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Thrombocytosis differential diagnosis

Introduction

Overview

Overview

Thrombocytosis Differential Diagnosis

Thrombocytosis Differential Diagnosis

Differentiating the diseases that can cause thrombocytosisΒ :

Category Condition Etiology Mechanism Inherited Acquried Clinical manifestations Paraβˆ’clinical findings Gold standard Associated findings
Demography History Symptoms Signs
Lab Findings Imaging
Fever Appearance Bleeding BP Splenomegaly Jaundice Other CBC PBS Bone marrow exam PT PTT
Increased megakaryocyte proliferation Accelerated platelet release Reduced platelet turnover Plt HB WBC
Autonomous thrombocytosis Hematologic malignancies Essential thrombocythemia[1]
  • Acquired mutation of JAK2, CALR, or MPL
+ – – – + Mean age >60 years old, female > male Β±
  • Flushing
+ Nl + – ↑↑ ↑ ↑ Nl Nl Bone marrow biopsy
  • Thrombo-hemorrhagic complications
Polycythemia vera[2]
  • Acquired mutation of JAK2
+ – – – + Mean age >60 years old –
  • Facial plethora
Β± Nl + – ↑ ↑↑ ↑ ↑ ↑ Bone marrow biopsy
  • Thrombo-hemorrhagic complications
Primary myelofibrosis[3] + – – – + Mean age >60 years old, male> female – + Nl + + ↑/↓ ↓ ↓ ↑ ↑ Bone marrow biopsy
  • Thrombo-hemorrhagic complications
  • Variable risk for development of acute leukemia
Chronic myeloid leukemia[4] + – – – + Mean age >50 years old, male> female History of exposure to: + + Nl + – ↑ ↓ ↑
  • ↑ Proportion of metamyelocytes and other white blood cells at various stages of maturation
↑ ↑ Bone marrow biopsy
  • Increase of immature myeloid cells
Acute myeloid leukemia[5]
  • Unknown
+ – – – + Median age of 63 years old + + Nl + + ↑/↓ ↓ ↑/↓
  • “Dry tap” on aspiration
  • Leukemic cells
↑ ↑ NA Bone marrow examination + clinical manifestation
Myelodysplastic syndromes[6] + – – Β± + Elderly Exposure to: Β± + Nl + + ↑/↓ ↓ ↓ Nl Nl NA Bone marrow examination + clinical manifestation
Condition Etiology Increased megakaryocyte proliferation Accelerated platelet release Reduced platelet turnover Inherited Acquried Demography History Fever Appearance Bleeding BP Splenomegaly Jaundice Other signs Plt HB WBC PBS Bone marrow exam PT PTT Imaging Gold standard Associated findings
Familial thrombocytosis[7][8] + – – + – Rare familial disease, middle age male and female –
  • Normal
– Nl – – – ↑ Nl Nl Nl Nl NA Genetic study
Reactive thrombocytosis Anemia/

blood loss[9]

