RESULTS Meta- analysis suggested that statin therapy is associated with a significant elevation of PON1 paraoxonase and arylesterase activities , but not PON1 protein concentration .
The PON1-enhancing effects of statins were robust in the sensitivity analyses and were independent of statin dose , treatment duration and changes in plasma low-density lipoprotein cholesterol concentration .
CONCLUSION The increase of paraoxonase and arylesterase activities with statins is a pleiotropic lipid-independent clinical benefit that may partly explain the putative effects of statins in preventing cardiovascular outcomes
BACKGROUND Decreased activity of the enzyme paraoxonase-1 ( PON1 ) has been demonstrated in cardiovascular diseases .
Statins , the forefront of pharmacotherapy for dyslipidemia , have been shown to enhance PON1 activity but clinical findings have not been conclusive .
OBJECTIVE To systematic ally review the clinical findings on the impact of statin therapy on PON1 status ( protein concentrations and activities of paraoxonase and arylesterase ) and calculate an effect size for the mentioned effects through meta- analysis of available data .
Effect of rosuvastatin versus atorvastatin treatment on paraoxonase-1 activity in men with established cardiovascular disease and a low HDL-cholesterol
ABSTRACT Objective : Paraoxonase-1 ( PON-1 ) is a high-density lipoprotein ( HDL ) associated enzyme involved in the protective mechanisms of HDL . Our aim was to compare the effect of treatment with rosuvastatin and atorvastatin on serum PON-1 activity . Methods : We performed a prespecified prospect i ve study in 68 patients , part of a larger , multicentre r and omized study – RADAR  ( Rosuvastatin and Atorvastatin in different Dosages And Reverse cholesterol transport ) . Patients aged 40–80 years , all men , with established cardiovascular disease and high-density lipoprotein cholesterol ( HDL‑C ) < 1.0 mmol/L ( < 40 mg/dL ) entered a 6-week dietary run-in period before receiving treatment with rosuvastatin 10 mg or atorvastatin 20 mg daily for 6 weeks . Doses were increased after 6 weeks to rosuvastatin 20 mg or atorvastatin 40 mg and after 12 weeks to rosuvastatin 40 mg or atorvastatin 80 mg daily . Serum PON-1 activity and lipid profile were determined at baseline , 6 and 18 weeks . Results : After 18 weeks , the rosuvastatin arm showed a significant increase of PON-1 activity ( 6.39 U/L , p = 0.02 ) whereas this was not observed in the atorvastatin arm ( 1.84 U/L , p = 0.77 ) . The difference between groups did not reach significance ( p = 0.11 ) . Both rosuvastatin and atorvastatin result ed in significant ( p = 0.0001 ) and similar increases in HDL‑C after 6 weeks [ 0.06 mmol/L ( 2.32 mg/dL ) vs. 0.05 mmol/L ( 1.93 mg/dL ) ] and after 18 weeks [ 0.10 mmol/L ( 3.87 mg/dL ) vs. 0.10 mmol/L ( 3.87 mg/dL ) ] . Conclusions : Rosuvastatin treatment result ed in a significant increment of serum PON-1 activity with increasing dose while this was not observed with atorvastatin
RESULTS Meta- analysis suggested that statin therapy is associated with a significant elevation of PON1 paraoxonase and arylesterase activities , but not PON1 protein concentration .
The PON1-enhancing effects of statins were robust in the sensitivity analyses and were independent of statin dose , treatment duration and changes in plasma low-density lipoprotein cholesterol concentration .
CONCLUSION The increase of paraoxonase and arylesterase activities with statins is a pleiotropic lipid-independent clinical benefit that may partly explain the putative effects of statins in preventing cardiovascular outcomes
BACKGROUND Decreased activity of the enzyme paraoxonase-1 ( PON1 ) has been demonstrated in cardiovascular diseases .
Statins , the forefront of pharmacotherapy for dyslipidemia , have been shown to enhance PON1 activity but clinical findings have not been conclusive .
OBJECTIVE To systematic ally review the clinical findings on the impact of statin therapy on PON1 status ( protein concentrations and activities of paraoxonase and arylesterase ) and calculate an effect size for the mentioned effects through meta- analysis of available data .