anti-inflammatory effect of statin and RA was investigated. Two researchers performed data extraction from eligible independently. Quality parameters and risk of bias in the included studies were assessed according to Cochrane's guidelines. The pooled Standardized Mean Difference (SMD) with a 95%CI was used to assess the anti-inflammatory effect of statin in patients with RA. RESULTS: Fifteen randomized controlled clinical, classified as "high quality" and with a relatively low risk of selection bias, were included in the meta-analysis. Of these, eight reported that there was no difference in the level of serum total lipids between the atorvastatin-treated and the conventional treatment group. However, the pooled analysis showed that atorvastatin could increase the level of serum amount of high-density lipoprotein (HDL) in RApatients by approximately x ± SD95% [HDL: SMD = 0.807, 95%CI = (0.187, 1.426), p = .011]. Meanwhile atorvastatin could reduce the level of serum low-density lipoprotein (LDL), total cholesterol (TC), and triglyceride (TG) in RApatient by x ± SD95% [LDL: SMD = -4.015, 95%CI = (-5.848, -2.183), p = .000; TC: SMD = -4.497, 95%CI = (-6.457, -2.537), p = .000; TG: SMD = -1.475, 95%CI = (-2.352, -0.599), p = .001]. Nine studies reported a change in C-Reactive Protein (CRP) after atorvastatin treatment, and the pooled analysis showed that atorvastatin decreased CRP in RApatients by x ± SD95% [SMD = -3.033, 95%CI = (-4.460, -1.606), p = .000]. Seven studies investigated the change of Erythrocyte Sedimentation Rate (ESR), and the pooled analysis showed that atorvastatin decreased ESR by x ± SD95% [SMD = -2.097, 95%CI = (-3.408, -0.786), p = .002]. Nine studies reported the improvement of disease activity score in RApatients after taking atorvastatin for 12 weeks, and the pooled analysis showed atorvastatin could decrease the DAS28 score in RApatients by x ± SD95% [SMD = -2.001, 95%CI = (-3.191, -0.811), p = .001]. CONCLUSIONS: Statins have a significant anti-inflammatory effect in RApatients. However, atorvastatin was superior to simvastatin both in terms of its anti-inflammatory and lipid-lowering activities.
Authors: Elena Myasoedova; Paras Karmacharya; Ali Duarte-Garcia; John M Davis; M Hassan Murad; Cynthia S Crowson Journal: Semin Arthritis Rheum Date: 2020-04-09 Impact factor: 5.532