Abstract
Sticky platelet syndrome (SPS) is a thrombophilic thrombocytopathy with familial occurrence
and autosomal dominant trait, characterized by an increased in vitro platelet aggregation
in response to low concentrations of adenosine diphosphate (ADP) and/or epinephrine
(EPI). According to aggregation pattern, three types of the syndrome can be identified
(hyperresponse after both reagents, Type I; EPI alone, Type II; ADP alone, Type III).
Clinically, the syndrome is associated with both venous and arterial thrombosis. In
pregnant women, complications such as fetal growth retardation and fetal loss have
been reported. The first thrombotic event usually occurs before 40 years of age and
without prominent acquired risk factors. Antiplatelet drugs generally represent adequate
treatment. The use of other antithrombotics is usually ineffective and may result
in the recurrence of thrombosis. In most patients, low doses of antiplatelet drugs
(acetylsalicylic acid, 80–100 mg/d) lead to normalization of hyperaggregability. Combination
of SPS with other thrombophilic disorders has been described. Despite several studies
investigating platelet glycoproteins' role in platelets' activation and aggregation,
the precise defect responsible for the syndrome remains unknown. The aim of this review
is to summarize authors' own experience about SPS and the clinical data indexed in
selected databases of medical literature (PubMed and Scopus).
Keywords
sticky platelet syndrome - platelet hyperaggregability - thrombophilia - platelet
disorders
