title: Hypercoagulability and high lipoprotein(a) levels in patients with type II diabetes mellitus.
abstract: Diabetes mellitus is associated with disturbances in hemostasis that could contribute to the development of diabetic vascular disease. We investigated the changes in parameters of blood coagulation and the fibrinolytic system and in plasma levels of lipoprotein(a)(Lp(a)) in 124 patients with type II diabetes mellitus and 44 healthy control subjects matched for age and body mass index (BMI) to determine whether hemostatic disturbances may lead to increased cardiovascular mortality. Median levels of fibrinogen (P < 0.0001), thrombin-antithrombin III complex (TAT) (P < 0.005), and plasminogen activator inhibitor-1 (PAI-1) activity (P < 0.05) in plasma were significantly elevated in diabetic patients compared with controls. The median concentration of Lp(a) was significantly higher in diabetic patients than in normal controls (18.2 vs. 12.6 mg/dl. P < 0.0005). Lp(a) levels tended to be elevated in patients with a prolonged history of diabetes. There was no evidence that Lp(a) levels were affected by metabolic control or by type of treatment. Twenty-two diabetics with coronary heart disease (CHD) had significantly higher levels of fibrinogen (P < 0.05), TAT (P < 0.05), and Lp(a) (24.7 vs. 13.7 mg/dl, P < 0.01) than the 51 patients without diabetic angiopathy. Our data indicate that impaired hemostatic balance in diabetes may cause hypercoagulability and may thus contribute to the increased cardiovascular mortality in diabetes.
authors.affiliation: Department of Laboratory Medicine, School of Medicine, Kanazawa University, Japan.
authors.forename: E
authors.initials: E
authors.lastname: Morishita
authors.forename: H
authors.initials: H
authors.lastname: Asakura
authors.forename: H
authors.initials: H
authors.lastname: Jokaji
authors.forename: M
authors.initials: M
authors.lastname: Saito
authors.forename: C
authors.initials: C
authors.lastname: Uotani
authors.forename: I
authors.initials: I
authors.lastname: Kumabashiri
authors.forename: M
authors.initials: M
authors.lastname: Yamazaki
authors.forename: K
authors.initials: K
authors.lastname: Aoshima
authors.forename: T
authors.initials: T
authors.lastname: Hashimoto
authors.forename: T
authors.initials: T
authors.lastname: Matsuda
mesh_terms: D000368:Aged; D000990:Antithrombin III / Q000032:analysis; D001778:Blood Coagulation Disorders / Q000097:blood* / Q000209:etiology; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000209:etiology / Q000401:mortality; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications; D003925:Diabetic Angiopathies / Q000097:blood / Q000150:complications; D004198:Disease Susceptibility; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D005342:Fibrinolysis; D006487:Hemostasis; D006801:Humans; D007564:Japan / Q000453:epidemiology; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000032:analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D012307:Risk Factors; D010959:Tissue Plasminogen Activator / Q000032:analysis; D000979:alpha-2-Antiplasmin / Q000032:analysis
chemical_list: D017270:Lipoprotein(a); D017395:Plasminogen Activator Inhibitor 1; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; D000990:Antithrombin III; D005340:Fibrinogen; D010447:Peptide Hydrolases; D010959:Tissue Plasminogen Activator