Coagulation and fibrinolytic system impairment in insulin dependent diabetes mellitus.
Selected coagulation and fibrinolytic parameters were assessed in 40 insulin dependent diabetes mellitus patients with varying degrees of metabolic control; 30 healthy subjects matched for age and sex formed the control group. Activated Partial Thromboplastin Time, Prothrombin Time, Fibrinogen, Factor VII, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, Plasminogen Activator Inhibitor-1, tissue-Plasminogen Activator were functionally evaluated. Antigenic levels of tissue-Plasminogen Activator, Thrombin-Antithrombin complexes and fibrinolytic specific product B beta 15-42 were also determined. Compared to the control group diabetic patients displayed significantly higher levels of Fibrinogen (p < 0.01), Factor VII (p < 0.01), Thrombin-Antithrombin complexes (p < 0.01) and Plasminogen Activator Inhibitor-1 activity (p < 0.01). Regardless of the normal level of the tissue-Plasminogen Activator-related antigen, diabetic patients had tissue-Plasminogen Activator activity lower than the control group (p < 0.05). Coagulation Factor VII and Thrombin-Antithrombin complexes were increased only in the patients with poor metabolic control (p < 0.01). Activated Partial Thromboplastin Time, Prothrombin Time, Antithrombin III, Protein C, Plasminogen, alpha 2-Plasmin Inhibitor, B beta 15-42 fibrin peptide were found to be in the normal range. Fibrinogen correlated positively with fasting blood glucose (p < 0.05) and Thrombin-Antithrombin complexes with glycosylated haemoglobin (p < 0.05), whereas Factor VII was positively correlated with glycemia (p < 0.01) and glycosylated haemoglobin (p < 0.05). Higher levels of Fibrinogen were found in patients affected by nephropathy (p < 0.005) or neuropathy (p < 0.05). These results demonstrate an impairment of the haemostatic balance in diabetic patients, that is a possible hypercoagulable state, which represents an important factor in the pathogenesis of atherosclerotic complications.
Carmassi
F
F
Institute of 2nd Medical Clinic, University of Pisa, Italy.
Morale
M
M
Puccetti
R
R
De Negri
F
F
Monzani
F
F
Navalesi
R
R
Mariani
G
G
D000328:Adult; D000595:Amino Acid Sequence; D000990:Antithrombin III / Q000378:metabolism; D001777:Blood Coagulation / Q000502:physiology*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood*; D003925:Diabetic Angiopathies / Q000209:etiology; D005167:Factor VII / Q000378:metabolism; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D008297:Male; D008969:Molecular Sequence Data; D009842:Oligopeptides / Q000737:chemistry; D010447:Peptide Hydrolases / Q000378:metabolism; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D010960:Plasminogen Activators / Q000097:blood; D013379:Substrate Specificity
D009842:Oligopeptides; D017395:Plasminogen Activator Inhibitor 1; C046193:antithrombin III-protease complex; D000990:Antithrombin III; D005167:Factor VII; D005340:Fibrinogen; D010447:Peptide Hydrolases; D010960:Plasminogen Activators