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Published on: November 10, 2017
Effect of atorvastatin on lipoprotein (a) and interleukin-10: a randomized placebo-controlled trial
C Hernández1, G Francisco, A Ciudin
1CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain.
Insights
Atorvastatin therapy effectively lowers lipoprotein (a) [Lp(a)] levels in hypercholesterolaemic patients. The study also found that atorvastatin increases interleukin-10 (IL-10) in a dose-dependent manner.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Biochemistry
Background:
- Hypercholesterolaemia poses a significant risk for cardiovascular disease (CVD).
- Lipoprotein (a) [Lp(a)] is an independent risk factor for atherosclerosis and CVD.
- Biomarkers of inflammation play a crucial role in the pathogenesis of cardiovascular events.
Purpose of the Study:
- To investigate the impact of atorvastatin on plasma Lp(a) levels.
- To assess the effect of atorvastatin on key inflammatory biomarkers.
- To evaluate these effects in hypercholesterolaemic patients without pre-existing cardiovascular disease.
Main Methods:
- A 12-week randomized, double-blind, placebo-controlled trial.
- Inclusion of 63 hypercholesterolaemic patients.
- Treatment groups: placebo, atorvastatin 10 mg/day, and atorvastatin 40 mg/day.
- Measurement of Lp(a), C-reactive protein (CRP), IL-6, IL-10, and TNF-Rs at baseline and follow-up points.
Main Results:
- Atorvastatin significantly reduced Lp(a) levels compared to placebo (P = 0.02 for 10 mg, P = 0.04 for 40 mg).
- Changes in Lp(a) were independently associated with baseline Lp(a) and CRP changes.
- A significant, dose-dependent increase in IL-10 was observed with atorvastatin therapy (P = 0.01).
- No significant changes were noted in CRP, IL-6, or TNF-Rs.
Conclusions:
- Twelve weeks of atorvastatin therapy is effective in reducing Lp(a) in dyslipidaemic patients without CVD.
- Atorvastatin demonstrates a novel, dose-dependent increase in IL-10 levels.
- These findings suggest potential pleiotropic effects of statins beyond lipid-lowering.
Aim:
This study aimed to determine the effect of atorvastatin therapy on plasma lipoprotein (a) [Lp(a)] and biomarkers of inflammation in hypercholesterolaemic patients free of cardiovascular disease.
Methods:
In this three-month randomized double-blind placebo-controlled trial, 63 hypercholesterolaemic patients were randomly treated with either placebo or atorvastatin (10 or 40 mg/day) for 12 weeks. Lp(a) and biomarkers of inflammation (C-reactive protein [CRP], interleukin [IL]-6 and -10, and tumour necrosis factor-alpha receptors [TNF-Rs]) were measured at study entry, and at four and 12 weeks of follow-up.
Results:
At the end of the study, patients allocated to atorvastatin (10 or 40 mg/day) presented with significantly lower Lp(a) levels than those taking placebo (10 [1-41]mg/dL versus 6 [1-38]mg/dL [P = 0.02] and 21 [1-138]mg/dL versus 15 [1-103]mg/dL [P = 0.04], respectively]. In multivariate analyses, the relative changes in Lp(a) were independently related to baseline Lp(a) levels and CRP changes. No significant changes in CRP, IL-6 and TNF-Rs were observed. In contrast, IL-10 (pg/mL) increased significantly in patients taking atorvastatin (2.14 [0.49-43]pg/mL versus 4.54 [0.51-37.5]pg/mL; P = 0.01), and was even more increased with the 40-mg dose than with 10mg.
Conclusion:
Our results suggest that 12-week atorvastatin is effective in reducing Lp(a) in dyslipidaemic patients free of CVD. Furthermore, this is also the first evidence that the drug increases IL-10 in a dose-dependent manner.
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