Diabetes mellitus: a hypercoagulable state

M E Carr1

  • 1Departments of Internal Medicine and Pathology, Medical College of Virginia, Virginia Commonwealth University, Box 980230, Richmond, VA 23298-0230, USA. mcarr@hsc.vcu.edu

Insights

Diabetes significantly increases thrombotic death risk, primarily from cardiovascular issues. This review explores how diabetes causes a hypercoagulable state, increasing clotting and reducing clot breakdown.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Endocrinology

Background:

  • Diabetes mellitus is a major risk factor for thrombotic events, with 80% of patients dying from thrombosis.
  • Cardiovascular complications account for 75% of these deaths, with cerebrovascular and peripheral vascular events comprising the remainder.
  • The vascular endothelium, crucial for preventing thrombosis, is impaired in diabetes, contributing to a prothrombotic state.

Purpose of the Study:

  • To review the evidence supporting diabetes as a hypercoagulable state.
  • To explore the roles of hyperglycemia and hyperinsulinemia in the development of this prothrombotic condition.

Main Methods:

  • Review of published literature on coagulation, fibrinolysis, and platelet function in diabetes.
  • Analysis of markers for coagulation activation, clotting factor levels, and anticoagulant protein levels.
  • Assessment of fibrinolytic system activity and platelet hyperactivity indicators.

Main Results:

  • Elevated markers of coagulation activation (e.g., prothrombin fragment 1+2, thrombin-antithrombin complexes).
  • Increased plasma levels of multiple clotting factors (fibrinogen, factors VII, VIII, XI, XII, kallikrein, von Willebrand factor) and decreased levels of anticoagulant protein C.
  • Inhibited fibrinolysis due to resistant clot structures and increased plasminogen activator inhibitor type 1 (PAI-1), alongside evidence of platelet hyperactivity.

Conclusions:

  • Diabetes is characterized by a hypercoagulable state, increasing the risk of thrombotic and cardiovascular events.
  • Endothelial dysfunction, coagulation activation, impaired fibrinolysis, and platelet hyperactivity are key contributors.
  • Hyperglycemia and hyperinsulinemia are implicated as potential drivers of these hemostatic abnormalities.

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