Vaskulárna medicína 2/2016

Sticky platelet syndrome

Platelet hyperaggregability after low concentrations of platelet agonists adenosine diphosphate (ADP) and/or epinephrine (EPI), referred to as sticky platelet syndrome (SPS), was first described by Holliday at the Ninth Conference on Stroke and Cerebral Circulation in Arizona in 1983. Clinical symptoms of SPS include unexplained arterial and venous thrombotic events, commonly occurring in stressful situations, and frequently recurrent under oral anticoagulant therapy. Furthermore, there is evidence for a causal relation between SPS and abortion. SPS is classified as type I (hyperaggregation after both ADP and EPI), type II (hyperaggregation after EPI alone) and type III (hyperaggregation after ADP alone). SPS type II seems to be the most common form. SPS is probably a hereditary, autosomal dominant thrombophilia, although the exact genetic cause has not as yet been identified. It has been suggested that defects of the platelet membrane glycoproteins or intracellular signal pathways involved in platelet activation and aggregation are responsible for the disorder.

Keywords: fetal loss syndrome, platelet hyperaggregability, single nucleotide polymorphism, sticky platelet syndrome, thrombosis