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Sticky platelet syndrome (SPS) is a disorder with familial occurrence and autosomal dominant trait characterized by platelet hyperaggregability in response to a low concentration of adenosine diphosphate (ADP) and/or epinephrine (EPI). The etiology of SPS may be associated with platelet microRNAs (miRNAs), which are considered as potential biomarkers of platelet function and antiplatelet therapy. We were monitoring the expression of platelet miRNAs in patients with laboratory diagnosed SPS and healthy controls. We have found a statistically significant increased expression of both miR-423-5p and miR-338-3p as well as a statistically significant decreased expression of miR-425-5p between the group of patients with diagnosed SPS type II and the group of healthy controls, which seems to be an interesting issue for a further research. [ABSTRACT FROM AUTHOR]

The knowledge on the etiology of thrombosis has increased tremendously over the past decades. Nevertheless, Virchow triad is still traditionally invoked to explain mechanisms leading to thrombosis, alleging concerted roles for abnormalities in blood composition, vessel wall components, and blood flow in the development of arterial and venous thrombosis. Recent decades have been focused primarily on describing abnormalities in blood composition, including defects of coagulation proteins and platelets. Although defects of coagulation factors are relatively well-described in the literature, prothrombotic platelet disorders are still less understood. One such defect, the Wien-Penzing defect was first described in 1991. Another platelet defect is sticky platelet syndrome (SPS). In this article, we review information about SPS, and we propose a new definition and standardization of diagnostic criteria. We also attempt to explain the causes and consequences of this condition. [ABSTRACT FROM AUTHOR]