title: Endogenous testosterone, fibrinolysis, and coronary heart disease risk in hyperlipidemic men.
abstract: To assess relationships of endogenous testosterone with fibrinolysis and coronary heart disease risk factors in 55 newly referred hyperlipidemic men, we studied the relationships of testosterone to basal fibrinolytic activity, lipids, lipoproteins, and apolipoproteins. Testosterone correlated positively with the major stimulator of fibrinolysis, tissue plasminogen activator activity (r = 0.30; p = 0.02) and correlated inversely with two independent coronary heart disease risk factors, plasminogen activator inhibitor activity, the major fibrinolysis inhibitor (r = -0.33; p = 0.01), and fibrinogen (r = -0.39; p = 0.004). Testosterone correlated inversely with plasma triglycerides (r = -0.33; p = 0.01). Stepwise multiple regression was done with fibrinolytic activities as the dependent variables, and age, Quetelet Index (relative ponderosity), apolipoprotein A-I, apolipoprotein B, triglyceride, testosterone, time of blood sampling, and lipoprotein (a) as explanatory variables. Testosterone was an inverse, independent predictor of fibrinogen (p = 0.002); 53% of the variance of fibrinogen could be accounted for by age and triglyceride level (positive; p = 0.001, p = 0.01), and by apolipoprotein A-I and testosterone (negative; p = 0.02, p = 0.002). Testosterone was an independent inverse predictor of tissue plasminogen activator antigen (p = 0.0008), with tissue plasminogen activator antigen correlating inversely with tissue plasminogen activator activity. Quetelet index and apolipoprotein B were independent negative predictors of tissue plasminogen activator activity (p = 0.02, p = 0.03); Quetelet index and triglycerides were independent positive predictors of plasminogen activator inhibitor activity (p = .0001, p = .0001) and alpha 2-antiplasmin (p = 0.0003, p = 0.009).(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Pathology, University of Cincinnati College of Medicine.
authors.forename: C J
authors.initials: CJ
authors.lastname: Glueck
authors.forename: H I
authors.initials: HI
authors.lastname: Glueck
authors.forename: D
authors.initials: D
authors.lastname: Stroop
authors.forename: J
authors.initials: J
authors.lastname: Speirs
authors.forename: T
authors.initials: T
authors.lastname: Hamer
authors.forename: T
authors.initials: T
authors.lastname: Tracy
mesh_terms: D016632:Apolipoprotein A-I / Q000032:analysis; D001055:Apolipoproteins B / Q000032:analysis; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000453:epidemiology*; D005340:Fibrinogen / Q000032:analysis; D005342:Fibrinolysis; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood*; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D008875:Middle Aged; D010958:Plasminogen / Q000032:analysis; D015849:Plasminogen Inactivators / Q000097:blood; D012307:Risk Factors; D013739:Testosterone / Q000097:blood*; D010959:Tissue Plasminogen Activator / Q000097:blood; D014280:Triglycerides / Q000097:blood; D000979:alpha-2-Antiplasmin / Q000032:analysis
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D017270:Lipoprotein(a); D015849:Plasminogen Inactivators; D014280:Triglycerides; D000979:alpha-2-Antiplasmin; D013739:Testosterone; D005340:Fibrinogen; D010958:Plasminogen; D010959:Tissue Plasminogen Activator