Soluble P-selectin as a marker of in vivo platelet activation

• Published in: Clinica chimica acta Vol. 399; no. 1; pp. 88 - 91
• Main Authors: Ferroni, Patrizia, Martini, Francesca, Riondino, Silvia, La Farina, Francesca, Magnapera, Agesilao, Ciatti, Filippo, Guadagni, Fiorella
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 2009
• Subjects: Antiplatelet drugs; Aspirin - therapeutic use; Biomarkers - blood; Cardiovascular Diseases - drug therapy; Female; Humans; Male; Middle Aged; P-Selectin - blood; Platelet Activation - drug effects; Platelet Activation - physiology; Platelet aggregation; Platelet Aggregation Inhibitors - therapeutic use; Risk Factors; Solubility; Soluble P-selectin; Time Factors; Soluble P-selectin; Antiplatelet drugs; Platelet aggregation
• ISSN: 0009-8981; 1873-3492
• DOI: 10.1016/j.cca.2008.09.018

Platelets are the major source of circulating sP-selectin. Elevated levels of this protein have been found in many atherothrombotic disorders. Thus, we investigated whether sP-selectin dosage might reflect platelet function in patients with risk factors for or with established cardiovascular diseases and whether its levels can be modulated by aspirin therapy. Plasma sP-selectin levels and light transmission platelet aggregometry (LTA) were analyzed in 152 outpatients. The effects of a 6-month aspirin therapeutic course on sP-selectin levels and LTA in 51 consecutive patients have been also investigated. Significant correlations were observed between sP-selectin and Mx% LTA in response to epinephrine ( p = 0.022) and arachidonic acid ( p = 0.006), or between sP-selectin and collagen lag-phase ( p = 0.016). Multiple regression analysis showed that the only predictors of sP-selectin levels were platelet number ( p < 0.001) and collagen-induced lag-phase ( p < 0.01). Aspirin-treated patients showed a significant reduction of sP-selectin levels by 13% ( p = 0.021) which significantly correlated with collagen-induced lag-phase ( p = 0.005). sP-selectin dosage could be proposed as a reliable marker of platelet activation in patients with major atherosclerotic risk factors either in the absence of clinically overt disease, and might represent a valid tool to asses in vivo platelet behavior.