Platelet activation in patients with the Raynaud phenomenon

Background: The Raynaud phenomenon (RP) is an exaggerated and reversible vasospasm of small arteries triggered by cold or emotional stress. Primary RP (PRP) term is used when the underlying condition is unknown. An altered regulation in vascular tone and/or release of soluble mediators from activated platelets plays a role in PRP through an increased oxidative stress. We assessed platelet activation and oxidative stress in patients with PRP by measuring platelet PAC-1, an index of glycoprotein (Gp) IIb/IIIa receptor activation, thromboxane A2 (TXA2), an index of platelet activation and 8-epi-prostaglandin F2 alpha (8-epi-PGF2 alpha), a marker of endogenous in vivo peroxidation. Methods: Eighteen asymptomatic patients with PRP (age 41.37 +/- 16.94 years; 17 women, 1 man) and 18 healthy subjects (age of 35.11 +/- 13.16 years; 16 women, 2 men) were studied. PAC-1 was analysed by flow cytometry while circulating TXB2, a stable metabolite of TXA2 and 8-epi-PGF2 alpha levels were assessed by ELISA kit. Results: Our results show a significant platelet activation in PRP patients as indicated by increased PAC-1 expression (65.29 +/- 15.24%; P < 0.001), TXB2 (1477.83 +/- 454.04 pg/mL; P= 0.003) and 8-epi-PGF2 alpha circulating levels (42.50 +/- 14.14 ng/mL; P < 0.001). An inverse correlation between the degree of PAC-1 expression and TXB2 levels (r=-0.527; P= 0.02) was also found in PRP patients, suggesting that downregulation of GpIIb/IIIa receptor expression may occur during thrombocytopoiesis, as a consequence of the chronic exposure to increased TXB2 concentration. Conclusions: Our study for the first time shows a marked activation of GpIIb/IIIa receptor in asymptomatic patients with PRP and supports antiplatelet therapy in PRP patients.