Thrombocytosis

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

Synonyms and keywords: Platelet count raised; thrombocythemia

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Thrombocytosis is the presence of high platelet counts in the blood, and can be either reactive or primary (also termed essential and caused by a myeloproliferative disease). Although often symptomless (particularly when it is a secondary reaction), it can predispose to thrombosis in some patients.

Definition

95% of the population will have a platelet count between 100,000 and 450,000 per mm³. Thrombocytosis is defined as >500,000. Extreme thrombocytosis is defined as >1,000,000. Generally, a normal platelet count ranges from 150,000 and 450,000 per mm³. These limits, however, are determined by the 2.5th lower and upper percentile, and a deviation does not necessary imply any form of disease. Nevertheless, counts over 750,000 (and especially over a million) are considered serious enough to warrant investigation and intervention.

References

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Historical Perspective

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Classification

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Pathophysiology

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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.

References

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Causes

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

Overview

Causes

Increase platelet counts can be due to a number of disease processes:

Essential (Primary)
- Essential thrombocytosis (a form of myeloproliferative disease)
- Other myeloproliferative disorders such as chronic myelogenous leukemia, polycythemia vera, myelofibrosis
Reactive (Secondary)
- Inflammation
- Surgery (which leads to an inflammatory state)
- Hyposplenism (decreased breakdown due to decreased function of the spleen)
- Hemorrhage and/or iron deficiency
- Drud Side Effect- Aztreonam, Ceftazidime, Ibuprofen

References

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Differentiating Thrombocytosis from other Diseases

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

Overview

Thrombocytosis Differential Diagnosis

Differentiating the diseases that can cause thrombocytosis :

