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ENFOQUE CLINICO Y DE LABORATORIO DEL AUMENTO DE LA FUNCION Y NUMERO DE PLAQUETAS

(especial para SIIC © Derechos reservados)
La trombosis es la manifestación clínica principal del síndrome de hiperactividad de las plaquetas y de la trombocitemia esencial. La heterogeneidad de los sitios afectados por la trombosis es una de las características que sugieren estos cuadros.
Autor:
Anna Dyszkiewicz-korpanty
Columnista Experto de SIIC

Institución:
Department of Medicine University Texas Southwestern Medical Center at Dallas Texas, USA

Artículos publicados por Anna Dyszkiewicz-korpanty
Coautores
Yu-Min Shen*  Ravindra Sarode**  Eberhard Mammen***  Eugene Frenkel**** 
MD, Assistant Professor, Internal Medicine. Department of Medicine, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas*
MD, Associate Professor of Pathology. Department of Pathology, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas**
MD, Professor of Obstetrics and Gynecology. Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI***
MD, Professor, Internal Medicine. Department of Medicine, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas****
Recepción del artículo
4 de Noviembre, 2004 		Primera edición
21 de Octubre, 2005 		Segunda edición, ampliada y corregida
7 de Junio, 2021

ENFOQUE CLINICO Y DE LABORATORIO DEL AUMENTO DE LA FUNCION Y NUMERO DE PLAQUETAS

Resumen
Las plaquetas desempeñan un papel crítico en la hemostasia, de manera tal que las alteraciones de la función y del número de plaquetas pueden desencadenar estados trombohemorrágicos. Está demostrado que el aumento de la reactividad plaquetaria (plaquetas hiperactivas) se observa en una variedad de estados clínicos o genéticos que pueden concluir en acontecimientos trombóticos. Además, el aumento de la función de las plaquetas puede coexistir con alteraciones en el número de éstas en situaciones de trombocitosis o trombocitemia. En este trabajo se realiza una revisión de los aspectos clínicos, fisiopatológicos y de laboratorio relacionados con el síndrome de hiperactividad plaquetaria. También se describe cómo reconocer los aspectos clínicos y el enfoque diagnóstico y terapéutico de la trombocitosis benigna con aumento en el número de plaquetas y de la lesión mieloproliferativa de la trombocitemia.

Palabras clave
Síndrome de hiperactividad de plaquetas, trombocitosis, trombocitemia


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CLINICAL AND LABORATORY APPROACH TO PLATELET HYPERFUNCTION AND INCREASED PLATELET NUMBER

Abstract
Platelets play a critical role in hemostasis, thus alterations of platelet function and number may result in clinical thrombohemorrhagic states. It has become clear that increased platelet reactivity (i.e. hyperactive platelets) can be observed in a variety of genetic and clinical states with resultant thrombotic events. In addition, platelet hyperfunction may co-exist with increased platelet number in the circumstances of thrombocytosis and thrombocythemia. Herein we review the clinical, pathophysiological and laboratory issues related to hyperactive platelet syndrome. In addition, clinical recognition, diagnostic and therapeutic approach to increased platelet number in the benign state of thrombocythosis and the myeloproliferative lesion of thrombocythemia are reviewed.

Key words
Hyperactive platelet syndrome, thrombocythosis, thrombocythemia


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Especialidades
Principal: Hematología
Relacionadas: Bioquímica, Diagnóstico por Laboratorio, Medicina Interna



