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

Figure 1 Arachidonic acid-induced human platelet aggregation and prostaglandin formation (Silver et al[3] 1973). Arachidonate acid (AA), 0.5 mmol/L induces a normal platelet aggregation curve (A). AA induces secretion of large amounts of prostaglandins after platelet aggregation, but little or no prostaglandins secretion occur after platelet aggregation induced by thrombin, collagen and epinephrin (B). AA, thrombin, collagen, epinephrine and ADP induce aggregation and secretion of rather equal amounts radioactivity from PRP preincubated with ¹⁴C-serotonin or ¹⁴C-adenine (C). These findings implicate that spontaneous in vivo shear induced aggregation of sticky JAK2 mutated platelet in the endarteriolar circulation is associated with high prostaglandin levels as the cause of the inflammatory pain and signs (redness, warmth and congestion) of erythromelalgia in JAK2-mutated thrombocythemia (Michiels et al[53] in 1985 and Michiels[80] in 2017).