+ – – – + Any – + Nl to ↓ – – Depends on the etilogy ↑ ↓ Nl Nl Nl NA Clinical manifestation
  • Required iron studies
Infection Chronic infections + + – – + Any + Β± Nl to ↓ – Β± Depends on the etilogy ↑ ↓ ↑ Nl Nl
  • Depends on the etiology
Culture Depends on the etilogy
Tuberculosis + + – – + Any
  • History of close contact
+
  • Cachectic
– Nl – – ↑ Nl ↑ Nl Nl
  • Cavitation on chest imaging
Clinical manifestation+ culture
Acute bacterial and viral infections + + – – + Any
  • History of close contact
+
  • Acutely ill
– Nl – – Depends on the etilogy ↑ ↑ Nl Nl
  • Depends on the etiology
Clinical manifestation+ culture
  • Depends on the etiology
Inflammation Vasculitides[10]
  • Unknown
+ + – Β± + Any
  • Family history of rheumatologic disorders
+
  • Acutely ill
+ Nl – – ↑ Nl to ↓ ↑ Nl to ↑ Nl to ↑
  • Depends on the type
Clinical manifestation+ culture
  • Depends on the type
Acute pancreatitis + + – – + Any +
  • Acutely ill
– Nl to ↓ – + ↑ Nl to ↓ ↑ Nl to ↑ Nl to ↑ Clinical manifestation
Malignancy[11] + + – Β± Β± Any
  • Prior malignancy
  • Exposure to chemicals
  • Family history of malignancy
+
  • Cachectic
– Nl to ↓ Depends on the type –
  • Tenderness
↑ Nl to ↓ ↑ Nl to ↑ Nl to ↑
  • Depends on the type
Biopsy
Condition Etiology Increased megakaryocyte proliferation Accelerated platelet release Reduced platelet turnover Inherited Acquried Demography History Fever Appearance Bleeding BP Splenomegaly Jaundice Other signs Plt HB WBC PBS Bone marrow exam PT PTT Imaging Gold standard Associated findings
Tissue damage Thermal burns[12] – + – – + Any
  • Thermal burn
+
  • Acutely ill
Β± Nl to ↓ – Β± ↑ Nl to ↓ ↑ Nl to ↑ Nl to ↑
  • Depend on the involvement
Clinical manifestation
Trauma[13] – + – – + Any Β±
  • Acutely ill
Β± Nl to ↓ – – ↑ Nl to ↓ ↑ Nl Nl
  • Depend on the involvement
  • Fracture on X-rays
Clinical manifestation
  • Sepsis
  • Associated with higher rates of complications
Myocardial infarction[14] – + – – + Elderly Β±
  • Acutely ill
  • Diaphoretic
– Nl to ↓ – – ↑ Nl to ↓ ↑ Nl Nl Clinical manifestation + enzymes elevation
Medication[15] Vincristine[16] – + – – + Any –
  • Cachectic
– Nl + – ↑ Nl to ↓ ↑ Nl to ↑ Nl to ↑
  • Depends on the etiology
Clinical manifestation + history of drug consumption
Epinephrine[17]
  • Unknown
  • Activation of chloride transport
+ + – – + Any –
  • Acutely ill
  • Diaphoretic
– Nl to ↓ – – ↑ ↑ ↑ Nl Nl
  • Depends on the etiology
Clinical manifestation + history of drug consumption
Glucocorticoids[18]
  • Stimulate megakaryocytopoiesis
+ + – – + Any + Nl to ↓ – – ↑ Nl to ↓ ↑ Nl to ↑ Nl to ↑
  • Depends on the etiology
Clinical manifestation + history of drug consumption
Antibiotics[19] + + – – + Any + Nl Β± Nl – –
  • Depends on the etiology
↑ Nl ↑ Nl Nl
  • Depends on the etiology
Clinical manifestation + history of drug consumption
Thrombopoietin[20][21]
  • Stimulate megakaryocytopoiesis
  • Thrombopoiesis
+ – – – + Any +
  • Chronically ill
– Nl to ↑ – –
  • Depends on the etiology
↑ ↑ ↑ Nl Nl
  • Depends on the etiology
Clinical manifestation + history of drug consumption
Condition Etiology Increased megakaryocyte proliferation Accelerated platelet release Reduced platelet turnover Inherited Acquried Demography History Fever Appearance Bleeding BP Splenomegaly Jaundice Other signs Plt HB WBC PBS Bone marrow exam PT PTT Imaging Gold standard Associated findings
Other Post-splenectomy or functional asplenia[22] – – + – + Any Β±
  • Normal
+ Nl Asplenia – – ↑ ↓ ↑ Nl Nl Clinical manifestation
Allergic reactions[23]
  • Unknown
  • Activation of chloride transport
+ + – – + Any –
  • Acutely ill
  • Diaphoretic
– Nl to ↓ – – ↑ ↑ ↑ Nl Nl
  • Depends on the etiology
Clinical manifestation
  • Poor prognosis
Exercise[24] + + – – + Athlete
  • Exercise
– Normal – Nl – – NA ↑ ↑ ↑ Nl Nl
  • Depends on the etiology
Clinical manifestation NA
Pseudothrombocytosis Mixed cryoglobulinemia[25]
  • Falsely elevated
– – – – – Any –
  • Atypical cutaneous ulcers
  • Palpable purpura
– Nl – – ↑ Nl to ↓ ↑
  • Cytoplasmic fragments
Nl Nl Nl NA Skin biopsy
Cytoplasmic fragments[26]
  • Falsely elevated
– – – – – Any NA – Normal – Nl – – NA ↑ Nl Nl
  • Cytoplasmic fragments
Nl Nl Nl Nl Repeat NA
References