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Bibliografía del artículo
  1. Heemskerk JW, Bevers EM, Lindhout T. Platelet activation and blood coagulation. Thromb Haemost. 2002; 88:186-93.
  2. Rao AK. Congenital disorders of platelet function: disorders of signal transduction and secretion. Am J Med Sci. 1998; 316:69-76.
  3. White JG, Key NS, King RA et al. The White platelet syndrome: a new autosomal dominant platelet disorder. Platelets. 2004; 15:173-84.
  4. Fujimoto TT, Sora M, Ide K et al. Glanzmann thrombasthenia associated with a 21-amino acid deletion (Leu817-Gln837) in glycoprotein IIb due to abnormal splicing in exon 25. Int J Hematol. 2004; 80:83-90.
  5. Mammen EF, Barnhart MI, Selik NR et al. “Sticky platelet syndrome”: a congenital platelet abnormality predisposing to thrombosis Folia Haematol Int Mag Klin Morphol Blutforsch 1988; 115:361-5.
  6. Mammen EF. Sticky platelet syndrome. Semin Thromb Hemost. 1999; 25:361-5.
  7. Rubenfire M, Blevins RD, Barnhart M et al. Platelet hyperaggregability in patients with chest pain and angiographically normal coronary arteries. Am J Cardiol. 1986; 57:657-60.
  8. Holiday PL, Mammen EF, Gilroy J et al. Sticky platelet syndrome and cerebral infarction in young adults. Ninth Int Joint Conf on Stroke and Cerebral Circulation. Phoenix, AZ; 1983.
  9. Mammen EF. Ten years’ experience with the “sticky platelet syndrome”. Clin Appl Thromb Hemost 1995;1:66-72.
  10. Bick RL. Sticky platelet syndrome: a common cause of unexplained arterial and venous thrombosis. Clin Appl Thromb Hemost 1998; 4:77-81.
  11. Andersen JA. Report: bleeding and thrombosis in women. Biomed Progress 1999; 12:40.
  12. Weber M, Gerdsen F, Gutensohn K, Schoder V et al. Enhanced platelet aggregation with TRAP-6 and collagen in platelet aggregometry in patients with venous thromboembolism. Thromb Res. 2002; 107:325-8.
  13. Michelson AD, Furman MI, Goldschmidt-Clermont P et al. Platelet GP IIIa Pl(A) polymorphisms display different sensitivities to agonists. Circulation. 2000; 101:1013-8.
  14. Feng D, Lindpaintner K, Larson MG et al. Increased platelet aggregability associated with platelet GPIIIa PlA2 polymorphism: the Framingham Offspring Study. Arterioscler Thromb Vasc Biol. 1999; 19:1142-7.
  15. Goodall AH, Curzen N, Panesar M et al. Increased binding of fibrinogen to glycoprotein IIIa-proline33 (HPA-1b, PlA2, Zwb) positive platelets in patients with cardiovascular disease. Eur Heart J. 1999; 20:742-7.
  16. Gardemann A, Humme J, Stricker J et al. Association of the platelet glycoprotein IIIa PlA1/A2 gene polymorphism to coronary artery disease but not to nonfatal myocardial infarction in low risk patients. Thromb Haemost. 1998; 80:214-7.
  17. Mikkelsson J, Perola M, Laippala P et al. Glycoprotein IIIa Pl(A) polymorphism associates with progression of coronary artery disease and with myocardial infarction in an autopsy series of middle-aged men who died suddenly. Arterioscler Thromb Vasc Biol. 1999; 19:2573-8.
  18. Ridker PM, Hennekens CH, Schmitz C et al. PIA1/A2 polymorphism of platelet glycoprotein IIIa and risks of myocardial infarction, stroke, and venous thrombosis. Lancet. 1997; 349:385-8.
  19. Kunicki TJ, Kritzik M, Annis DS et al. Hereditary variation in platelet integrin alpha 2 beta 1 density is associated with two silent polymorphisms in the alpha 2 gene coding sequence. Blood.1997; 89:1939-43.
  20. Santoso S, Kunicki TJ, Kroll H et al. Association of the platelet glycoprotein Ia C807T gene polymorphism with nonfatal myocardial infarction in younger patients. Blood. 1999; 93:2449-53.
  21. Carlsson LE, Santoso S, Spitzer C et al. The alpha2 gene coding sequence T807/A873 of the platelet collagen receptor integrin alpha2beta1 might be a genetic risk factor for the development of stroke in younger patients. Blood. 1999; 93:3583-6.
  22. Von Beckerath N, Koch W, Mehilli J et al. Glycoprotein Ia gene C807T polymorphism and risk for major adverse cardiac events within the first 30 days after coronary artery stenting. Blood. 2000; 95:3297-301.
  23. Morita H, Kurihara H, Imai Y et al. Lack of association between the platelet glycoprotein Ia C807T gene polymorphism and myocardial infarction in Japanese. An approach entailing melting curve analysis with specific fluorescent hybridization probes. Thromb Haemost. 2001; 85:226-30.
  24. Baker RI, Eikelboom J, Lofthouse EY et al. Platelet glycoprotein I b alpha Kozak polymorphism is associated with an increased risk of ischemic stroke. Blood. 2001; 98:36-40.
  25. Hsieh K, Funk M, Schillinger M et al. Vienna Stroke Registry. Impact of the platelet glycoprotein Ib alpha Kozak polymorphism on the risk of ischemic cerebrovascular events: a case-control study. Blood Coagul Fibrinolysis. 2004; 15:469-73.
  26. Yongbin N, Dayi H, Hong YW et al. Association of genetic polymorphisms in the fibrinogen and platelet glycoprotein genes with unstable angina in Chinese patients. Clin Cardiol. 2004; 27:455-8.
