REFERENCES
1. Gross S, Keefer V, Newman AJ. The Platelets in Iron-Deficiency Anemia. I. The Response to Oral and Parenteral Iron. Pediatrics 1964;34:315-23.
2. Wang JL, Huang LT, Wu KH, Lin HW, Ho MY, Liu HE. Associations of reactive thrombocytosis with clinical characteristics in pediatric diseases. Pediatr Neonatol 2011;52:261-6.
3. Nelson ND, Marcogliese A, Bergstrom K, Scheurer M, Mahoney D, Bertuch AA. Thrombopoietin Measurement as a Key Component in the Evaluation of Pediatric Thrombocytosis. Pediatr Blood Cancer 2016;63:1484-7.
4. Kucine N, Viny AD, Rampal R, et al. Genetic analysis of five children with essential thrombocytosis identified mutations in cancer-associated genes with roles in transcriptional regulation. Haematologica 2016;101:e237-9.
5. Westwick J, Watson-Williams EJ, Krishnamurthi S, et al. Platelet activation during steady state sickle cell disease. J Med 1983;14:17-36.
6. Eder AF, Yau YY, West K. The effect of iron balance on platelet counts in blood donors. Transfusion 2017;57:304-12.
7. Ganti AK, Moazzam N, Laroia S, Tendulkar K, Potti A, Mehdi SA. Predictive value of absent bone marrow iron stores in the clinical diagnosis of iron deficiency anemia. In Vivo 2003;17:389-92.
8. Rumi E, Pietra D, Ferretti V, et al. JAK2 or CALR mutation status defines subtypes of essential thrombocythemia with substantially different clinical course and outcomes. Blood 2014;123:1544-51.
9. Nangalia J, Massie CE, Baxter EJ, et al. Somatic CALR mutations in myeloproliferative neoplasms with nonmutated JAK2. N Engl J Med 2013;369:2391-405.
10. Tefferi A, Lasho TL, Abdel-Wahab O, et al. IDH1 and IDH2 mutation studies in 1473 patients with chronic-, fibrotic- or blast-phase essential thrombocythemia, polycythemia vera or myelofibrosis. Leukemia 2010;24:1302-9.
11. McNamara CJ, Panzarella T, Kennedy JA, et al. The mutational landscape of accelerated- and blast-phase myeloproliferative neoplasms impacts patient outcomes. Blood Adv 2018;2:2658-71.
12. Lin CC, Hou HA, Chou WC, et al. SF3B1 mutations in patients with myelodysplastic syndromes: the mutation is stable during disease evolution. Am J Hematol 2014;89:E109-15.
13. McClure RF, Ewalt MD, Crow J, et al. Clinical Significance of DNA Variants in Chronic Myeloid Neoplasms: A Report of the Association for Molecular Pathology. J Mol Diagn 2018;20:717-37.
14. 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.
15. Budde U, van Genderen PJ. Acquired von Willebrand disease in patients with high platelet counts. Semin Thromb Hemost 1997;23:425-31.
16. Lancellotti S, Dragani A, Ranalli P, et al. Qualitative and quantitative modifications of von Willebrand factor in patients with essential thrombocythemia and controlled platelet count. J Thromb Haemost 2015;13:1226-37.
17. Bodo I, Eikenboom J, Montgomery R, et al. Platelet-dependent von Willebrand factor activity. Nomenclature and methodology: communication from the SSC of the ISTH. J Thromb Haemost 2015;13:1345-50.
18. Flood VH, Gill JC, Morateck PA, et al. Common VWF exon 28 polymorphisms in African Americans affecting the VWF activity assay by ristocetin cofactor. Blood 2010;116:280-6.
19. The Diagnosis, Evaluation, and Management of von Willebrand Disease2007 December 2007. Report No.: NIH Publication No. 08-5832.
20. Nichols WL, Hultin MB, James AH, et al. von Willebrand disease (VWD): evidence-based diagnosis and management guidelines, the National Heart, Lung, and Blood Institute (NHLBI) Expert Panel report (USA). Haemophilia 2008;14:171-232.