References

  1. ↑ BriΓ¨re, Jean B (2007). Orphanet Journal of Rare Diseases. 2 (1): 3. doi:10.1186/1750-1172-2-3. ISSNΒ 1750-1172. Missing or empty |title= (help)
  2. ↑ Arber, D. A.; Orazi, A.; Hasserjian, R.; Thiele, J.; Borowitz, M. J.; Le Beau, M. M.; Bloomfield, C. D.; Cazzola, M.; Vardiman, J. W. (2016). “The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia”. Blood. 127 (20): 2391–2405. doi:10.1182/blood-2016-03-643544. ISSNΒ 0006-4971.
  3. ↑ Tefferi, Ayalew; Lasho, Terra L.; Jimma, Thitina; Finke, Christy M.; Gangat, Naseema; Vaidya, Rakhee; Begna, Kebede H.; Al-Kali, Aref; Ketterling, Rhett P.; Hanson, Curtis A.; Pardanani, Animesh (2012). “One Thousand Patients With Primary Myelofibrosis: The Mayo Clinic Experience”. Mayo Clinic Proceedings. 87 (1): 25–33. doi:10.1016/j.mayocp.2011.11.001. ISSNΒ 0025-6196.
  4. ↑ Thompson, Philip A.; Kantarjian, Hagop M.; Cortes, Jorge E. (2015). “Diagnosis and Treatment of Chronic Myeloid Leukemia in 2015”. Mayo Clinic Proceedings. 90 (10): 1440–1454. doi:10.1016/j.mayocp.2015.08.010. ISSNΒ 0025-6196.
  5. ↑ Rose-Inman, Hayley; Kuehl, Damon (2014). “Acute Leukemia”. Emergency Medicine Clinics of North America. 32 (3): 579–596. doi:10.1016/j.emc.2014.04.004. ISSNΒ 0733-8627.
  6. ↑ Natelson, Ethan A.; Pyatt, David (2013). “Acquired Myelodysplasia or Myelodysplastic Syndrome: Clearing the Fog”. Advances in Hematology. 2013: 1–11. doi:10.1155/2013/309637. ISSNΒ 1687-9104.
  7. ↑ Ding, J. (2004). “Familial essential thrombocythemia associated with a dominant-positive activating mutation of the c-MPL gene, which encodes for the receptor for thrombopoietin”. Blood. 103 (11): 4198–4200. doi:10.1182/blood-2003-10-3471. ISSNΒ 0006-4971.
  8. ↑ Wiestner, A.; Padosch, S. A.; Ghilardi, N.; Cesar, J. M.; Odriozola, J.; Shapiro, A.; Skoda, R. C. (2000). “Hereditary thrombocythaemia is a genetically heterogeneous disorder: exclusion of TPO and MPL in two families with hereditary thrombocythaemia”. British Journal of Haematology. 110 (1): 104–109. doi:10.1046/j.1365-2141.2000.02169.x. ISSNΒ 0007-1048.
  9. ↑ Kuter, David J. (1996). “The Physiology of Platelet Production”. Stem Cells. 14 (S1): 88–101. doi:10.1002/stem.5530140711. ISSNΒ 1066-5099.
  10. ↑ Hamblin T, Oscier D (September 1978). “Polyarteritis presenting with thrombocytosis and palliated by plasma exchange”. Postgrad Med J. 54 (635): 615–7. PMCΒ 2425233. PMIDΒ 82963.
  11. ↑ Yang, Chen; Jiang, Hui; Huang, Shaozhuo; Hong, Hui; Huang, Xiaowen; Wang, Xiaojie; Liao, Weixin; Wang, Xueyi; Chen, Xuewen; Jiang, Liming (2018). “The prognostic role of pretreatment thrombocytosis in gastric cancer”. Medicine. 97 (31): e11763. doi:10.1097/MD.0000000000011763. ISSNΒ 0025-7974.
  12. ↑ Dinsdale, R. J.; Devi, A.; Hampson, P.; Wearn, C. M.; Bamford, A. L.; Hazeldine, J.; Bishop, J.; Ahmed, S.; Watson, C.; Lord, J. M.; Moiemen, N.; Harrison, P. (2017). “Changes in novel haematological parameters following thermal injury: A prospective observational cohort study”. Scientific Reports. 7 (1). doi:10.1038/s41598-017-03222-w. ISSNΒ 2045-2322.
