Key result
Diabetes induces a procoagulant state through platelet-vascular activation, increased fibrinogen, and hypofibrinolysis, suggesting a role for targeted antiplatelet and profibrinolytic therapies.
This review highlights the procoagulant mechanisms in diabetes and suggests that specific antiplatelet and profibrinolytic therapies may be relevant for reducing morbidity and mortality.
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Hypothesis-generating for targeted therapies in diabetes; prospective trials needed before any practice change.
Major known effects of the metabolic derangements of diabetes in haemostasis are induction of platelet-vascular activation by hyperglycaemia, the increase in fibrinogen, modification of fibrin substrate by glucose and hypofibrinolysis related to insulin resistance. The platelet effects are specifically expressed during high shear stress and may be relevant in particular for developing of micro-angiopathy. Hypofibrinolysis, increased fibrinogen and modifications of fibrin may aggravate microthrombosis and organ damage and contribute to precipitation of coronary and cerebral infarction. In addition to specific anti-diabetic medication to reduce the haemostatic effects, specific antiplatelet and profibrinolytic treatments may be relevant for reducing further the morbidity and mortality in diabetics for both micro- and macro-angiopathy.
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Kluft et al. (2002) conducted a review in Diabetes. Diabetes was evaluated. Diabetes induces a procoagulant state through platelet-vascular activation, increased fibrinogen, and hypofibrinolysis, suggesting a role for targeted antiplatelet and profibrinolytic therapies.
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