Sticky Platelet Syndrome: An Unusual Presentation of Arterial Ischemia

Bojalian, M.O.; Akingba, A. George; Andersen, Judith C.; Swerdlow, Paul; Bove, P; Brown, O. William; Rubin, J.R.

doi:10.1016/j.avsg.2009.12.005

Cited by 18 publications

(12 citation statements)

References 9 publications

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“…This condition increases the risk of acute thrombosis in different territories, such as myocardial infarction, ischemic optic neuropathy, recurrent venous thromboembolism, transient ischemic attacks and strokes, kidney graft infarction, arterial microemboli in the fingers, peripheral arterial occlusion, as well as recurrent strokes under anticoagulation therapy …”

Section: Discussionmentioning

confidence: 99%

Livedoid vasculopathy (LV) associated with sticky platelets syndrome type 3 (SPS type 3) and enhanced activity of plasminogen activator inhibitor (PAI‐1) anomalies

et al. 2013

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Section: Discussionmentioning

confidence: 99%

Livedoid vasculopathy (LV) associated with sticky platelets syndrome type 3 (SPS type 3) and enhanced activity of plasminogen activator inhibitor (PAI‐1) anomalies

et al. 2013

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“…The concomitant occurrence of SPS with other well-defined thrombophilias (elevated factor VIII, antiphospholipid syndrome, prothrombin G20201A, and hyperhomocysteinemia) were subsequently reported. 29,[33][34][35][36][37] In fact, as shown by Ruiz-Argüelles et al, most patients with SPS phenotype might display other thrombophilic conditions, both inherited and acquired. Thus, the coexistence of SPS with other conditions may be required in some cases for the development of vaso-occlusive episodes and clinical manifestation, in accordance with the concept of multifactorial thrombophilia.…”

Section: The Discovery Of Sps: From Its Initial Description To Full Cmentioning

confidence: 99%

Sticky Platelet Syndrome: History and Future Perspectives

Kubisz

Ruíz‐Argüelles

Staško

et al. 2014

Semin Thromb Hemost

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The sticky platelet syndrome (SPS) is a thrombophilic qualitative platelet disorder with familial occurrence and autosomal dominant trait, characterized by increased in vitro platelet aggregation after low concentrations of adenosine diphosphate and/or epinephrine. Its clinical manifestation includes arterial thrombosis, pregnancy complications (fetal growth retardation and fetal loss), and less often venous thromboembolism. SPS was considered to be a rare thrombophilic disorder, but it can be found relatively often as a cause of unexplained thrombosis, particularly among patients with arterial thrombosis such as stroke. The syndrome was recognized as a distinct disorder in 1983 by Holiday and further characterized in the 1980s and 1990s, with Mammen and Bick providing the key findings. Although recognized for more than 30 years, significant issues, namely the syndrome's etiology, inheritance, and epidemiology, remain unclear. The aim of the first part of this review is to summarize the previous 35 years of the research into, and to provide a brief historical account of, SPS. The history section is focused particularly on the work of two most prominent investigators: Eberhard F. Mammen and Rodger L. Bick. The second part summarizes the present understanding of the syndrome and outlines unresolved issues and the trends in which the future research is likely to continue.

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“…There are no universal recommendations, and treatment should be individualized; however, treatment is often rather accompanied by complications related to the adverse events of medication (especially bleeding) or thrombosis recurrence. 16,30 Fig . 2 Treatment algorithm of SPS.…”

Section: Therapy Of Sticky Platelet Syndromementioning

confidence: 99%

Sticky Platelet Syndrome

Kubisz

Staško

Holly

2013

Semin Thromb Hemost

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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).

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Sticky Platelet Syndrome: An Unusual Presentation of Arterial Ischemia

Cited by 18 publications

References 9 publications

Livedoid vasculopathy (LV) associated with sticky platelets syndrome type 3 (SPS type 3) and enhanced activity of plasminogen activator inhibitor (PAI‐1) anomalies

Livedoid vasculopathy (LV) associated with sticky platelets syndrome type 3 (SPS type 3) and enhanced activity of plasminogen activator inhibitor (PAI‐1) anomalies

Sticky Platelet Syndrome: History and Future Perspectives

Sticky Platelet Syndrome

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