Key result
Hyperglycemia significantly decreased protein C antigen and activity in insulin-dependent diabetic patients compared to matched controls, which was restored to normal by insulin-induced euglycemia.
Why the study?
Does hyperglycemia reduce Protein C levels and activity in patients with insulin-dependent diabetes?
Observational (n=30)
Does hyperglycemia reduce Protein C levels and activity in patients with insulin-dependent diabetes?
Hyperglycemia acutely reduces Protein C levels in insulin-dependent diabetes, suggesting a mechanism for increased thrombotic risk that can be mitigated by strict glycemic control.
Answers are grounded in this paper and cite their sources.
Hyperglycemia may reduce protein C in insulin-dependent diabetes; leaves open whether euglycemia mitigates thrombotic risk.
In 30 insulin-dependent diabetic patients protein C (PC) antigen and PC activity were significantly lower than those of matched control healthy subjects. An inverse correlation between fasting plasma glucose and both PC concentration and activity was present in diabetics, while a direct correlation between PC concentration and PC activity was observed. Induced hyperglycemia in diabetic and normal subjects was able to decrease both PC antigen levels and PC activity, and heparin reversed in part this effect. In diabetic patients euglycemia obtained by insulin infusion restored to normal the depressed PC levels. Heparin did not alter both the basal PC concentration and activity in healthy controls. These data stress the major role of hyperglycemia in determining PC decrease in diabetics, and suggest that PC reduction is probably associated to hyperglycemia-enhanced thrombin formation.
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Ceriello et al. (1990) conducted an observational in Insulin-Dependent Diabetes (n=30). Hyperglycemia vs. Euglycemia and healthy controls was evaluated on Protein C (PC) antigen and PC activity. Hyperglycemia significantly decreased protein C antigen and activity in insulin-dependent diabetic patients compared to matched controls, which was restored to normal by insulin-induced euglycemia.
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