  27. Afshar-Kharghan V, Li CQ, Khoshnevis-Asl MJ et al. Kozak sequence polymorphism of the glycoprotein (GP) Ibalpha gene is a major determinant of the plasma membrane levels of the platelet GP Ib-IX-V complex. Blood. 1999; 94:186-91.
  28. Lopez JA, Ludwig EH, McCarthy BJ. Polymorphism of human glycoprotein Ib alpha results from a variable number of tandem repeats of a 13-amino acid sequence in the mucin-like macroglycopeptide region. Structure/function implications. J Biol Chem.1992 May; 267:10055-61.
  29. Fontana P, Dupont A, Gandrille S et al. Adenosine diphosphate-induced platelet aggregation is associated with P2Y12 gene sequence variations in healthy subjects. Circulation. 2003; 108:989-95.
  30. Fontana P, Gaussem P, Aiach M et al. P2Y12 H2 haplotype is associated with peripheral arterial disease: a case-control study.Circulation. 2003; 108:2971-3.
  31. Rand ML, Leung R, Packham MA. Platelet function assays. Transfus Apheresis Sci. 2003; 28:307-17.
  32. Yngen M, Li N, Hjemdahl P, Wallen NH. Insulin enhances platelet activation in vitro. Thromb Res. 2001; 104:85.
  33. Zdrojewski Z, Lizakowski S, Raszeja-Specht A et al. Influence of spontaneous platelet aggregation on progression of glomerular disease. Nephron. 2002; 92:36-42.
  34. Juhan I, Vague P, Buonocore M et al. Effects of insulin on erythrocyte deformability in diabetics--relationship between erythrocyte deformability and platelet aggregation. Scand J Clin Lab Invest Suppl. 1981; 156:159-64.
  35. Cho NH, Becker D, Dorman JS et al. Spontaneous whole blood platelet aggregation in insulin-dependent diabetes mellitus: an evaluation in an epidemiologic study. Thromb Haemost. 1989; 61:127-30.
  36. Mandal S, Sarode R, Dash S et al. Hyperaggregation of platelets detected by whole blood platelet aggregometry in newly diagnosed noninsulin-dependent diabetes mellitus. Am J Clin Pathol. 1993; 100:103-7.
  37. Golanski J, Golanski R, Chizynski K et al. Platelet hyperreactivity after coronary artery bypass grafting: the possible relevance to glycoprotein polymorphisms. A preliminary report. Platelets 2001; 12:241-7.
  38. Heilmann E, Hynes LA, Burstein SA et al. Fluorescein derivatization of fibrinogen for flow cytometric analysis of fibrinogen binding to platelets. Cytometry. 1994 1;17:287-93.
  39. Faraday N, Goldschmidt-Clermont P, Dise K et al. Quantitation of soluble fibrinogen binding to platelets by fluorescence-activated flow cytometry. J Lab Clin Med. 1994; 123:728-40.
  40. Aupeix K, Hugel B, Martin T, Bischoff P et al. The significance of shed membrane particles during programmed cell death in vitro, and in vivo, in HIV-1 infection. J Clin Invest. 1997; 99:1546-54.
  41. Mahla E, Lang T, Vicenzi MN, Werkgartner G et al. Thromboelastography for monitoring prolonged hypercoagulability after major abdominal surgery. Anesth Analg. 2001; 92:572-7.
  42. Pihusch R, Rank A, Gohring P et al. Platelet function rather than plasmatic coagulation explains hypercoagulable state in cholestatic liver disease. J Hepatol. 2002; 37:548-55.
  43. Frossard M, Fuchs I, Leitner JM et al. Platelet function predicts myocardial damage in patients with acute myocardial infarction. Circulation. 2004; 110:1392-7.
  44. Knobler H, Savion N, Shenkman B et al. Shear-induced platelet adhesion and aggregation on subendothelium are increased in diabetic patients. Thromb Res. 1998; 90:181-90.
  45. Eto K, Ochiai M, Isshiki T et al. Platelet aggregability under shear is enhanced in patients with unstable angina pectoris who developed acute myocardial infarction. Jpn Circ J. 2001; 65:279-82.
  46. Hekimsoy Z, Payzin B, Ornek T et al. Mean platelet volume in Type 2 diabetic patients. J Diabetes Complications. 2004; 18:173-6.
  47. Mimidis K, Papadopoulos V, Kotsianidis J et al. Alterations of platelet function, number and indexes during acute pancreatitis. Pancreatology. 2004; 4:22-7.
  48. Bath P, Algert C, Chapman N et al; PROGRESS Collaborative Group. Association of mean platelet volume with risk of stroke among 3134 individuals with history of cerebrovascular disease. Stroke. 2004; 35:622-6.
  49. Collins CE, Cahill MR, Newland AC et al. Platelets circulate in an activated state in inflammatory bowel disease. Gastroenterology. 1994; 106:840-5.
  50. Wallen NH, Held C, Rehnqvist N et al. Effects of mental and physical stress on platelet function in patients with stable angina pectoris and healthy controls. Eur Heart J. 1997; 18:807-15.
  51. Buyukasyk NS, Ileri M, Alper A et al. Increased blood coagulation and platelet activation in patients with infective endocarditis and embolic events. Clin Cardiol. 2004; 27:154-8.
  52. Goette A, Weber M, Lendeckel U et al. Effect of physical exercise on platelet activity and the von-Willebrand-factor in patients with persistent lone atrial fibrillation.J Interv Card Electrophysiol. 2004; 10:139-46.
  53. Born GVR. Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature 1962;194: 927-9.
  54. Jarvis GE. Platelet aggregation in whole blood. Impedance and particle counting methods. In: Methods in molecular biology, vol.272: Platelets and megakaryocytes, Vol. 1: Functional assays, eds. Gibbins JM, Mahaut- Smith MP. Humana Press Inc., 2004, Totowa, NJ ,77-87.
