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JOURNAL ARTICLE
META-ANALYSIS
REVIEW
Effects of Statin Therapy in Patients with Systemic Lupus Erythematosus.
Southern Medical Journal 2016 November
OBJECTIVES: Systemic lupus erythematosus (SLE) is associated with a significant risk of cardiovascular mortality. The use of statins for lipid modulation and the prevention of cardiovascular disease in this population also may impart pleiotropic anti-inflammatory and immunomodulatory effects. Our aim was to identify studies that compared the use of statins and placebo or no statin therapy in patients with SLE.
METHODS: A meta-analysis was conducted on the follow-up measures of serum lipid levels, inflammatory markers, and disease activity, which was measured using the SLE Disease Activity Index (SLEDAI) score. The mean difference (MD) was calculated by the inverse variance method under a fixed or random-effects model, as appropriate.
RESULTS: A total of eight studies met our inclusion criteria, including five randomized controlled trials. The total number of patients was 814 (statins 446, placebo/no statins 368), and follow-up ranged from 1 month to 7 years. The total cholesterol (MD -23.48 mg/dL, 95% confidence interval [CI] -34.57 to -12.39, P < 0.0001), low-density lipoprotein (MD -20.7 mg/dL, 95% CI -30.51 to -10.89, P < 0.0001), and high-sensitivity C-reactive protein (MD -0.40 mg/dL, 95% CI -0.64 to -0.16, P = 0.001) levels were significantly reduced by statin therapy. There was no change with statin use in serum levels of high-density lipoprotein and conventional C-reactive protein, and there was no difference in the SLEDAI score.
CONCLUSIONS: The use of statins in SLE reduced the serum lipid and high-sensitivity C-reactive protein levels, which suggests a role for the primary prevention of cardiovascular disease. Statins did not affect the SLEDAI score, and therefore their use for modifying SLE disease activity levels is not presently supported.
METHODS: A meta-analysis was conducted on the follow-up measures of serum lipid levels, inflammatory markers, and disease activity, which was measured using the SLE Disease Activity Index (SLEDAI) score. The mean difference (MD) was calculated by the inverse variance method under a fixed or random-effects model, as appropriate.
RESULTS: A total of eight studies met our inclusion criteria, including five randomized controlled trials. The total number of patients was 814 (statins 446, placebo/no statins 368), and follow-up ranged from 1 month to 7 years. The total cholesterol (MD -23.48 mg/dL, 95% confidence interval [CI] -34.57 to -12.39, P < 0.0001), low-density lipoprotein (MD -20.7 mg/dL, 95% CI -30.51 to -10.89, P < 0.0001), and high-sensitivity C-reactive protein (MD -0.40 mg/dL, 95% CI -0.64 to -0.16, P = 0.001) levels were significantly reduced by statin therapy. There was no change with statin use in serum levels of high-density lipoprotein and conventional C-reactive protein, and there was no difference in the SLEDAI score.
CONCLUSIONS: The use of statins in SLE reduced the serum lipid and high-sensitivity C-reactive protein levels, which suggests a role for the primary prevention of cardiovascular disease. Statins did not affect the SLEDAI score, and therefore their use for modifying SLE disease activity levels is not presently supported.
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