Category	Condition		Etiology	Mechanism			Inherited	Acquried	Clinical manifestations									Para−clinical findings								Gold standard	Associated findings
									Demography	History	Symptoms			Signs				Para−clinical findings
											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					Fever	Appearance	Bleeding	BP	Splenomegaly	Jaundice	Other	Plt	HB	WBC	PBS	Bone marrow exam	PT	PTT
Autonomous thrombocytosis	Hematologic malignancies	Essential thrombocythemia^[1]	Acquired mutation of JAK2, CALR, or MPL	+	–	–	–	+	Mean age >60 years old, female > male	Vascular occlusive events and hemorrhages	±	Flushing	+	Nl	+	–	Erythromelalgia Transient ischemic attacks Priapism Decreased visual acuity	↑↑	↑	↑	Large platelets Megakaryocyte fragments Platelet aggregates	Increased cellularity Hyperplasia and clustering of megakaryocytes Bone marrow reticulin may be increased with no collagen fibrosis	Nl	Nl	Splenomegaly on abdominal CT VTE on spiral chest CT DVT on ultrasound	Bone marrow biopsy	Thrombo-hemorrhagic complications
		Polycythemia vera^[2]	Acquired mutation of JAK2	+	–	–	–	+	Mean age >60 years old	Family history of polycythemia vera Ashkenazi Jewish descent	–	Facial plethora	±	Nl	+	–	Erythromelalgia Pruritus Tinnitus Blurred vision Lymphadenopathy	↑	↑↑	↑	Panmyelosis including prominent erythroid, granulocyte, and megakaryocyte proliferation	Panmyelosis including prominent erythroid, granulocyte, and megakaryocyte proliferation Pleomorphic, mature megakaryocytes	↑	↑	Splenomegaly or splenic infarcts on imaging Increased radiographic attenuation of cerebral arteries, veins and dural sinuses on CT scan or MRI	Bone marrow biopsy	Thrombo-hemorrhagic complications
		Primary myelofibrosis^[3]	Bone marrow fibrosis Mutation in JAK2, CALR, or MPL	+	–	–	–	+	Mean age >60 years old, male> female	Other myeloproliferative disorders Radiation exposure Chemicals exposure	–	Pallor Bruising Skin nodules	+	Nl	+	+	Fatigue Abdominal pain Early satiety Dyspnea Lymphadenopathy	↑/↓	↓	↓	Decreased number of erythroid, granulocyte, and megakaryocyte proliferation	Proliferation and atypia of megakaryocytes Reticulin or collagen fibrosis Hypercellular bone marrow	↑	↑	Diffuse bone sclerosis on CT	Bone marrow biopsy	Thrombo-hemorrhagic complications Variable risk for development of acute leukemia
		Chronic myeloid leukemia^[4]	Translocation (9;22), the Philadelphia chromosome BCR-ABL1 oncogene	+	–	–	–	+	Mean age >50 years old, male> female	History of exposure to: Ionizing radiation Formaldehyde Benzene	+	Pallor Bruises Petechiae Ulcers Vesicles	+	Nl	+	–	Fatigue Abdominal pain Early satiety Dyspnea Lymphadenopathy	↑	↓	↑	Immature leukocytes Leukemic blasts Leukoerythroblastic features Giant platelets Blast crisis	↑ Proportion of metamyelocytes and other white blood cells at various stages of maturation	↑	↑	Enlarged lymph nodes and splenomegaly on CT scan	Bone marrow biopsy	Increase of immature myeloid cells
		Acute myeloid leukemia^[5]	Unknown	+	–	–	–	+	Median age of 63 years old	History of hematological disorder History of chemotherapy and ionizing radiation	+	Pallor Leukemia cutis Bruising Petechiae Ecchymosis	+	Nl	+	+	Fatigue Bone tenderness Early satiety	↑/↓	↓	↑/↓	Leukemic blasts Leukoerythroblastic features Giant platelets	“Dry tap” on aspiration Leukemic cells	↑	↑	NA	Bone marrow examination + clinical manifestation	Infections of variable severity Cranial nerve palsy
		Myelodysplastic syndromes^[6]	Unknown Mutation	+	–	–	±	+	Elderly	Exposure to: Chemotherapy Radiation therapy Tobacco smoke	±	Petechiae Purpura Diffuse erythematous rash	+	Nl	+	+	Shortness of breath Fatigue	↑/↓	↓	↓	Large platelets Ovalomacrocytosis Basophilic stippling Howell-Jolly body Pelger-Huet anomaly Ring sideroblasts	Impaired myeloid maturation Dyserythropoiesis Dysgranulopoiesis Dysmegakaryocytopoiesis Hypercellular bone marrow Fibrosis	Nl	Nl	NA	Bone marrow examination + clinical manifestation	Thrombosis at unusual sites Thrombosis in younger patients Might transformed to acute leukemia