  55. Riess H, Braun G, Brehm G et al. Critical evaluation of platelet aggregation in whole human blood. Am J Clin Pathol. 1986; 85:50-6.
  56. Dyszkiewicz-Korpanty A, Frenkel EP, Sarode R. Approach to the assessment of platelet function: comparison between optical-based platelet-rich plasma and impedance -based whole blood aggregation methods. Clin Appl Thromb Hemost 2004; 10(4): in press.
  57. De La Cruz JP, Paez MV, Carmona JA et al. Antiplatelet effect of the anaesthetic drug propofol: influence of red blood cells and leucocytes.Br J Pharmacol. 1999; 128:1538-44.
  58. Klein B, Faridi A, Von Tempelhoff GF et al. A whole blood flow cytometric determination of platelet activation by unfractionated and low molecular weight heparin in vitro. Thromb Res. 2002; 108:291-6.
  59. Ruf A, Patscheke H. Flow cytometric detection of activated platelets: comparison of determining shape change, fibrinogen binding, and P-selectin expression. Semin Thromb Hemost. 1995; 21:146-51.
  60. Heilmann E, Hynes LA, Burstein SA et al. Fluorescein derivatization of fibrinogen for flow cytometric analysis of fibrinogen binding to platelets . Cytometry 1994; 17:287-293.
  61. Faraday N, Goldshmidt-ClermontP, Dise K et al. Quantitation of soluble fibrinogen binding to platelets by florescence- activated flow cytometry. J Lab Clin Med 1994; 123:728-40.
  62. Michelson AD, Rajasekhar D, Bednarek FJ et al. Platelet and platelet-derived microparticle surface factor V/Va binding in whole blood: differences between neonates and adults. Thromb Haemost. 2000; 84:689-94.
  63. Michelson AD, Barnard MR, Krueger LA et al. Circulating monocyte-platelet aggregates are a more sensitive marker of in vivo platelet activation than platelet surface P-selectin: studies in baboons, human coronary intervention, and human acute myocardial infarction. Circulation. 2001; 104:1533-7.
  64. Furman MI, Barnard MR, Krueger LA et al. Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarction. J Am Coll Cardiol. 2001; 38:1002-6.
  65. Michelson AD, Barnard MR, Krueger LA et al. Flow cytometry. In: Platelets, ed. Michelson AD, Academic Press, Elsevier Science, 2002, San Diego, CA, USA& London, UK, 297-315.
  66. Gum PA, Kottke-Marchant K, Poggio ED et al. Profile and prevalence of aspirin resistance in patients with cardiovascular disease. Am J Cardiol. 2001; 88:230-5.
  67. Gum PA, Kottke-Marchant K, Welsh PA et al. A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease. J Am Coll Cardiol. 2003; 41:961-5.
  68. Alberts MJ, Bergman DL, Molner E et al. Antiplatelet effect of aspirin in patients with cerebrovascular disease. Stroke. 2004 ; 35:175-8.
  69. Gurbel PA, Bliden KP, Hiatt BL et al. Clopidogrel for coronary stenting: response variability, drug resistance, and the effect of pretreatment platelet reactivity. Circulation. 2003; 107:2908-13.
  70. Lau WC, Gurbel PA, Watkins PB et al. Contribution of hepatic cytochrome P450 3A4 metabolic activity to the phenomenon of clopidogrel resistance. Circulation. 2004; 109:166-71.
  71. Undas A, Brummel K, Musial J et al. Pl(A2) polymorphism of beta(3) integrins is associated with enhanced thrombin generation and impaired antithrombotic action of aspirin at the site of microvascular injury. Circulation. 2001; 104:2666-72.
  72. Dropinski J, Sanak M, Wegrzyn W et al. Platelet glycoprotein IIIa polymorphism and complementary actions of aspirin and clopidogrel in coronary artery disease. In: Proceedings in coronary artery disease. Ed. Monduzzi, Medimond Inc, Florence, Italy, 2003, 515-19.
  73. Angiolillo DJ, Fernandez-Ortiz A, Bernardo E et al. PlA polymorphism and platelet reactivity following clopidogrel loading dose in patients undergoing coronary stent implantation.Blood Coagul Fibrinolysis. 2004; 15:89-93.
  74. Mukherjee D, Topol EJ. Pharmacogenomics in cardiovascular diseases. Curr Probl Cardiol. 2003; 28:317-47.
  75. Frenkel EP, Bick RL. Prothrombin G20210A gene mutation, heparin cofactor II defects, primary (essential) thrombocythemia, and thrombohemorrhagic manifestations. Semin Thromb Hemost. 1999; 25:375-86.
  76. Frenkel EP, Mammen EF. Sticky platelet syndrome and thrombocythemia. Hematol Oncol Clin North Am. 2003; 17:63-83.
  77. Schafer AI. Thrombocytosis. N Engl J Med. 2004; 350:1211-9.
  78. Frenkel EP. The clinical spectrum of thrombocytosis and thrombocythemia. Am J Med Sci. 1991; 301:69-80.
  79. Vardiman JB, Harris NL. Chronic myeloproliferative diseases: Introduction, In Pathology and genetics of tumours of haematopoietic and lymphoid tissues, H.N. Jaffe ES, Stein H, Vardiman JW, Editor. 2001, IARC Press: Lyon, 17-19.
  80. Ruggeri M, Tosetto A, Frezzato M et al. The rate of progression to polycythemia vera or essential thrombocythemia in patients with erythrocytosis or thrombocytosis. Ann Intern Med. 2003; 139:470-5.
  81. Kaushansky K. Regulation of megakaryopoiesis, In Thrombosis and hemorrhage, S. AI, Editor. 2003, Williams & Wilkins: Philadelphia, USA, 120-139.