  13. ↑ Salim, Ali; Hadjizacharia, Pantelis; DuBose, Joseph; Kobayashi, Leslie; Inaba, Kenji; Chan, Linda S.; Margulies, Daniel R. (2009). “What is the Significance of Thrombocytosis in Patients With Trauma?”. The Journal of Trauma: Injury, Infection, and Critical Care. 66 (5): 1349–1354. doi:10.1097/TA.0b013e318191b8af. ISSNΒ 0022-5282.
  14. ↑ Nanavati, Amit; Patel, Nainesh; Burke, James (2012). “Thrombocytosis and Coronary Occlusion”. JACC: Cardiovascular Interventions. 5 (6): e18–e19. doi:10.1016/j.jcin.2011.12.018. ISSNΒ 1936-8798.
  15. ↑ Frye JL, Thompson DF (February 1993). “Drug-induced thrombocytosis”. J Clin Pharm Ther. 18 (1): 45–8. PMIDΒ 8473359.
  16. ↑ Feliu, E.; Cervantes, F.; Blade, J.; Rozman, C. (1980). “Thrombocytosis in Quiescent Chronic Granulocytic Leukaemia after Vincristine and 6-Mercaptopurine Therapy”. Acta Haematologica. 64 (4): 224–226. doi:10.1159/000207258. ISSNΒ 0001-5792.
  17. ↑ Spalding A, Vaitkevicius H, Dill S, MacKenzie S, Schmaier A, Lockette W (February 1998). “Mechanism of epinephrine-induced platelet aggregation”. Hypertension. 31 (2): 603–7. PMIDΒ 9461228.
  18. ↑ Neel, Jennifer A.; Snyder, Laura; Grindem, Carol B. (2012). “Thrombocytosis: a retrospective study of 165 dogs”. Veterinary Clinical Pathology. 41 (2): 216–222. doi:10.1111/j.1939-165X.2012.00416.x. ISSNΒ 0275-6382.
  19. ↑ Scharf RE (November 2012). “Drugs that affect platelet function”. Semin. Thromb. Hemost. 38 (8): 865–83. doi:10.1055/s-0032-1328881. PMIDΒ 23111864.
  20. ↑ Hitchcock IS, Kaushansky K (April 2014). “Thrombopoietin from beginning to end”. Br. J. Haematol. 165 (2): 259–68. doi:10.1111/bjh.12772. PMIDΒ 24499199.
  21. ↑ Teofili, Luciana; Giona, Fiorina; Martini, Maurizio; Torti, Lorenza; Cenci, Tonia; FoΓ , Robin; Leone, Giuseppe; Larocca, Luigi M. (2010). “Thrombopoietin Receptor Activation, Thrombopoietin Mimetic Drugs, and Hereditary Thrombocytosis: Remarks on Bone Marrow Fibrosis”. Journal of Clinical Oncology. 28 (19): e317–e318. doi:10.1200/JCO.2010.29.0387. ISSNΒ 0732-183X.
  22. ↑ Vlachaki E, Kalogeridis A, Neokleous N, Perifanis V, Klonizakis F, Ioannidou E, Klonizakis I (May 2012). “Absence of JAK2V617F mutation in patients with beta-thalassemia major and thrombocytosis due to splenectomy”. Mol. Biol. Rep. 39 (5): 6101–5. doi:10.1007/s11033-011-1425-7. PMIDΒ 22203487.
  23. ↑ Randi ML, Rossi C, Fabris F, Zerbinati P, Girolami A (December 1995). “Atopic dermatitis and allergic diseases with thrombocytosis: a possible link”. Ann. Allergy Asthma Immunol. 75 (6 Pt 1): 530–2. PMIDΒ 8603285.
  24. ↑ Beck WR, Scariot PP, Gobatto CA (2014). “Primary and secondary thrombocytosis induced by exercise and environmental luminosity”. Bratisl Lek Listy. 115 (10): 607–10. PMIDΒ 25573725.
  25. ↑ Patel KJ, Hughes CG, Parapia LA (January 1987). “Pseudoleucocytosis and pseudothrombocytosis due to cryoglobulinaemia”. J. Clin. Pathol. 40 (1): 120–1. PMCΒ 1140844. PMIDΒ 3818970.
  26. ↑ Akinci, Sema; Hacibekiroglu, Tuba; Basturk, Abdulkadir; Bakanay, Sule Mine; Guney, Tekin; Dilek, Imdat (2013). “Pseudothrombocytosis due to Microerythrocytosis: A Case of Beta Thalassemia Minor Complicated with Iron Deficiency Anemia”. Acta Haematologica. 130 (2): 61–63. doi:10.1159/000346434. ISSNΒ 1421-9662.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]