Coagulation-induced shedding of platelet glycoprotein VI mediated by factor Xa.

This study evaluated shedding of the platelet collagen receptor, glycoprotein VI (GPVI) in human plasma. Collagen or other ligands induce metalloproteinase-mediated GPVI ectodomain shedding, generating approximately 55-kDa soluble GPVI (sGPVI) and approximately 10-kDa platelet-associated fragments. In the absence of GPVI ligands, coagulation of platelet-rich plasma from healthy persons induced GPVI shedding, independent of added tissue factor, but inhibitable by metalloproteinase inhibitor, GM6001.

Resolution of platelet function defects with imatinib therapy in a patient with chronic myeloid leukaemia in chronic phase.

Platelet function defects are frequently found in patients with chronic myeloid leukaemia. Major clinical bleeding, however, is a rare and infrequently reported complication. Platelet function abnormalities have also not been previously correlated with molecular monitoring of BCR-ABL in chronic myeloid leukaemia.