Sticky platelet syndrome is a term used by some^[1][2][3][4] to describe a disorder of platelet function.^[5]

It was first described by Mammen in 1983.^[6]

It is inherited in an autosomal dominant pattern.^[7] It has not been associated with a specific gene, and it is not recognized as an entity in OMIM.

Among researchers using the term, it has been described as a coagulation disorder that can present in conjunction with protein S deficiency and Factor V Leiden.^[8] It is not currently known if sticky platelet syndrome is a distinct condition, or if it represents part of the presentation of a more well characterized coagulation disorder.

SPS is diagnosed by demonstrating platelet hyperaggregability. In a lab test called aggregometry platelet stickyness is stimulated with epinephrine (EPI) and/or adenosine diphosphate (ADP).^[9] This test is not possible for patients being treated with acetylsalicylic acid until that substance has sufficiently cleared from their system.

Those diagnosed are usually treated with taking a low dose (80–100 mg) Aspirin a day.^[10] Anticoagulants (e.g. Warfarin, Coumadin) or clopidogrel (Plavix) are often additionally prescribed following formation of a medically significant clot. Thrombelastography is more commonly being used to diagnose hypercoagulability and monitor anti-platelet therapy.

Critics of the diagnosis complain that case evidence is spotty and lacking controlled clinical studies.^[11]