Sticky platelet syndrome | |
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Specialty | Hematology |
Sticky platelet syndrome (SPS) is a heritable disorder of platelet function in which platelet hyperaggregation leads to hypercoagulability.[1][2][3][4][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.
It 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 has not been widely studied[9] and is not widely known.[10]
Symptoms are related to hypercoagulability,[9] usually presenting as venous thromboembolisms, arterial thrombosis,[9] myocardial infarction, angina, and stroke.[1]
The syndrome is believed to be hereditary.[11]
SPS is diagnosed by demonstrating platelet hyperaggregability. In a lab test called aggregometry, platelet stickiness is stimulated with epinephrine (EPI) and/or adenosine diphosphate (ADP).[12] This test is not possible for patients being treated with acetylsalicylic acid until that substance has sufficiently cleared from their system.[citation needed]
Treatment usually consists of a daily low dose (80–100 mg) of aspirin.[13] Anticoagulants (e.g. warfarin) or antiplatelets (clopidogrel) 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.[citation needed]