Thrombocytosis pathophysiology: Difference between revisions
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Latest revision as of 15:48, 30 August 2015
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Thrombocytosis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Thrombocytosis pathophysiology On the Web |
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American Roentgen Ray Society Images of Thrombocytosis pathophysiology |
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Risk calculators and risk factors for Thrombocytosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Faizan Sheraz, M.D. [2]
Overview
Pathophysiology
Thrombocytosis is either reactive or autonomous. In one study of 91 patients with platelet count >600,000, 70% were reactive and 22% autonomous. In 280 patients with platelet count >1,000,000 82% were reactive and 14% were autonomous. 8% had both. Among reactive causes of thrombocytosis, infection (30%), Post-surgical (15%), Both (30%), Malignancy (10%), Post splenectomy (10%) and acute blood loss/iron deficiency (10%) are the most common causes.
Autonomous causes of thrombocytosis include Essential Thrombocytosis, Chronic Myelogenous Leukemia (CML), Polycythemia Vera, Agnogenic Myeloid Metaplasia and Myelodysplasia. The degree of thrombocytosis does not help determine whether the thrombocytosis is reactive or not.