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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvOTU2ODA2LW92ZXJ2aWV3\nDrugs & Diseases > Pediatrics: General Medicine\nPediatric Myelofibrosis\nAuthor: Trisha Simone Tavares, MD, FAAP; Chief Editor: Robert J Arceci, MD, PhD more...\nSections Pediatric Myelofibrosis\nApproach Considerations\nBone Marrow Aspirate and Biopsy\nSupportive Care and Monitoring\nHematopoietic Stem Cell Transplantation\nVitamin D Analogs\nMyelofibrosis (bone marrow fibrosis) is characterized by the presence of excessive collagen and reticulin fibers in bone marrow. In most patients, it arises secondary to other disease processes. Pediatric myelofibrosis is uncommon; much of what is known about it is extrapolated from the adult literature or reported from isolated cases in children. See the image below.\nPhotomicrograph of a peripheral smear of a patient with agnogenic myeloid metaplasia (idiopathic myelofibrosis) shows findings of leukoerythroblastosis, giant platelets, and few teardrop cells.\nPatients with a condition predisposing to myelofibrosis present with a history of that disease. There may be a family history or a history of exposure to ionizing radiation. A detailed family history may identify an affected relative.\nClinical symptoms may be mild; some patients are asymptomatic at presentation. Manifestations of disease may include, but are not limited to, the following:\nPallor (anemia)\nBruising, petechiae, or bleeding (thrombocytopenia)\nBone pain\nLeft upper quadrant pain\nSplenomegaly (frequent), hepatomegaly, or lymphadenopathy [1]\nStigmata of a predisposing condition\nSee Presentation for more detail.\nLaboratory testing may include the following:\nEvaluation for peripheral blood abnormalities (eg, normocytic anemia, thrombocytopenia, or leukocytosis with left shift)\nEndocrinologic testing (eg, hyper- or hypoparathyroidism)\nRheumatologic evaluation\nBlood urea nitrogen (BUN) and creatinine testing (to rule out renal dysfunction)\nCoombs (direct antiglobulin) test\nPurified protein derivative (PPD) test\nChromosomal analysis in any child with onset before age 2 years\nThe following imaging studies may be helpful:\nAbdominal ultrasonography\nAbdominal computed tomography (CT)\nPositron emission tomography (PET)\nOther studies include the following:\nBone marrow aspiration and biopsy\nCytogenetic analysis (to exclude other myeloid neoplasms)\nSee Workup for more detail.\nWhen secondary childhood myelofibrosis is identified, treatment should be directed at the underlying process.\nSupportive care of myelofibrosis typically includes the following:\nTransfusions (red blood cells [RBCs] or platelets)\nProphylaxis against opportunistic infections in some patients with neutropenia\nAggressive treatment of fever and suspected infections\nIntravenous immunoglobulin and bisphosphonates in selected cases\nMedications that may be helpful include the following:\nThalidomide and lenalidomide\nJanus kinase inhibitors (eg, ruxolitinib)\nOther treatment measures that may be considered include the following:\nSee Treatment and Medication for more detail.\nBone marrow fibrosis, known as myelofibrosis, was originally described in 1879 and is characterized by the presence of excessive collagen and reticulin fibers in bone marrow. This is an uncommon condition in children, and much of what is known is extrapolated from the adult literature or reported from isolated pediatric cases.\nIn most patients, the condition arises secondary to other disease processes. [2] In particular, myelofibrosis is frequently associated with malignancy (eg, acute megakaryoblastic leukemia [AMKL]). (See Clinical and Workup.)\nMyelofibrosis may be observed prior to a clear diagnosis of acute leukemia [3] at the time of diagnosis of leukemia, [4] or as a late event in patients previously treated for leukemia. Numerous nonmalignant conditions have also been reported in association with myelofibrosis. (See Treatment.)\nImportantly, primary or idiopathic myelofibrosis (IMF) is also described. [5, 6, 7]\nNote the image below.\nPatients can be expected to develop complications secondary to decreased production of functional white blood cells (infection), decreased numbers of red blood cells (anemia), and decreased numbers of platelets (bleeding).\nSplenomegaly may lead to hypersplenism, thereby worsening cytopenias.\nThere is an increased risk of myelodysplasia and myeloid leukemia.\nA single case report described subcutaneous lymphoma arising in a child with IMF. [8]\nSee Prognosis.\nEarly onset myelofibrosis is occasionally inherited in a recessive pattern. Counsel parents about the possibility of a second affected child.\nIn normal marrow, the fine fibrous collagen network is faintly perceptible after conventional staining techniques with silver impregnation. Although not unique to this condition, increased staining is a hallmark of myelofibrosis.