title: Effects of statins on oxidative stress and primed polymorphonuclear leukocytes in hyperlipidemic patients.
abstract: Inflammation and oxidative stress are among the factors that have been implicated in the pathogenesis of hyperlipidemia. In metabolic syndrome and hyperlipidemic patients, peripheral polymorphonuclear leukocytes (PMNL) are primed and they release uncontrolled superoxide that contributes to oxidative stress and inflammation. Recent studies have demonstrated that the anti-hyperlipidemic drug, Atrovastatin effects improvement in endothelial function, exhibits anti-oxidative characteristics and reduces lipid markers of oxidation. To evaluate possible nontraditional effects of treatment with Atrovastatin on PMNL priming, oxidative stress and inflammation in hyperlipidemia, 50 non-smoking hyperlipidemic patients were treated for 6 months with Atrovastatin and compared to age and gender-matched healthy controls. PMNL priming was assessed by the rate of superoxide release from separated, phorbol ester-stimulated PMNL and by PMNL-CD11b levels. Inflammation was reflected by blood inflammatory markers including albumin, transferrin, C-reactive protein (CRP) and fibrinogen levels, white blood cells (WBC), PMNL counts and PMNL apoptosis. Atrovastatin treatment showed a reduction in PMNL priming, PMNL apoptosis, fibrinogen and CRP levels concomitant with decreased lipid levels. Atrovastatin may be preferred for hyperlipidemic patients owing to its combined anti-PMNL priming and anti-inflammatory effects in addition to its anti-atherogenic effects.
authors.affiliation: Department of Internal Medicine B, Ziv Medical Center, Safed, Israel. raymond.f@ziv.health.gov.il
authors.forename: R
authors.initials: R
authors.lastname: Farah
authors.forename: F
authors.initials: F
authors.lastname: Jubran
authors.forename: R
authors.initials: R
authors.lastname: Khamisy-Farah
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000187:drug effects; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D039481:CD11b Antigen / Q000032:analysis; D002478:Cells, Cultured; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006949:Hyperlipidemias / Q000188:drug therapy*; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy; D007958:Leukocyte Count; D008297:Male; D009504:Neutrophils / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects*; D010703:Phorbol Esters / Q000494:pharmacology; D011758:Pyrroles / Q000627:therapeutic use*; D013481:Superoxides / Q000378:metabolism
chemical_list: D015415:Biomarkers; D039481:CD11b Antigen; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; C509295:ITGAM protein, human; D010703:Phorbol Esters; D011758:Pyrroles; D013481:Superoxides; D000069059:Atorvastatin