Coagulation and fibrinolytic systems in type I diabetes: effects of venous occlusion and insulin-induced hypoglycaemia.
1. The effects of venous occlusion on the coagulation and fibrinolytic systems were investigated in six patients with type 1 (insulin-dependent) diabetes and 11 age- and sex-matched non-diabetic control subjects. The coagulation parameters (fibrinogen, prothrombin time, partial thromboplastin time with kaolin, von Willebrand factor antigen) did not differ between patients and control subjects either before or after 20 min of venous occlusion. No rise was observed in von Willebrand factor antigen after venous occlusion in either group. 2. In the diabetic patients, chronic activation of the fibrinolytic system was found at baseline, which was indicated by a shortened euglobulin lysis time (P < 0.01), increased tissue plasminogen activator activity (P < 0.05) and decreased plasminogen activator inhibitor type 1 antigen level (P < 0.05), when compared with control subjects. In both groups venous occlusion resulted in significant increments in all measurements, except plasminogen activator inhibitor type 1 antigen level. The post-occlusion values did not differ between the two groups, except the plasminogen activator inhibitor type 1 antigen level, which remained significantly lower in the diabetic patients. The mean increments in each parameter did not differ between the two groups. 3. Coagulation and fibrinolysis were assessed in response to acute insulin-induced hypoglycaemia. Von Willebrand factor antigen levels increased significantly in both groups, with no difference in maximal increments. Significant activation of the fibrinolytic system occurred in response to hypoglycaemia, demonstrated by shortened euglobulin lysis time and increased fibrin plate lysis, tissue plasminogen activator antigen level and tissue plasminogen activator activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Department of Haematology, Royal Infirmary of Edinburgh, U.K.
I
I
Wieczorek
A C
AC
Pell
B
B
McIver
I R
IR
MacGregor
C A
CA
Ludlam
B M
BM
Frier
D000208:Acute Disease; D000328:Adult; D001132:Arm / Q000098:blood supply; D001324:Autoantigens / Q000032:analysis; D001777:Blood Coagulation / Q000502:physiology*; D003251:Constriction, Pathologic; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000276:immunology; D005260:Female; D005342:Fibrinolysis / Q000502:physiology; D006801:Humans; D007003:Hypoglycemia / Q000097:blood / Q000139:chemically induced; D007328:Insulin / Q000009:adverse effects; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000276:immunology; D014680:Veins
D001324:Autoantigens; D007328:Insulin; D017395:Plasminogen Activator Inhibitor 1