title: Pitavastatin increases HDL particles functionally preserved with cholesterol efflux capacity and antioxidative actions in dyslipidemic patients.
abstract: OBJECTIVE
  Although statins increase the plasma concentration of high-density lipoprotein cholesterol (HDL-C), it has not been elucidated whether the increased HDL particles possess normal antiatherosclerotic properties. Pitavastatin functions to increase the plasma HDL-C level and decrease the lowdensity lipoprotein cholesterol (LDL-C) level. In the present study, we sought to examine the qualitative changes in HDL during pitavastatin treatment.
  
  
  METHODS
  A total of 30 patients with dyslipidemia were treated with 2 mg of pitavastatin for four weeks. The cholesterol efflux capacity and activities of the antioxidative enzymes paraoxonase-1 (PON-1) and platelet-activating factor acetylhydrolase (PAF-AH) were evaluated using polyethethylene glycol-treated HDL fractions before and after pitavastatin treatment.
  
  
  RESULTS
  Pitavastatin treatment decreased the serum LDL-C level by 39% and increased the serum HDL-C level by 9% (p＜0.05). In addition, pitavastatin increased the phospholipid content of HDL by 7.8% (p＜0.05). The pitavastatin-induced increase in the HDL-C level coincided with an increase in the cholesterol efflux capacity of the isolated HDL fraction of 8.6% (p＜0.05). The post-pitavastatin treatment activity of HDL-associated PON-1 (paraoxonase and arylesterase) was increased by 9% (p＜0.05) and 11% (p＜0.05), respectively, while the HDL-associated PAF-AH activity was not affected by pitavastatin.
  
  
  CONCLUSIONS
  In addition to its LDL-C-lowering effects, pitavastatin elevates the HDL-C level and enhances the cholesterol efflux capacity and antioxidative properties of HDL. Pitavastatin therefore increases the amount of functional HDL without attenuating HDL quality.
authors.affiliation: Division of Cardiovascular Medicine , Kobe University Graduate School of Medicine.
authors.forename: Maki
authors.initials: M
authors.lastname: Miyamoto-Sasaki
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Yasuda
authors.forename: Tomoko
authors.initials: T
authors.lastname: Monguchi
authors.forename: Hideto
authors.initials: H
authors.lastname: Nakajima
authors.forename: Kenta
authors.initials: K
authors.lastname: Mori
authors.forename: Ryuji
authors.initials: R
authors.lastname: Toh
authors.forename: Tatsuro
authors.initials: T
authors.lastname: Ishida
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Hirata
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000378:metabolism; D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000378:metabolism; D043303:Aryldialkylphosphatase / Q000378:metabolism; D050197:Atherosclerosis / Q000517:prevention & control; D002784:Cholesterol / Q000378:metabolism; D008076:Cholesterol, HDL / Q000187:drug effects*; D050171:Dyslipidemias / Q000188:drug therapy* / Q000378:metabolism*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D010972:Platelet Activating Factor / Q000378:metabolism; D011092:Polyethylene Glycols / Q000378:metabolism; D011804:Quinolines / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D008076:Cholesterol, HDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D010972:Platelet Activating Factor; D011804:Quinolines; D011092:Polyethylene Glycols; D002784:Cholesterol; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human; C108475:pitavastatin