Secondary Thrombocytosis

  • Author: Koyamangalath Krishnan, MD, FRCP, FACP; Chief Editor: Srikanth Nagalla, MBBS, MS, FACP  more...
 
Updated: Apr 14, 2016
 

Background

Platelets are acute-phase reactants; therefore, they increase in response to various stimuli, including systemic infections, inflammatory conditions, bleeding, and tumors.[1, 2, 3] This 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]

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Pathophysiology

Secondary thrombocytosis (reactive thrombocytosis) may be due to the overproduction of proinflammatory cytokines, such as interleukin (IL)-1, IL-6, and IL-11, that occurs in chronic inflammatory, infective, and malignant states.[6, 7, 8, 9] The presence of elevated IL-1, IL-6, C-reactive protein (CRP), granulocyte colony-stimulating factor (G-CSF), and granulocyte-macrophage colony-stimulating factor (GM-CSF) in individuals with these conditions suggests that these cytokines may be involved in secondary thrombocytosis.

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Epidemiology

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]

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,[11] 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 x 109/L or greater), 82% had secondary thrombocytosis.[12]

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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.[11, 13]

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Contributor Information and Disclosures
Author

Koyamangalath Krishnan, MD, FRCP, FACP Dishner Endowed Chair of Excellence in Medicine, Professor of Medicine, James H Quillen College of Medicine at East Tennessee State University

Koyamangalath Krishnan, MD, FRCP, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society of Hematology, Royal College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Devapiran Jaishankar, MBBS Associate Professor, Division of Oncology, East Tennessee State University, James H Quillen College of Medicine

Devapiran Jaishankar, MBBS is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Hematology, American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Marcel E Conrad, MD Distinguished Professor of Medicine (Retired), University of South Alabama College of Medicine

Marcel E Conrad, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American Association of Blood Banks, American Chemical Society, American College of Physicians, American Physiological Society, American Society for Clinical Investigation, American Society of Hematology, Association of American Physicians, Association of Military Surgeons of the US, International Society of Hematology, Society for Experimental Biology and Medicine, SWOG

Disclosure: Partner received none from No financial interests for none.

Chief Editor

Srikanth Nagalla, MBBS, MS, FACP Associate Professor of Medicine, Division of Hematology and Oncology, UT Southwestern Medical Center

Srikanth Nagalla, MBBS, MS, FACP is a member of the following medical societies: American Society of Hematology, Association of Specialty Professors

Disclosure: Nothing to disclose.

Acknowledgements

Wadie F Bahou, MD Chief, Division of Hematology, Hematology/Oncology Fellowship Director, Professor, Department of Internal Medicine, State University of New York at Stony Brook

Wadie F Bahou, MD is a member of the following medical societies: American Society of Hematology

Disclosure: Nothing to disclose.

References
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  2. Mantadakis E, Tsalkidis A, Chatzimichael A. Thrombocytosis in childhood. Indian Pediatr. 2008 Aug. 45(8):669-77. [Medline].

  3. Mata Fernández C, Pérez-Miranda Castillo J, Galarón García P, Cela de Julián E, Beléndez Bieler C. [Thrombocytosis in the oncology-haematology clinic: description, aetiological diagnosis and progression thrombocytosis] [Spanish]. An Pediatr (Barc). 2008 Jul. 69(1):10-4. [Medline]. [Full Text].

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  6. Tefferi A, Ho TC, Ahmann GJ, Katzmann JA, Greipp PR. Plasma interleukin-6 and C-reactive protein levels in reactive versus clonal thrombocytosis. Am J Med. 1994 Oct. 97(4):374-8. [Medline].

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  8. Araneda M, Krishnan V, Hall K, et al. Reactive and clonal thrombocytosis: proinflammatory and hematopoietic cytokines and acute phase proteins. South Med J. 2001 Apr. 94(4):417-20. [Medline].

  9. Haidopoulou K, Goutaki M, Lemonaki M, Kavga M, Papa A. Reactive thrombocytosis in children with viral respiratory tract infections. Minerva Pediatr. 2011 Aug. 63(4):257-62. [Medline].

  10. Khan PN, Nair RJ, Olivares J, Tingle LE, Li Z. Postsplenectomy reactive thrombocytosis. Proc (Bayl Univ Med Cent). 2009 Jan. 22(1):9-12. [Medline]. [Full Text].

  11. Indolfi G, Catania P, Bartolini E, et al. Incidence and clinical significance of reactive thrombocytosis in children aged 1 to 24 months, hospitalized for community-acquired infections. Platelets. 2008 Sep. 19(6):409-14. [Medline].

  12. Buss DH, Cashell AW, O'Connor ML, Richards F 2nd, Case LD. Occurrence, etiology, and clinical significance of extreme thrombocytosis: a study of 280 cases. Am J Med. 1994 Mar. 96(3):247-53. [Medline].

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  14. Chanet V, Tournilhac O, Dieu-Bellamy V, et al. Isolated spleen agenesis: a rare cause of thrombocytosis mimicking essential thrombocythemia. Haematologica. 2000 Nov. 85(11):1211-3. [Medline]. [Full Text].

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  16. Kulnigg-Dabsch S, Schmid W, Howaldt S, Stein J, Mickisch O, Waldhör T, et al. Iron deficiency generates secondary thrombocytosis and platelet activation in IBD: the randomized, controlled thromboVIT trial. Inflamm Bowel Dis. 2013 Jul. 19(8):1609-16. [Medline].

  17. Tsantes AE, Dimoula A, Bonovas S, Mantzios G, Tsirigotis P, Zoi K, et al. The role of the Platelet Function Analyzer (PFA)-100 and platelet aggregometry in the differentiation of essential thrombocythemia from reactive thrombocytosis. Thromb Res. 2009 Aug 5. [Medline].

  18. Alberio L. Do we need antiplatelet therapy in thrombocytosis? Pro. Diagnostic and pathophysiologic considerations for a treatment choice. Hamostaseologie. 2015 Feb 24. 35 (2):[Medline].

  19. Harrison MT, Short P, Williamson PA, Singanayagam A, Chalmers JD, Schembri S. Thrombocytosis is associated with increased short and long term mortality after exacerbation of chronic obstructive pulmonary disease: a role for antiplatelet therapy?. Thorax. 2014 Jul. 69(7):609-15. [Medline].

  20. Cohen JG, Tran AQ, Rimel BJ, Cass I, Walsh CS, Karlan BY, et al. Thrombocytosis at secondary cytoreduction for recurrent ovarian cancer predicts suboptimal resection and poor survival. Gynecol Oncol. 2014 Mar. 132(3):556-9. [Medline].

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