Secondary Thrombocytosis

Updated: Jul 10, 2020
  • Author: Devapiran Jaishankar, MBBS; Chief Editor: Srikanth Nagalla, MBBS, MS, FACP  more...
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Practice Essentials

Platelets are acute-phase reactants; therefore, platelet counts increase in response to various stimuli, including systemic infections, inflammatory conditions, bleeding, and tumors. [1, 2, 3] This phenomenon is called reactive or secondary thrombocytosis, which is a benign form of thrombocytosis. In contrast, clonal thrombocytosis (primary or essential thrombocytosis) is an unregulated abnormality of platelet production due to a clonal expansion of bone marrow progenitor cells. [4, 5]  

Secondary thrombocytosis is usually identified on routine laboratory evaluation, as most patients are asymptomatic, However, patients may have symptoms related to the primary condition that may have precipitated the thrombocytosis (see Presentation). If the clinical presentation does not clearly differentiate between primary (clonal) and secondary thrombocytosis, further tests may be indicated to exclude or confirm a diagnosis of disorders that cause clonal thrombocytosis (see Workup).

The primary treatment of secondary thrombocytosis should address the underlying cause of the thrombocytosis. For patients with platelet counts in excess of 1,000,000/μL, aspirin 65 mg daily may be considered to minimize the rare development of stroke or thrombosis (see Treatment).



The pathophysiology of secondary thrombocytosis may vary, depending on the cause of thrombocytosis. Elevated platelet counts can be due to megakaryocyte proliferation; decreased platelet sequestration; or increased cytokine production, which stimulates platelet production.

Megakaryocyte proliferation can be seen with iron deficiency or blood loss. Decreased platelet sequestration occurs in conditions such as asplenia. Overproduction of proinflammatory cytokines, such as interleukin (IL)-1, IL-6, and IL-11, occurs in chronic inflammatory, infective, and malignant states. [6, 7, 8, 9]  Elevated levels of IL-1, IL-6, C-reactive protein (CRP), granulocyte colony-stimulating factor (G-CSF), and granulocyte-macrophage colony-stimulating factor (GM-CSF) lead to megakaryocyte growth and increased production of platelets​ as part of secondary thrombocytosis.



Secondary thrombocytosis (reactive thrombocytosis) is a relatively common condition. The incidence varies with the underlying condition. The incidence of postsplenectomy secondary thrombocytosis is approximately 75-82%. [10]  In a retrospective review of patients with iron deficiency anemia, the prevalence of reactive thrombocytosis was found to be 31%. [11]

Overall, secondary thrombocytosis occurs in 3-13% of hospitalized children. However, in a Greek study of children 10 days to 8 years old who were hospitalized with viral pneumonia, [9] and an Italian study of children 1 to 24 months old who were hospitalized for community-acquired infections, [12] approximately half had thrombocytosis.

Secondary thrombocytosis is more common than primary thrombocytosis. In a series from a large US university hospital that included 280 patients with extreme thrombocytosis (platelet count of 1,000 × 109/L or greater), 82% had secondary thrombocytosis. [13]


Race-, Sex-, and Age-related Demographics

No race predilection exists for secondary thrombocytosis (reactive thrombocytosis). No sex predilection exists for secondary thrombocytosis, except that iron deficiency is more prevalent in females during childbearing years. No age predilection exists for secondary thrombocytosis. [12, 14]