	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]		Mutation in TPO and MPL	+	–	–	+	–	Rare familial disease, middle age male and female	Family history of thrombocytosis	–	Normal	–	Nl	–	–	–	↑	Nl	Nl	Giant platelets Platelet conglomerates Bizarre forms Megakaryocytic fragments	Proliferation of megakaryocytes	Nl	Nl	NA	Genetic study	Polyclonal hematopoiesis Familial polycythemia vera Familial primary myelofibrosis
Reactive thrombocytosis	Anemia/ blood loss^[9]	Iron deficiency Blood loss Hemolysis	Unknown Proliferation of megakaryocytes	+	–	–	–	+	Any	History of bleeding or iron deficiency	–	Pallor	+	Nl to ↓	–	–	Depends on the etilogy	↑	↓	Nl	Microcytic anemia Megakaryocytic fragments	Proliferation of megakaryocytes	Nl	Nl	NA	Clinical manifestation	Required iron studies
	Infection	Chronic infections	Proliferation of megakaryocytes	+	+	–	–	+	Any	History of immunodeficiency	+	Pallor	±	Nl to ↓	–	±	Depends on the etilogy	↑	↓	↑	Microcytic anemia Megakaryocytic fragments	Proliferation of megakaryocytes	Nl	Nl	Depends on the etiology	Culture	Depends on the etilogy
		Tuberculosis	Proliferation of megakaryocytes	+	+	–	–	+	Any	History of close contact	+	Cachectic	–	Nl	–	–		↑	Nl	↑	Large platelets	Proliferation of megakaryocytes	Nl	Nl	Cavitation on chest imaging	Clinical manifestation+ culture
		Acute bacterial and viral infections	Proliferation of megakaryocytes	+	+	–	–	+	Any	History of close contact	+	Acutely ill	–	Nl	–	–	Depends on the etilogy	↑		↑	Large platelets	Proliferation of megakaryocytes	Nl	Nl	Depends on the etiology	Clinical manifestation+ culture	Depends on the etiology
	Inflammation	Vasculitides^[10]	Unknown	+	+	–	±	+	Any	Family history of rheumatologic disorders	+	Acutely ill	+	Nl	–	–	Arthritis	↑	Nl to ↓	↑	Microcytic anemia Megakaryocytic fragments	Proliferation of megakaryocytes	Nl to ↑	Nl to ↑	Depends on the type	Clinical manifestation+ culture	Depends on the type
		Acute pancreatitis	Proliferation of megakaryocytes	+	+	–	–	+	Any	Alcohol consumption Gallstone Hypertriglyceridemia Obesity	+	Acutely ill	–	Nl to ↓	–	+	Abdominal tenderness N/V Dyspnea	↑	Nl to ↓	↑	Large platelets	Proliferation of megakaryocytes	Nl to ↑	Nl to ↑	Diffusely enlarged and hypoechoic pancreas on abdominal ultrasound Focal or diffuse enlargement of the pancreas with heterogeneous enhancement on abdominal CT scan	Clinical manifestation	Rarely progress to severe inflammation and necrosis Organ failure
		Malignancy^[11]	Proliferation of megakaryocytes Accelerated platelet release	+	+	–	±	±	Any	Prior malignancy Exposure to chemicals Family history of malignancy	+	Cachectic	–	Nl to ↓	Depends on the type	–	Tenderness	↑	Nl to ↓	↑	Microcytic anemia Megakaryocytic fragments	Proliferation of megakaryocytes	Nl to ↑	Nl to ↑	Depends on the type	Biopsy	Potential effective predictor of overall survival Venous thromboembolism
	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]	Accelerated platelet release	–	+	–	–	+	Any	Thermal burn	+	Acutely ill	±	Nl to ↓	–	±	Fatigue Tenderness Burn Dyspnea	↑	Nl to ↓	↑	Megakaryocytic fragments Large numbers of microspherocytes	Increased production of neutrophils	Nl to ↑	Nl to ↑	Depend on the involvement	Clinical manifestation	Sepsis
		Trauma^[13]	Accelerated platelet release	–	+	–	–	+	Any	Physical trauma Accident	±	Acutely ill	±	Nl to ↓	–	–	Tenderness Fracture	↑	Nl to ↓	↑	Megakaryocytic fragments Large numbers of microspherocytes	Increased production of neutrophils	Nl	Nl	Depend on the involvement Fracture on X-rays	Clinical manifestation	Sepsis Associated with higher rates of complications
