Induction and possible role of fibrinolysis in diabetes mellitus.
This article reviews the evidence supporting a relationship between an enhanced tissue injury, increased fibrin formation, defective fibrinolysis, and the evolution of the complications of late diabetic disease. Particular attention is drawn to the role of a defective endothelial cell mediated fibrinolysis with respect to increased fibrin formation and a delayed tissue repair in diabetic patients. Reviewed are studies that indicate that it is possible in patients with diabetes by means of sulfonylurea compounds to increase endothelial cell-produced t-PA without affecting PAI-1. It is advocated that potent compounds should be searched for, with the capability to modify the hemostatic process of the diabetic endothelial cell in order to express more fibrinolytic activity independent of the patient's metabolic state in an attempt to delay the complications of late diabetes.
Gram
J
J
Department of Clinical Chemistry, Ribe County Hospital, Esbjerg, Denmark.
Jespersen
J
J
D003920:Diabetes Mellitus / Q000378:metabolism / Q000503:physiopathology*; D003925:Diabetic Angiopathies / Q000378:metabolism; D005337:Fibrin / Q000096:biosynthesis; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans
D005337:Fibrin