\nThe fibrous network observed in myelofibrosis is collagenous. Collagen types I, III, IV, and V are increased, with the most significant increased noted in type III. Fibrosis of the bone marrow presumably reflects overgrowth of the normal marrow matrix. [9] This can be observed in association with several diseases and has even been reported to have prognostic significance in childhood acute lymphoblastic leukemia. [10] Overgrowth has been shown to be related to the secretion of profibrotic cytokines and myeloproliferative growth factors. [11]\nIn cases of acute myelofibrosis of childhood (C-AMF), myelofibrosis may be secondary to the release of granules by abnormal megakaryocytes. In addition to platelet-derived growth factor (PDGF), these granules contain transforming growth factor-beta (TGF-b) and epidermal growth factor (EGF), both of which can stimulate proliferation of fibroblasts. TGF-b synthesis appears to be regulated by nuclear factor kappaB (NF-kB). Interestingly, the overexpression of an immunophilin, FK506-binding protein 51, has been observed in myelofibrosis megakaryocytes, and this protein appears, in turn, to activate NF-kB. [12]\nMatrix homeostasis results from a balance between the deposition of the matrix and its removal. The former is regulated by various growth factors, most notably PDGF, whereas the latter presumably reflects the activity of collagenase-expressing monocytes, macrophages, and granulocytes. Thus, the diseases associated with myelofibrosis can be classified according to whether the basic defect is matrix overproduction, underresorption, or both.\nMarrow blood flow and microvessel density are also increased in patients with myelofibrosis, most likely due to an increase in circulating endothelial cell progenitors.\nSome investigators believe that the abnormal fibrotic marrow stroma directly enhances the circulation and dissemination of hematopoietic precursors. [13] This leads to extramedullary hematopoiesis in the liver, spleen, lymph nodes, or (occasionally) kidneys, causing myeloid metaplasia in these organs, which then become enlarged. Hypersplenism, if present, exacerbates cytopenias.\nThe gain-of-function V617F mutation in the Janus kinase 2 (JAK2) gene (on 9p) is seen in many adult patients with IMF. [14] Its presence correlates with a shift from thrombopoiesis toward increased erythropoiesis and may also predict progression to massive splenomegaly and leukemic transformation. [15, 16]\nAmong adults with IMF, conventional cytogenetic analysis of the marrow reveals an abnormal clone in approximately one third of patients. Using a comparative genomic hybridization technique, Al-Assar et al studied IMF marrow specimens and found chromosomal imbalances in 21 of 25 cases. [17] Gains of 9p, 13q, 2q, 3p, and 12q were among the most commonly seen abnormalities. Isolated del(20q) or del(13q) appears to confer a better prognosis. All other abnormalities confer an independent adverse effect on survival and are also associated with higher JAK2V617F mutational frequency. [18]\nA study by Livun et al suggested that in primary myelofibrosis, several genes related to bone marrow homeostasis are aberrantly expressed, with the investigators finding upregulation of cyclo-oxygenase 2 (COX2) and down-regulation of chemokine (C-X-C motif) receptor 4 (CXCR4), paired box 5 (PAX5) C-terminus, and hypoxia inducible factor 1A (HIF1A). [19]\nPredisposing conditions\nClassification of myelofibrosis includes the following: primary (idiopathic) C-AMF, secondary (malignant) C-AMF, and secondary (nonmalignant) C-AMF.\nCauses of secondary (malignant) C-AMF include:\nAcute erythroblastic (M6) leukemia [20]\nAcute megakaryoblastic (M7) leukemia (AMKL)\nALL [21]\nEssential thrombocythemia [22]\nHodgkin disease (reported cases in adults only)\nCauses of secondary (nonmalignant) C-AMF include:\nHemophagocytic lymphohistiocytosis [23]\nSickle cell anemia (a single case report) [24]\nFanconi anemia\nVitamin D deficiency\nInfectious conditions - Tuberculosis, [25] visceral leishmaniasis, [26] histoplasmosis (reported cases in adults only) [27]\nRenal osteodystrophy\nSystemic lupus erythematosus [28]\nGray platelet syndrome\nOsteopetrosis\nHyperparathyroidism\nHypoparathyroidism (reported cases in adults only)\nPernicious anemia (reported cases in adults only)\nGaucher disease (reported cases in adults only)\nExposure to radiation, thorium dioxide, benzene (reported cases in adults only)\nOccurrence in the United States\nApproximately 100 cases of pediatric myelofibrosis have been reported worldwide. This is likely an underrepresentation, because cases associated with acute myeloid leukemia (AML) (the most common association) are not generally reportable.