		Myocardial infarction^[14]	Accelerated platelet release	–	+	–	–	+	Elderly	Acute coronary syndrome Diabetes mellitus	±	Acutely ill Diaphoretic	–	Nl to ↓	–	–	Chest pain Dyspnea N/V Coma	↑	Nl to ↓	↑	Megakaryocytic fragments Large numbers of microspherocytes	Proliferation of megakaryocytes	Nl	Nl	Hypokinetic heart on echocardiogram	Clinical manifestation + enzymes elevation	Acute pulmonary edema Poor prognosis
	Medication^[15]	Vincristine^[16]	Increased megakaryocytic differentiation	–	+	–	–	+	Any	Malignancy Drug consumption	–	Cachectic	–	Nl	+	–	Abdominal pain Diarrhea Dizziness	↑	Nl to ↓	↑	Megakaryocytic fragments Large numbers of microspherocytes	Proliferation of megakaryocytes	Nl to ↑	Nl to ↑	Depends on the etiology	Clinical manifestation + history of drug consumption	Neuropathy
		Epinephrine^[17]	Unknown Activation of chloride transport	+	+	–	–	+	Any	Anaphylaxis Respiratory diseases	–	Acutely ill Diaphoretic	–	Nl to ↓	–	–	Dizziness Tremor Anxiety Dyspnea	↑	↑	↑	Megakaryocytic fragments	Proliferation of megakaryocytes	Nl	Nl	Depends on the etiology	Clinical manifestation + history of drug consumption	Thromboembolic complications
		Glucocorticoids^[18]	Stimulate megakaryocytopoiesis	+	+	–	–	+	Any	Malignancy Autoimmune diseases	+	Obese	Easy bruising	Nl to ↓	–	–	Abdominal pain Muscle weakness Growth failure Pubertal delay	↑	Nl to ↓	↑	Megakaryocytic fragments Large numbers of microspherocytes	Proliferation of megakaryocytes	Nl to ↑	Nl to ↑	Depends on the etiology	Clinical manifestation + history of drug consumption	Thromboembolic complications Cushing syndrome Diabetes mellitus
		Antibiotics^[19]	Unclear Stimulate megakaryocytopoiesis Acute phase reactant	+	+	–	–	+	Any	Infection	+	Nl	±	Nl	–	–	Depends on the etiology	↑	Nl	↑	Megakaryocytic fragments	Proliferation of megakaryocytes	Nl	Nl	Depends on the etiology	Clinical manifestation + history of drug consumption	Poor prognosis Thrombosis
		Thrombopoietin^[20]^[21]	Stimulate megakaryocytopoiesis Thrombopoiesis	+	–	–	–	+	Any	Malignancy Chemotherapy	+	Chronically ill	–	Nl to ↑	–	–	Depends on the etiology	↑	↑	↑	Megakaryocytic fragments Large platelets	Proliferation of megakaryocytes	Nl	Nl	Depends on the etiology	Clinical manifestation + history of drug consumption	Poor prognosis Thrombosis
	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]	Reduced platelet turnover	–	–	+	–	+	Any	Prior surgical removal of the spleen Sickle cell disease	±	Normal	+	Nl	Asplenia	–	–	↑	↓	↑	Howell-Jolly bodies Nucleated RBCs	Proliferation of megakaryocytes	Nl	Nl	Small or no spleen on CT scan	Clinical manifestation	Incidental laboratory finding Thrombosis
		Allergic reactions^[23]	Unknown Activation of chloride transport	+	+	–	–	+	Any	Anaphylaxis Respiratory diseases	–	Acutely ill Diaphoretic	–	Nl to ↓	–	–	Dizziness Tremor Anxiety Dyspnea	↑	↑	↑	Megakaryocytic fragments	Proliferation of megakaryocytes	Nl	Nl	Depends on the etiology	Clinical manifestation	Poor prognosis
		Exercise^[24]	Increased megakaryocyte proliferation	+	+	–	–	+	Athlete	Exercise	–	Normal	–	Nl	–	–	NA	↑	↑	↑	Megakaryocytic fragments	Proliferation of megakaryocytes	Nl	Nl	Depends on the etiology	Clinical manifestation	NA
Pseudothrombocytosis	Mixed cryoglobulinemia^[25]		Falsely elevated	–	–	–	–	–	Any	Malignancy Autoimmune disease Infection	–	Atypical cutaneous ulcers Palpable purpura	–	Nl	–	–	Headache Confusion Blurry or loss of vision Joint pain Generalized weakness	↑	Nl to ↓	↑	Cytoplasmic fragments	Nl	Nl	Nl	NA	Skin biopsy	Vasculitis Neuropathy Raynaud phenomenon
Pseudothrombocytosis	Cytoplasmic fragments^[26]		Falsely elevated	–	–	–	–	–	Any	NA	–	Normal	–	Nl	–	–	NA	↑	Nl	Nl	Cytoplasmic fragments	Nl	Nl	Nl	Nl	Repeat	NA

