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]

Signs and symptoms

Symptoms are related to hypercoagulability, ^[9] usually presenting as venous thromboembolisms, arterial thrombosis, ^[9] myocardial infarction, angina, and stroke. ^[1]

Cause

The syndrome is believed to be hereditary. ^[11]

Diagnosis

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

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]}

References