Primed polymorphonuclear leukocytes constitute a possible link between inflammation and oxidative stress in hyperlipidemic patients: effect of statins.
OBJECTIVE
Oxidative stress (OS) and inflammation and are among the mechanisms that have been recently implicated in pathogenesis of hyperlipidemia. Peripheral polymorphonuclear leukocytes (PMNLs) are primed in metabolic syndrome patients, which include hyperlipidemic patients, releasing uncontrolled superoxide contributing to OS and inflammation. Recent studies have attributed additional anti-ischemic and antioxidative characteristics to the antihyperlipidemic antiatherogenic drug, simvastatin. The aim of this paper was to evaluate the possible non-traditional effect of five months' simvastatin treatment on PMNL priming and inflammation in hyperlipidemia.


METHODS
Thirty non-smoking hyperlipidemic patients were treated for 5 months with Simvastatin and compared with age and gender-matched healthy controls (HC). PMNL priming was assessed by the rate of superoxide release from separated, phorbol ester-stimulated PMNLs and by PMNL-CD11b levels. Inflammation was reflected by blood albumin, transferrin, C-reactive protein (CRP) and fibrinogen levels, white blood cells (WBC), PMNL counts and by PMNL apoptosis.


RESULTS
Five months of simvastatin treatment showed a decrease in lipid levels, concomitantly with reduction in PMNL priming, PMNL apoptosis, fibrinogen and CRP levels.


CONCLUSIONS
PMNLs are primed in hyperlipidemic patients contributing to OS and inflammation in these patients. Treating these patients with Simvastatin may be beneficial due to its combined anti-PMNL priming and anti-inflammatory effects, in addition to its traditional antiatherogenic characteristics.
Farah
R
R
Departement of Internal Medicine F, Western Galilee Hospital, Nahariya, Israel. raymond.f@ziv.health.gov.il
Shurtz-Swirski
R
R
Dorlechter
F
F
D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use*; D006949:Hyperlipidemias / Q000188:drug therapy* / Q000209:etiology* / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy* / Q000209:etiology* / Q000378:metabolism; D009504:Neutrophils / Q000187:drug effects* / Q000502:physiology*; D018384:Oxidative Stress / Q000187:drug effects*; D019821:Simvastatin / Q000494:pharmacology* / Q000627:therapeutic use*
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D019821:Simvastatin