References

↑ Brière, Jean B (2007). Orphanet Journal of Rare Diseases. 2 (1): 3. doi:10.1186/1750-1172-2-3. ISSN 1750-1172. Missing or empty |title= (help)
↑ 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. ISSN 0006-4971.
↑ 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. ISSN 0025-6196.
↑ 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. ISSN 0025-6196.
↑ 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. ISSN 0733-8627.
↑ 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. ISSN 1687-9104.
↑ 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. ISSN 0006-4971.
↑ 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. ISSN 0007-1048.
↑ Kuter, David J. (1996). “The Physiology of Platelet Production”. Stem Cells. 14 (S1): 88–101. doi:10.1002/stem.5530140711. ISSN 1066-5099.
↑ Hamblin T, Oscier D (September 1978). “Polyarteritis presenting with thrombocytosis and palliated by plasma exchange”. Postgrad Med J. 54 (635): 615–7. PMC 2425233. PMID 82963.
↑ 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. ISSN 0025-7974.
↑ 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. ISSN 2045-2322.
↑ 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. ISSN 0022-5282.
↑ 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. ISSN 1936-8798.
↑ Frye JL, Thompson DF (February 1993). “Drug-induced thrombocytosis”. J Clin Pharm Ther. 18 (1): 45–8. PMID 8473359.
↑ 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. ISSN 0001-5792.
↑ 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. PMID 9461228.
↑ 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. ISSN 0275-6382.
↑ Scharf RE (November 2012). “Drugs that affect platelet function”. Semin. Thromb. Hemost. 38 (8): 865–83. doi:10.1055/s-0032-1328881. PMID 23111864.
↑ Hitchcock IS, Kaushansky K (April 2014). “Thrombopoietin from beginning to end”. Br. J. Haematol. 165 (2): 259–68. doi:10.1111/bjh.12772. PMID 24499199.
↑ Teofili, Luciana; Giona, Fiorina; Martini, Maurizio; Torti, Lorenza; Cenci, Tonia; Foà, 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. ISSN 0732-183X.
↑ 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. PMID 22203487.
↑ 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. PMID 8603285.
↑ Beck WR, Scariot PP, Gobatto CA (2014). “Primary and secondary thrombocytosis induced by exercise and environmental luminosity”. Bratisl Lek Listy. 115 (10): 607–10. PMID 25573725.
↑ Patel KJ, Hughes CG, Parapia LA (January 1987). “Pseudoleucocytosis and pseudothrombocytosis due to cryoglobulinaemia”. J. Clin. Pathol. 40 (1): 120–1. PMC 1140844. PMID 3818970.
↑ 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. ISSN 1421-9662.

Epidemiology and Demographics

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Risk Factors

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Screening

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Natural History, Complications and Prognosis

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Diagnosis

Treatment

Medical Therapy | Surgery | Prevention | Future or Investigational Therapies | Cost Effectiveness of Therapy

Case Studies

Case #1

Acknowledgements

The content on this page was first contributed by: BIDMC Resident Report by Duane Pinto, M.D.

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Template:WikiDoc Sources

[Brière2007-1] Brière, Jean B (2007). Orphanet Journal of Rare Diseases. 2 (1): 3. doi:10.1186/1750-1172-2-3. ISSN 1750-1172. Missing or empty |title= (help)

[ArberOrazi2016-2] 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. ISSN 0006-4971.

[TefferiLasho2012-3] 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. ISSN 0025-6196.

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Thrombocytosis

Overview

References

References

References

Overview

Pathophysiology

References

Overview

Causes

References

Overview

Thrombocytosis Differential Diagnosis

References

References

References

References

References

Diagnosis

Treatment

Case Studies

Acknowledgements

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