Aspirin cures erythromelalgia and cerebrovascular disturbances in JAK2-thrombocythemia through platelet-cycloxygenase inhibition

Figure 15 Shear induced platelet activation of constitutively JAK2^V617F hypersensitive sticky platelet with increased CD62p and CD 63 expression) in thrombocythemra vera of JAK2^V617F-positive ET and PV patients is the cause of a broad spectrum of platelet-mediated arteriolar inflammatory and thrombotic manifestations of erythromelalgia, digital ischemic complications, superficial thrombophlebitis, MIAs, TIAs, adrenal microvascular thrombosis and TIAs or even stroke and acute coronary syndrome in particular when thrombocythemia[79,80] is associated with increased activated leucocytes and erythrocyte count of polycythemia vera (increased cellular blood viscosity (Figure 12). In this process of in vivo platelet activation and secretion, reversible VWF-platelet aggregates activate endothelial cells to secrete thrombomoduline (TM) and sVCAM[79,80], whereas secreted PDGM accounts for the fibromuscular intimal proliferation (inset left) followed by occlusion of arterioles by VWF-rich platelet thrombi (inset right). After reversible aggration the platelets recirculate as exhausted platelets with secondary storage pool deficiency and impaired platelet functional defects. The platelet - Von Willebrand factor (VWF) interactions leads to proteolysis of large vWF multimers at increasing platelet counts from below to above 1000 × 10⁹/L (Figure 13 right and Figure 16 peak 1 and 4).