Progress in the Understanding of Sticky Platelet Syndrome

Abstract

The knowledge on the etiology of thrombosis has increased tremendously over the past decades. Nevertheless, Virchow triad is still traditionally invoked to explain mechanisms leading to thrombosis, alleging concerted roles for abnormalities in blood composition, vessel wall components, and blood flow in the development of arterial and venous thrombosis. Recent decades have been focused primarily on describing abnormalities in blood composition, including defects of coagulation proteins and platelets. Although defects of coagulation factors are relatively well-described in the literature, prothrombotic platelet disorders are still less understood. One such defect, the Wien-Penzing defect was first described in 1991. Another platelet defect is sticky platelet syndrome (SPS). In this article, we review information about SPS, and we propose a new definition and standardization of diagnostic criteria. We also attempt to explain the causes and consequences of this condition.

Primary Thrombophilia in Mexico XIII: Localization of the Thrombotic Events in Mexican Mestizos With the Sticky Platelet Syndrome

“…7,10 There is limited data about the prevalence of this entity in the whole population; some data indicate that up to 15% of the general population displays the phenotype of the SPS, whereas more than 60% of persons with a clinical marker of thrombophilia are found to display the SPS phenotype. 7,11,14–19 Other authors have found that the SPS is identified in approximately 21% of unexplained arterial thrombotic episodes and 13% of unexplained venous thromboembolism 3,13 ; one of the possible reasons to explain these differences is the way to define the SPS; we and others 1,7,11,18,19 have elected the criteria proposed by Mammen and Bick 12,14,20–24 aiming to produce comparable results, but not all authors have employed the same criterion. 12…”

“…1,2 Sticky platelet syndrome is an autosomal dominant disease with qualitative platelet alterations and familial occurrence characterized by platelet hyperreactivity with increased platelet aggregability in response to low concentrations of platelet agonists: epinephrine (EPI), adenosine diphosphate (ADP), or both. 1–4 The diagnosis is based on platelet aggregometry, and according to this study, there are 3 types 5 :Type I: Hyperaggregation after EPI and ADP.Type II: Hyperaggregation after EPI alone.Type III: Hyperaggregation after ADP alone.…”

“…1,4–7 The clinical manifestations involve venous and arterial thrombosis, fetal loss, and fetal growth retardation. 1,3,6,8,9 In this study, we analyze the localization of both the arterial and venous thrombotic events in a cohort of Mexican mestizo patients with the SPS.…”

Glycoprotein VI Gene Variants Affect Pregnancy Loss in Patients With Platelet Hyperaggregability

“…5,6 Patients with SPS present with arterial and/or venous thrombosis and fetal loss. 5–12 Although the first patient with SPS was reported in 1983, 13 many physicians remain unfamiliar with this platelet defect and do not consider SPS when screening for thrombophilic risk factors. The diagnosis and classification of SPS relies on platelet aggregometry tests employing appropriate dilutions of 2 platelet aggregation inducers: ADP and EPI.…”

“…The diagnosis and classification of SPS relies on platelet aggregometry tests employing appropriate dilutions of 2 platelet aggregation inducers: ADP and EPI. 5,6,12…”