  82. Wang JC, Chen C, Novetsky AD et al. Blood thrombopoietin levels in clonal thrombocytosis and reactive thrombocytosis. Am J Med, 1998. 104:451-5.
  83. Hsu HC, Tsai WH, Jiang ML et al. Circulating levels of thrombopoietic and inflammatory cytokines in patients with clonal and reactive thrombocytosis. J Lab Clin Med, 1999; 134:392-7.
  84. Folman CC, Ooms M, Kuenen BB et al. The role of thrombopoietin in post-operative thrombocytosis. Br J Haematol, 2001; 114:126-33.
  85. Ishiguro A, Suzuki Y, Mito M et al. Elevation of serum thrombopoietin precedes thrombocytosis in acute infections. Br J Haematol. 2002; 116:612-8.
  86. Kaser A, Brandacher G, Steurer W et al. Interleukin-6 stimulates thrombopoiesis through thrombopoietin: role in inflammatory thrombocytosis. Blood. 2001; 98:2720-5.
  87. Wolber EM, Fandrey J, Frackowski U et al. Hepatic thrombopoietin mRNA is increased in acute inflammation. Thromb Haemost. 2001; 86:1421-4.
  88. Espanol I, Hernandez A, Cortes M et al. Patients with thrombocytosis have normal or slightly elevated thrombopoietin levels. Haematologica. 1999; 84:312-6.
  89. Marta R, Goette N, Lev P et al. Increased levels of plasma interleukin-6 soluble receptor in patients with essential thrombocythemia. Haematologica. 2004; 89:657-63.
  90. Horikawa Y, Matsumura I, Hashimoto K et al. Markedly reduced expression of platelet c-mpl receptor in essential thrombocythemia. Blood 1997;90:4031-8.
  91. Li J, Xia Y, Kuter DJ. The platelet thrombopoietin receptor number and function are markedly decreased in patients with essential thrombocythaemia. Br J Haematol. 2000; 111:943-53.
  92. Mesa RA, Hanson CA, Li CY et al. Diagnostic and prognostic value of bone marrow angiogenesis and megakaryocyte c-Mpl expression in essential thrombocythemia. Blood. 2002; 99:4131-7.
  93. Teofili L, Pierconti F, Di Febo A et al. The expression pattern of c-mpl in megakaryocytes correlates with thrombotic risk in essential thrombocythemia. Blood. 2002. 100:714-7.
  94. Axelrad AA, Eskinazi D, Correa PN et al. Hypersensitivity of circulating progenitor cells to megakaryocyte growth and development factor (PEG-rHu MGDF) in essential thrombocythemia. Blood. 2000. 96:3310-21.
  95. Kuroda H, Matsunaga T, Terui T et al. Decrease of Smad4 gene expression in patients with essential thrombocythaemia may cause an escape from suppression of megakaryopoiesis by transforming growth factor-beta1. Br J Haematol. 2004. 124:211-20.
  96. Michiels JJ, Juvonen E. Proposal for revised diagnostic criteria of essential thrombocythemia and polycythemia vera by the Thrombocythemia Vera Study Group. Semin Thromb Hemost. 1997; 23:339-47.
  97. Imbert MP, Thiele R, Vardiman J et al. Essential thrombocythaemia, in pathology and genetics of tumours of haematopoietic and lymphoid tissues, Eds. Jaffe ES, Stein H, Vardiman JW, 2001, IARC Press: Lyon, 39-41.
  98. Laszlo J. Myeloproliferative disorders (MPD): myelofibrosis, myelosclerosis, extramedullary hematopoiesis, undifferentiated MPD, and hemorrhagic thrombocythemia. Semin Hematol. 1975;12:409-32.
  99. Iland HJ, Laszlo J, Peterson P et al. Essential thrombocythemia: clinical and laboratory characteristics at presentation. Trans Assoc Am Physicians.1983; 96:165-74.
  100. Iland HJ, Laszlo J, Case DC Jr. et al. Differentiation between essential thrombocythemia and polycythemia vera with marked thrombocytosis. Am J Hematol. 1987;25:191-201.
  101. Gilbert HS. Diagnosis and treatment of thrombocythemia in myeloproliferative disorders. Oncology (Huntingt). 2001;15: 989-96, 998; discussion 999-1000, 1006, 1008.
  102. Murphy S. Thrombocytosis and thrombocythaemia. Clin Haematol. 1983;12:89-106.
  103. Schafer AI. Bleeding and thrombosis in the myeloproliferative disorders. Blood. 1984;64:1-12.
  104. Schilling RF. Platelet millionaires. Lancet.1980; 2:372-3.
  105. Hoagland HC and Silverstein MN. Primary thrombocythemia in the young patient. Mayo Clin Proc. 1978;53:578-80.
  106. Griesshammer M, Klippel S, Strunck E et al. PRV-1 mRNA expression discriminates two types of essential thrombocythemia. Ann Hematol. 2004;83:364-70.
  107. Klippel S, Strunck E, Temerinac S et al. Quantification of PRV-1 mRNA distinguishes polycythemia vera from secondary erythrocytosis. Blood. 2003; 102:3569-74.
  108. Klippel S, Strunck E, Busse CE et al. Biochemical characterization of PRV-1, a novel hematopoietic cell surface receptor, which is overexpressed in polycythemia rubra vera. Blood. 2002; 100:2441-8.
  109. Cilloni D, Carturan S, Gottardi E et al. Usefulness of the quantitative assessment of PRV-1 gene expression for the diagnosis of polycythemia vera and essential thrombocythemia patients. Blood. 2004;103: 2428; author reply 2429.
  110. Tefferi A., T.L. Lasho, A.P. Wolanskyj et al. Neutrophil PRV-1 expression across the chronic myeloproliferative disorders and in secondary or spurious polycythemia. Blood. 2004;103: 3547-8.
