Sepsis and related syndromes account for a high morbidity and mortality cau
sed by the development of multiorgan failure. Pathogenesis of sepsis is com
plex, involving humoral as well as cellular factors. Since the role of plat
elets is still undefined in this concern, we investigated CD63, CD62P, CD36
, and CD31 expression on platelets of patients in septic shock (n=18) using
a flow cytometric assay in whole blood. Samples were drawn within 24 hours
of onset. We found thrombocytopenia accompanied by a significantly higher
expression of CD63, CD62P, and CD31 and a significant downregulation of CD3
6 in comparison to healthy volunteers (n=18), Changes in CD63 and CD62P exp
ression indicates platelet activation. Because CD62P, CD36, and CD31 mediat
e interaction of platelets with leukocytes, subendothelial matrix and proba
bly endothelial cells as well as platelet adhesion/aggregation, our finding
s suggest an involvement of platelets in leukocyte/endothelial cell interac
tion in septic shock. We suspect that thrombocytopenia is not due to bone m
arrow depression, but rather is due to consumption of highly activated plat
elets in the microcirculation. We feel that our observations may offer a ra
tionale for potentially beneficial effects of antiplatelet therapy in sepsi
s; however, further studies have to evaluate its beneficial impact as well
as its potential risk for bleeding complications. (C) 1999 Elsevier Science
Ltd. All rights reserved.