Ciprofibrate increases plasma concentration of platelet-derived growth factor AB in patients with advanced atherosclerosis and hyperlipidemia independently of its hypolipidemic effects

Fibrates, besides their hypolipidemic action, share alternative effects, su ch as decreased plasma fibrinogen and uric acid levels. Because of their co mplex action, additional effects have been investigated. A group of 23 pati ents with clinical signs of atherosclerosis and hyperlipoproteinemia was ra ndomly allocated after a 1-month washout period and treated with either 100 mg/d of ciprofibrate or 100 mg/d of aspirin for 2 months. Patients were th en treated with a combination of these two agents for the next 2 months. Ci profibrate decreased plasma concentrations of triglycerides (-29%) and very -low-density lipoprotein cholesterol (-27%) in monotherapy and a larger red uction was observed if ciprofibrate was added to the aspirin therapy: trigl ycerides (-39%), very-low-density lipoprotein cholesterol (-33%). total cho lesterol (-18%), low-density lipoprotein cholesterol (-17%), and increased high-density lipoprotein cholesterol (+36%). Ciprofibrate increased plasma levels of platelet-derived growth factor (PDGF) AB in both monotherapy pati ents (+162.9 pg/ml, +297%) and in aspirin-pretreated patients (+129.8 pg/ml , +134%); the increase of PDGF AB platelet store was significant only in as pirin-pretreated patients (+11.1 ng/ml, +51%). Aspirin in monotherapy did n ot modulate either plasma or platelet store of PDGF AB. Ciprofibrate did no t inhibit thromboxane B-2 synthesis in platelets. Aspirin did not influence plasma thromboxane B-2 concentration at all, whereas it decreased thrombox ane B-2 platelet production markedly in monotherapy (-85%) and in combinati on with ciprofibrate (-91%). Ciprofibrate increases PDGF AB content, which is amplified by aspirin pretreatment without correlation with its hypolipid emic action. The increase of PDGF production is suggested to participate in plaque stabilization.