  111. Temerinac S., S. Klippel, E. Strunck et al. Cloning of PRV-1, a novel member of the uPAR receptor superfamily, which is overexpressed in polycythemia rubra vera. Blood. 2000; 95:2569-76.
  112. Palmqvist L, Goerttler P, Wasslavik C et al. Comparison of methods for polycythemia rubra vera-1 mRNA quantification in whole-blood leukocytes and purified granulocytes. Clin Chem.2004; 50:644-7.
  113. Liu E, Jelinek J, Pastore YD et al. Discrimination of polycythemias and thrombocytoses by novel, simple, accurate clonality assays and comparison with PRV-1 expression and BFU-E response to erythropoietin. Blood. 2003; 101:3294-301.
  114. Florensa L, Besses C, Zamora L et al. Endogenous erythroid and megakaryocytic circulating progenitors, HUMARA clonality assay, and PRV-1 expression are useful tools for diagnosis of polycythemia vera and essential thrombocythemia. Blood. 2004; 103:2427-8.
  115. Mesa RA, Silverstein MN, Jacobsen SJ et al. Population-based incidence and survival figures in essential thrombocythemia and agnogenic myeloid metaplasia: an Olmsted County Study, 1976-1995. Am J Hematol. 1999; 61:10-5.
  116. McIntyre KJ, Hoagland HC, Silverstein MN et al. Essential thrombocythemia in young adults. Mayo Clin Proc.1991; 66:149-54.
  117. Murphy S, Iland H, Rosenthal D et al. Essential thrombocythemia: an interim report from the Polycythemia Vera Study Group. Semin Hematol. 1986; 23:177-82.
  118. Randi ML, Putti MC, Fabris F et al. Features of essential thrombocythaemia in childhood: a study of five children. Br J Haematol. 2000; 108:86-9.
  119. Van Genderen PJ and Michiels JJ. Erythromelalgia: a pathognomonic microvascular thrombotic complication in essential thrombocythemia and polycythemia vera. Semin Thromb Hemost 1997; 23:357-63.
  120. Michiels JJ, Abels J, Steketee J et al. Erythromelalgia caused by platelet-mediated arteriolar inflammation and thrombosis in thrombocythemia. Ann Intern Med, 1985; 102:466-71.
  121. Michiels JJ, Ten Kate FW, Vuzevski VD et al. Histopathology of erythromelalgia in thrombocythaemia. Histopathology.1984; 8:669-78.
  122. Griesshammer M, Bangerter M, Van Vliet HH et al. Aspirin in essential thrombocythemia: status quo and quo vadis. Semin Thromb Hemost. 1997; 23:371-7.
  123. Schroer K. Aspirin and platelets: the antiplatelet action of aspirin and its role in thrombosis treatment and prophylaxis. Semin Thromb Hemost.1997; 3:349-356.
  124. Preston FE, Emmanuel IG, Winfield DA et al. Essential thrombocythaemia and peripheral gangrene. Br Med J.1974; 3:48-52.
  125. Bellucci S, Janvier M, Tobelem G et al. Essential thrombocythemias. Clinical evolutionary and biological data. Cancer.1986; 8:2440-7.
  126. Murphy S, Peterson P, Iland H et al. Experience of the Polycythemia Vera Study Group with essential thrombocythemia: a final report on diagnostic criteria, survival, and leukemic transition by treatment. Semin Hematol. 1997; 34:29-39.
  127. Pearson TC. Primary thrombocythaemia: diagnosis and management. Br J Haematol. 1991; 78:145-8.
  128. Jantunen R, Juvonen E, Ikkala E et al. Essential thrombocythemiadiagnosis: causes of diagnostic evaluation and presence of positive diagnostic findings. Ann Hematol. 1998;77:101-6.
  129. Koudstaal PJ and Koudstaal A. Neurologic and visual symptoms in essential thrombocythemia: efficacy of low-dose aspirin. Semin Thromb Hemost. 1997;23:365-70.
  130. Budde U and Van Genderen PJ. Acquired von Willebrand disease in patients with high platelet counts. Semin Thromb Hemost. 1997; 23:425-31.
  131. Kondo T, Okabe M, Sanada M et al. Familial essential thrombocythemia associated with one-base deletion in the 5’-untranslated region of the thrombopoietin gene. Blood. 1998; 92:1091-6.
  132. Murphy S. Diagnostic criteria and prognosis in polycythemia vera and essential thrombocythemia. Semin Hematol. 1999;36(Suppl 2):9-13.
  133. Wehmeier A, Sudhoff T and Meierkord F. Relation of platelet abnormalities to thrombosis and hemorrhage in chronic myeloproliferative disorders. Semin Thromb Hemost. 1997; 23:391-402.
  134. Cincotta R, Higgins JR, Tippett C et al. Management of essential thrombocythaemia during pregnancy. Aust N Z J Obstet Gynaecol. 2000;40:33-7.
  135. Falconer J, Pineo G, Blahey W et al. Essential thrombocythemia associated with recurrent abortions and fetal growth retardation. Am J Hematol. 1987; 25:345-7.
  136. Mercer B, Drouin J, Jolly E et al. Primary thrombocythemia in pregnancy: a report of two cases. Am J Obstet Gynecol. 1988;159:127-8.
  137. Snethlage W and Ten Cate JW. Thrombocythaemia and recurrent late abortions: normal outcome of pregnancies after antiaggregatory treatment. Case report. Br J Obstet Gynaecol. 1986;93:386-8.
  138. Ding J, Komatsu H, Wakita A et al. Familial essential thrombocythemia associated with a dominant-positive activating mutation of the c-MPL gene, which encodes for the receptor for thrombopoietin. Blood. 2004; 103:4198-200.
  139. Cortelazzo S, Viero P, Finazzi G et al. Incidence and risk factors for thrombotic complications in a historical cohort of 100 patients with essential thrombocythemia. J Clin Oncol. 1990; 8:556-62.
