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Platelets in diabetes: the role in the hemostatic regulation in atherosclerosis
D Tschoepe1, P Roesen, B Schwippert
1Cellular Hemostasis Group, Diabetes Research Institute, Heinrich Heine University, Duesseldorf, Germany.
Insights
Diabetic patients experience increased vascular complications due to activated platelets. Research shows larger platelets with enhanced function contribute to this heightened thrombotic risk in diabetes mellitus.
Area of Science:
- Cardiovascular Medicine
- Diabetology
- Hematology
Background:
- Vascular diseases are the primary cause of mortality in diabetic patients.
- Diabetes mellitus leads to specific microcirculatory disturbances and accelerated macroangiopathy.
- A prethrombotic state in diabetics increases the risk of thrombotic events and acute blood flow interruption.
Purpose of the Study:
- To investigate the role of platelet activation in diabetic vascular complications.
- To identify the mechanisms behind the increased functional properties of platelets in diabetes mellitus.
Main Methods:
- Utilized flow cytometry (Duesseldorf III method) to test activation markers (CD62, CD63, thrombospondin).
- Analyzed platelet size, thromboxane formation capacity, and glycoprotein receptors (GPIb, GPIIb/IIIa).
Main Results:
- Diabetic platelets exhibit enhanced functional properties.
- Larger platelets with increased thromboxane formation and more glycoprotein receptors are released.
- Predominantly large platelets circulate in an activated state in diabetes mellitus.
Conclusions:
- The megakaryocyte-platelet system is activated in diabetes mellitus.
- Activated, larger platelets contribute significantly to the thrombotic diathesis in diabetics.
- Understanding these platelet alterations is crucial for managing diabetic vascular complications.
Abstract:
Vascular diseases and related complications still represent the main cause of death in diabetic patients. Neuropathy, nephropathy, retinopathy, and disturbed nutritive tissue perfusion may result from reduced capillary microcirculation. These disturbances are diabetes specific. Macroangiopathy does not differ structurally from atherosclerotic lesions of nondiabetic subjects, but leads to accelerated cerebral, coronary, and peripheral artery disease. Occurrence of life-terminating thrombotic events, which are superimposed on those vascular lesions, are increased. Thus, morbidity and mortality of diabetics depend mainly on vascular complications. Normal blood flow is a prerequisite of adequate organ perfusion and results from vasomotion, plasma components, corpuscular blood elements, vascular architecture, and the undisturbed interaction of these components at the endothelial interface. Functional thromboresistance of the endothelial layer is reduced in the diabetic state. Increased intravascular thrombin generation, reduced fibrinolytic potential, and hyperactive platelets lead to a prethrombotic state. This thrombotic diathesis increases the permanent danger of acute flow interruption. Activated platelets operate by three mechanisms: (1) Microembolization of the capillaries; (2) local progression of preexisting vascular lesions by secretion of constrictive, mitogenic, and oxidative substances; (3) trigger of the prognosis-limiting arterial thrombotic event. We were able to show that the increased functional properties of diabetic platelets result from the primary release of larger platelets with enhanced thromboxane formation capacity and increased numbers of functional glycoprotein receptors GPIb and GPIIb/IIIa, which are synthesized in the megakaryocytes. The megakaryocyte-platelet system is turned on in diabetes mellitus. It could be demonstrated with the Duesseldorf III method of flow cytometric activation marker testing (CD62, CD63, thrombospondin) that predominantly large platelets circulate in an activated state in diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)