Horm Metab Res 1997; 29(12): 631-635
DOI: 10.1055/s-2007-979115
Minisymposium Clinical Research

© Georg Thieme Verlag Stuttgart · New York

Platelet-Leukocyte-Cross-Talk in Diabetes Mellitus

D. Tschoepe1 , U. Rauch2 , B. Schwippert1
  • 1Diabetes Research Institute at the Heinrich Heine University of Duesseldorf, Cellular Haemostasis and Clinical Angiology Group, Duesseldorf, Germany
  • 2FU Berlin, Klinikum Benjamin Franklin, Dpt. f. Cardiology, Pulmonology and Angiology, Berlin, Germany
Further Information

Publication History

1997

1997

Publication Date:
23 April 2007 (online)

Abstract

The physiological meaning of platelets has been best documented for acute coronary syndromes where platelets act as “first responsive elements” triggering the final occlusive thrombus after plaque rupture has occurred. This situation is particularly relevant for patients with NIDDM-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 towards the hemostatic function of platelets. Meanwhile, a variety of particularly important platelet features have been identified: a) promotion of liquid phase coagulation; b) regulation of the local vascular tone; c) active modulation of tissue modeling at lesion sites; d) adhesion molecule-mediated communication with a variety of corpuscular blood (and non-blood cells). With emerging recognition of the latter role, the patho-physiological 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 populations of circulating platelets have been identified expressing activation dependent adhesion molecules such as activated α2β3 (CPIIbIIIa), lysosomal GP53, thrombospondin or, perhaps most importantly “P-selectin” (CD62 p). This suggests that these adhesion molecules among others can also mediate platelet-leukocyte interactions potentially 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 state outlining new pharmacological concepts for intervention.