  140. Cortelazzo S, Finazzi G, Ruggeri M et al. Hydroxyurea for patients with essential thrombocythemia and a high risk of thrombosis. N Engl J Med. 1995; 332:1132-6.
  141. Landolfi R, Marchioli R and Patrono C. Mechanisms of bleeding and thrombosis in myeloproliferative disorders. Thromb Haemost. 1997; 78:617-21.
  142. Schafer AI. Management of thrombocythemia. Curr Opin Hematol. 1996;3:341-6.
  143. Regev A, Stark P, Blickstein D et al. Thrombotic complications in essential thrombocythemia with relatively low platelet counts. Am J Hematol. 1997;56:168-72.
  144. Frenkel EP. The clinical spectrum of thrombocytosis and thrombocythemia. In: University of Texas Southwestern Medical Center Internal Medicine Grand Rounds. 1990. Dallas, TX.
  145. Frenkel EP. Polycythemia vera, myelofibrosis, and primary (essential) thrombocythemia. In: Medical Oncology: Basic Principles and Clinical Management, Ed. P.S. Calabresse,1993, McGraw Hill: New York, USA, 503-515.
  146. Frenkel EP. Myeloproliferative disorders: Polycythemia vera, thrombocythemia and myelofibrosis, in Textbook of Internal Medicine, W. Kelly, Editor. 1997, Lippincott-Raven: Philadelphia, USA, 1388-1392.
  147. Ravandi-Kashani F and Schafer AI. Microvascular disturbances, thrombosis, and bleeding in thrombocythemia: current concepts and perspectives. Semin Thromb Hemost. 1997;23:479-88.
  148. Manoharan A, Gemmell R, Brighton T et al. Thrombosis and bleeding in myeloproliferative disorders: identification of at-risk patients with whole blood platelet aggregation studies. Br J Haematol.1999;105:618-25.
  149. Sacher RA, Jacobson RJ and McGill M. Functional and morphological studies of platelet reactivity with vessel wall subendothelium in chronic myeloproliferative disease. Br J Haematol, 1981;49:43-52.
  150. Boughton BJ, Allington MJ and King A. Platelet and plasma beta thromboglobulin in myeloproliferative syndromes and secondary thrombocytosis. Br J Haematol. 1978; 40:125-32.
  151. Wehmeier A, Fricke S, Scharf RE et al. A prospective study of haemostatic parameters in relation to the clinical course of myeloproliferative disorders. Eur J Haematol 1990; 45:191-7.
  152. Wu K. Platelet hyperaggregability and thrombosis in patients with thrombocythemia. Ann Intern Med. 1978; 88:7-11.
  153. Bellucci S, Ignatova E, Jaillet N et al. Platelet hyperactivation in patients with essential thrombocythemia is not associated with vascular endothelial cell damage as judged by the level of plasma thrombomodulin, protein S, PAI-1, t-PA and vWF. Thromb Haemost. 1993; 70:736-42.
  154. Gisslinger H, Rodeghiero F, Ruggeri M et al. Homocysteine levels in polycythaemia vera and essential thrombocythaemia. Br J Haematol. 1999; 105:551-5.
  155. Fiedler W, Henke RP, Ergun S et al. Derivation of a new hematopoietic cell line with endothelial features from a patient with transformed myeloproliferative syndrome: a case report. Cancer. 2000; 88:344-51.
  156. Mesa RA, Hanson CA, Rajkumar SV et al. Evaluation and clinical correlations of bone marrow angiogenesis in myelofibrosis with myeloid metaplasia. Blood. 2000;96:3374-80.
  157. Verheul HM, Jorna AS, Hoekman K et al. Vascular endothelial growth factor-stimulated endothelial cells promote adhesion and activation of platelets. Blood. 2000;96:4216-21.
  158. Usuki K, Iki S, Endo M et al. Influence of thrombopoietin on platelet activation in myeloproliferative disorders. Br J Haematol. 1997; 97:530-7.
  159. Cacciola RR, Di Francesco E, Ferlito C et al. Vascular endothelial growth factor and thrombopoietin in patients with essential thrombocythemia and polycythemia vera and thrombotic complications. Acta Haematol. 2003; 110:202-3.
  160. Kornblihtt LI, Heller PG, Correa G et al. Associated thrombophilic defects in essential thrombocythaemia: their relationship with clinical manifestations. Thromb Res. 2003; 112:131-5.
  161. Barbui T and Finazzi G. Clinical parameters for determining when and when not to treat essential thrombocythemia. Semin Hematol. 1999;36 (1 Suppl 2):14-8.
  162. Bazzan M, Tamponi G, Schinco P et al. Thrombosis-free survival and life expectancy in 187 consecutive patients with essential thrombocythemia. Ann Hematol. 1999;78:539-43.
  163. Michiels JJ. Normal life expectancy and thrombosis-free survival in aspirin treated essential thrombocythemia. Clin Appl Thromb Hemost. 1999; 5:30-6.
  164. Rozman C, Giralt M, Feliu E et al. Life expectancy of patients with chronic nonleukemic myeloproliferative disorders. Cancer. 1991; 67:2658-63.
  165. Finazzi G, Ruggeri M, Rodeghiero F et al. Second malignancies in patients with essential thrombocythaemia treated with busulphan and hydroxyurea: long-term follow-up of a randomized clinical trial. Br J Haematol. 2000;110:577-83.
  166. Randi ML, Rossi C, Fabris F et al. Aspirin seems as effective as myelosuppressive agents in the prevention of rethrombosis in essential thrombocythemia. Clin Appl Thromb Hemost. 1999; 5:131-5.
