PLATELET-LEUKOCYTE-CROSS-TALK IN DIABETES-MELLITUS

The physiological meaning of platelets has been best documented for ac ute coronary syndromes where platelets act as ''first responsive eleme nts'' triggering the final occlusive thrombus after plaque rupture has occurred. This situation is particularly relevant for patients with N IDDM-type diabetes regularly showing complicated plaque architecture. Predictive power for acute ischemic events e.g. following angioplasty has been proven, and this has dominated the attention exclusively towa rds the hemostatic function of platelets. Meanwhile, a variety of part icularly important platelet features have been identified: a) promotio n of liquid phase coagulation; b) regulation of the local vascular ton e; c) active modulation of tissue modeling at lesion sites; d) adhesio n molecule-mediated communication with a variety of corpuscular blood (and non-blood cells). With emerging recognition of the latter role, t he pathophysiological scope of platelets exceeds the well-established role as microemboli, local atherosclerosis amplifiers and triggers of gross thrombosis. In diabetes mellitus of either type, increased popul ations of circulating platelets have been identified expressing activa tion dependent adhesion molecules such as activated alpha(2) beta(3), (GPIIbIIIa), lysosomal GP53, thrombospondin or, perhaps most important ly ''P-selectin'' (CD62 p). This suggests that these adhesion molecule s among others can also mediate platelet-leukocyte interactions potent ially resulting in inflammatory tissue damaging processes in addition to the immanent tendency towards (micro-)thrombosis. This review works out a more general view on the meaning of platelet activation beyond hemostaseology and updates the actual knowledge of platelet-leukocyte communication checkpoints with particular reference to the diabetic st ate outlining new pharmacological concepts for intervention.