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Abstract Protein C is a vitamen K dependent protease which circulates in plasma as a zymogen and is rapidly activated in vivo by’ throrubin (Vehar & Davie, 1980; Comp & Esmon 198 4). Activated protein C inactivates factors V andVIII and therefore it is a powerfull anticoagulant (Harlar et al, 1982). Endothelial cells markedly accelrate the activation of protein C by thrombin (Owen and Esmon, 1981 ; Esmon et iii, 1982 aj.Unlike the antith— rombin in endothelial cell interaction, the acceleration of protein C by endothelial cells is not blocked by platelet factor IV (Owen & Esmon, 1981). Th activity of protein C is further enhanced by another vitamen K dependent protein (proteins ) which binds protein C (Walker, 1981). Protein C must play3 an important role in vivo because heterozygous deficiency of protein C is associated with congenital thrombotic disease (Griffin et al,. 1981) and deficiency of an inhibition of protein C causes combined factor V and VIII deficiency (Marlar et al, 1981). Abnormalities in the plasmatic coagulant• system have been repeteadly described in patients with diabetes mellitus and have been linked to vascular disease common in those patients. A reduction in the amount of immunologically detectable factor VIII related protein C (Betn et al l98O Vukovich and Schernthafler, 1984) or factor VIII coagulant antigen (Christeet al, 1984) as well as an increase in fibrinolysis has been reported in diabetes mellitus. - These haenostatic abnormalities may be caused by increased activation of protein C in the circulation resulting in an enhanced clearance from the blood plasma This study aims at 1. Estimation of plasma protein C level in diabetics (IDDs and NIDDS) and its possible role in vascular complications in these patients. 2. Finding a correlation between plasma protein C level, blood glucose level and duration of diabetic state. |