  167. Pearson TC, Bareford D, Craig J et al. The management of “low-risk” and “intermediate-risk” patients with primary thrombocythaemia. MPD (UK) Study Group. Br J Haematol. 1999; 106:833-4.
  168. Ruggeri M, Finazzi G, Tosetto A et al. No treatment for low-risk thrombocythaemia: results from a prospective study. Br J Haematol. 1998; 103:772-7.
  169. Tefferi A. Risk-based management in essential thrombocythemia. In: The American Society of Hematology Education Program Book, Eds. GH Schechter, R Schrier, SL,1999, The American Society of Hematology: New Orleans, USA, 172-177.
  170. Johansson P, Ricksten A, Wennstrom L et al. Increased risk for vascular complications in PRV-1 positive patients with essential thrombocythaemia. Br J Haematol. 2003; 123:513-6.
  171. Millard FE, Hunter CS, Anderson M et al. Clinical manifestations of essential thrombocythemia in young adults. Am J Hematol. 1990; 33:27-31.
  172. Sterkers Y, Preudhomme C, Lai JL et al. Acute myeloid leukemia and myelodysplastic syndromes following essential thrombocythemia treated with hydroxyurea: high proportion of cases with 17p deletion. Blood. 1998; 91:616-22.
  173. De Bergsagel DE, Frenkel EP, Alfrey CP Jr. et al. Megaloblastic Erythropoiesis Induced by Hydroxyurea (Nsc-32065). Cancer Chemother Rep, 1964; 40:15-7.
  174. Frenkel EP, Skinner WN and Smiley JD. Studies on a Metabolic Defect Induced by Hydroxyurea (Nsc-32065). Cancer Chemother Rep.1964; 40:19-22.
  175. Frenkel EP and Arthur C. Induced ribotide reductive conversion defect by hydroxyurea and its relationship to megaloblastosis. Cancer Res. 1967; 27:1016-9.
  176. Van den Anker-Lugtenburg PJ and Sizoo W. Myelodysplastic syndrome and secondary acute leukemia after treatment of essential thrombocythemia with hydroxyurea. Am J Hematol. 1990;33:152.
  177. Finazzi G, Ruggeri M, Rodeghiero F et al. Efficacy and safety of long-term use of hydroxyurea in young patients with essential thrombocythemia and a high risk of thrombosis. Blood. 2003;101:3749.
  178. Fenaux P, Simon M, Caulier MT et al. Clinical course of essential thrombocythemia in 147 cases. Cancer. 1990; 66:549-56.
  179. Hehlmann R, Jahn M, Baumann B et al. Essential thrombocythemia. Clinical characteristics and course of 61 cases. Cancer. 1988; 61:2487-96.
  180. Chott A, Gisslinger H, Thiele J et al. Interferon-alpha-induced morphological changes of megakaryocytes: a histomorphometrical study on bone marrow biopsies in chronic myeloproliferative disorders with excessive thrombocytosis. Br J Haematol. 1990; 74:10-16.
  181. Elliott MA and Tefferi A. Interferon-alpha therapy in polycythemia vera and essential thrombocythemia. Semin Thromb Hemost. 1997; 23:463-72.
  182. Giles FJ, Singer CR, Gray AG et al. Alpha-interferon therapy for essential thrombocythaemia. Lancet.1988; 2:70-2.
  183. Gisslinger H, Ludwig H, Linkesch W et al. Long-term interferon therapy for thrombocytosis in myeloproliferative diseases. Lancet. 1989. 1(8639):634-7.
  184. Petit JJ, Callis M and Fernandez de Sevilla A. Normal pregnancy in a patient with essential thrombocythemia treated with interferon-alpha 2b. Am J Hematol. 1992; 40:80.
  185. Silver RT. Interferon in the treatment of myeloproliferative diseases. Semin Hematol 1990; 27(3 Suppl 4):6-14.
  186. Gillespie E. Anagrelide: a potent and selective inhibitor of platelet cyclic AMP phosphodiesterase enzyme activity. Biochem Pharmacol. 1988; 37:2866-8.
  187. Abe Andes W, Noveck RJ and Fleming JS. Inhibition of platelet production induced by an antiplatelet drug, anagrelide, in normal volunteers. Thromb Haemost. 1984; 52:325-8.
  188. Anagrelide Study Group. Anagrelide, a therapy for thrombocythemic states: experience in 577 patients. Am J Med. 1992; 92:69-76.
  189. Pescatore SL and Lindley C. Anagrelide: a novel agent for the treatment of myeloproliferative disorders. Expert Opin Pharmacother. 2000; 1:537-46.
  190. Silverstein MN, Petitt RM, Solberg LA Jr. et al. Anagrelide: a new drug for treating thrombocytosis. N Engl J Med. 1988;318:1292-4.
  191. Solberg LA Jr, Tefferi A, Oles KJ et al. The effects of anagrelide on human megakaryocytopoiesis. Br J Haematol. 1997; 99:174-80.
  192. Tefferi A, Silverstein MN, Petitt RM et al. Anagrelide as a new platelet-lowering agent in essential thrombocythemia: mechanism of actin, efficacy, toxicity, current indications. Semin Thromb Hemost. 1997; 23:379-83.
  193. Thiele J, Kvasnicka HM, Fuchs N et al. Anagrelide-induced bone marrow changes during therapy of chronic myeloproliferative disorders with thrombocytosis. an immunohistochemical and morphometric study of sequential trephine biopsies. Haematologica 2003; 88:1130-8.
  194. Birgegard G, Bjorkholm M, Kutti J et al. Adverse effects and benefits of two years of anagrelide treatment for thrombocythemia in chronic myeloproliferative disorders. Haematologica. 2004;89:520-527.
  195. Storen EC, Tefferi A. Long-term use of anagrelide in young patients with essential thrombocythemia. Blood. 2001; 97:863-6.
 
 
 
 
 
 
 
 
 
 
 
 
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