Hamostaseologie 2016; 36(04): 227-240
DOI: 10.5482/HAMO-14-11-0074
Review
Schattauer GmbH

Do we need antiplatelet therapy in thrombocytosis? Pro

Diagnostic and pathophysiologic considerations for a treatment choiceBrauchen wir Antithrombotika bei Thrombozytose? ProDiagnostische und pathophysiologische Überlegungen bei der Therapiewahl
Lorenzo Alberio
1   Service of Hematology and Central Hematology Laboratory, University Hospital of Lausanne, Switzerland
› Author Affiliations
Further Information

Publication History

Received 23 November 2014

Accepted in revised form: 13 February 2015

Publication Date:
18 December 2017 (online)

Summary

Thrombocytosis (defined as platelets >450 × 109/l) has several aetiologies. After having excluded spurious thrombocytosis (e. g., due to microspherocytes, schistocytes, cryoglobulins, or bacteria), the differential diagnosis of true thrombocytosis encompasses secondary causes (as diverse as inflammation, infection, malignancy, iron deficiency, or asplenia), primary hereditary (rare forms of familial thrombocytosis) and primary acquired entities (either in the context of a myelodys-plastic syndrome or more frequently a myeloproliferative neoplasia). This manuscript addresses the following aspects: 1) diagnostic approach to thrombocytosis; 2) various mechanisms leading to a high platelet count; 3) potential of some of these mechanisms to modulate platelet function, producing hyper-reactive platelets and thus exerting a direct impact on the thrombotic risk; 4) indication of anti-thrombotic treatment in patients with thrombocytosis. There is a single prospective randomized clinical trial showing the benefit of acetyl-salicylic acid in polycythaemia vera. For other types of primary thrombocytosis and for secondary forms, treatment decisions have to be individualized according to the patient thrombotic and bleeding risks, taking into account the mechanism causing thrombocytosis. This manuscript discusses experimental and clinical data suggesting that besides patients with essential thrombocythaemia and other forms of primary thrombocytosis also those with thrombocytosis in the context of chronic inflammation, malignancy, or exposure to high altitude might benefit from anti-platelet treatment.

Zusammenfassung

Die Thrombozytose (definiert als Thrombo -zytenzahl >450 × 109/l) hat unterschiedliche Ursachen. Zuerst soll eine Pseudo-Thrombozytose (z. B. verursacht durch Mikrosphärozyten, Fragmentozyten, Kryoglobuline oder Bakterien) ausgeschlossen werden. Die Differenzialdiagnose einer echten Thrombozytose beinhaltet sekundäre Ursachen (z. B. Entzündung, Infektion, Neoplasie, Eisenmangel oder Asplenie), primäre hereditäre Formen (die seltenen familiären Thrombozytosen) und primäre erworbene Formen (am häufigsten eine myeloproliferative Neoplasie, seltener myelodysplastische Syndrome). Dieses Manuskript beschäftigt sich mit folgenden Aspekten: 1) diagnostische Abklärung einer Thrombozytose; 2) Mechanismen, die eine Thrombozytose verursachen können; 3) Die Frage, ob einige dieser Mechanismen die Produktion hyper-reaktiver Thrombozyten bewirken und somit direkt das thrombotische Risiko zu erhöhen. 4) Die Indikationen einer anti-aggregatorischen Behandlung bei Patienten mit Thrombozytose. Es gibt nur eine prospektive, randomisierte Studie, welche die Wirksamkeit von Aspirin bei Patienten mit Polycythämia vera belegt. Für die übrigen primären Thrombozytosen und für alle sekundären Formen muss die Behandlungsentscheidung individualisiert getroffen werden. Das thrombotische und das Blutungsrisiko sind abzuwägen, der die Thrombozytose verursachende Mechanismus ist zu berücksichtigen. Dieses Manuskript beschreibt die experimentellen und klinischen Daten, die den Nutzen einer anti-aggregatorischen Behandlung für myeloproliferative Neoplasien und sekundäre Thrombozytosen im Rahmen von z. B. einer chronischen Entzündung, eines Eisenmangels oder Tumors oder beim Aufent-halt in extremen Höhen nahelegen.

 
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