\nInternational occurrence\nCases of pediatric myelofibrosis have been described in association with tuberculosis (in Pakistan) and visceral leishmaniasis (in Sudan). Thus, myelofibrosis is presumably more common in areas of endemicity for these diseases. Detailed epidemiologic data are not available. Autosomal recessive familial myelofibrosis appears to be more common among children from Saudi Arabia. [29, 30, 31]\nSex- and age-related demographics\nIn published cases of pediatric myelofibrosis, females outnumber males by a ratio of approximately 2:1.\nIn infants, the presentation may be atypical and lack some of the classic clinical features.\nA large percentage of published cases of pediatric myelofibrosis occurs in children younger than 3 years. These younger patients are more likely to have Down syndrome, rickets, or a familial (possibly autosomal recessive) form of myelofibrosis. Among older patients, AML, systemic lupus erythematosus, and tuberculosis are the most common associations.\nThe prognosis of childhood myelofibrosis varies depending on the clinical context in which it occurs. With appropriate treatment for rickets, tuberculosis, systemic lupus erythematosus, and other conditions, the myelofibrosis may completely resolve.\nIdiopathic acute myelofibrosis of childhood may be a fulminant disease. Without effective therapy, life expectancy is typically less than 1 year. Potentially effective and/or curative treatments include chemotherapy and allogeneic bone marrow transplantation (BMT). Treatment with medications may also result in a temporary amelioration of the disease. Occasionally, pediatric patients have a more indolent course than what is observed in adults. With supportive care alone, they may survive for many years.\nIn adult patients with myelofibrosis, several alternative prognostic scoring systems (PSSs) are available. [32, 33] Neither the patient's symptoms nor the percentage of circulating blasts is taken into account in the Mayo Clinic PSS (in contrast to other PSSs). A retrospective review of 334 patients with myelofibrosis showed the Mayo Clinic PSS to be more effective than other PSSs in terms of (1) identifying long-lived patients and (2) delineating an intermediate-risk disease category. [33] The Mayo PSS assigns a score of 1-4 by allotting 1 point for each of the following:\nHemoglobin level more than 10 g/dL\nWhite blood cell (WBC) count less than 4 or more than 30 X 109/L\nPlatelet count less than 100 X 109/L\nAbsolute monocyte count at or above 1 X 109/L\nA new prognostic scoring system for primary myelofibrosis has been determined based on data collected during a study conducted by the International Working Group for Myelofibrosis Research and Treatment. [34]\nMultivariate analysis identified the following risk factors:\nAge older than 65 years\nConstitutional symptoms\nHemoglobin less than 10 g/dL\nCirculating blast cells 1% or greater\nPediatric patients were included in this study but not in sufficient numbers to analyze as a separate group.\nMorbidity and mortality\nMyelofibrosis causes, or accompanies conditions that cause, disruption of normal hematopoiesis. Patients may experience anemia, neutropenia, and/or thrombocytopenia. Patients may also experience pain secondary to hepatosplenomegaly. Neutropenia may lead to opportunistic infections. Thrombocytopenia may lead to hemorrhage.\nClinical Presentation\nSong MK, Park BB, Uhm JE. Understanding Splenomegaly in Myelofibrosis: Association with Molecular Pathogenesis. Int J Mol Sci. 2018 Mar 18. 19 (3):[Medline]. [Full Text].\nNaithani R, Tyagi S, Choudhry VP. Secondary myelofibrosis in children. J Pediatr Hematol Oncol. 2008. 30(3):196-8. [Medline].\nInoue S, Limsuwan A, McQueen R. Spontaneous resolution of myelofibrosis and pancytopenia followed by the development of acute myeloid leukemia with an extramedullary mass. J Pediatr Hematol Oncol. 1998 May-Jun. 20(3):268-70. [Medline].\nMaj JS, Roslan K, Fic-Sikorska B. Acute myelofibrosis in children: report on two cases. Acta Haematol Pol. 1996. 27(1):79-84. [Medline].\nBoxer LA, Camitta BM, Berenberg W. Myelofibrosis-myeloid metaplasia in childhood. Pediatrics. 1975 Jun. 55(6):861-5. 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Role for the nuclear factor kappaB pathway in transforming growth factor-beta1 production in idiopathic myelofibrosis: possible relationship with FK506 binding protein 51 overexpression. Cancer Res. 2005 Apr 15. 65(8):3281-9. [Medline].\nWolf BC, Neiman RS. Myelofibrosis with myeloid metaplasia: pathophysiologic implications of the correlation between bone marrow changes and progression of splenomegaly. Blood. 1985 Apr. 65(4):803-9. [Medline].\nAlghasham N, Alnouri Y, Abalkhail H, Khalil S. Detection of mutations in JAK2 exons 12-15 by Sanger sequencing. Int J Lab Hematol. 2016 Feb. 38 (1):34-41. [Medline].\nBarosi G, Bergamaschi G, Marchetti M, et al. JAK2 V617F mutational status predicts progression to large splenomegaly and leukemic transformation in primary myelofibrosis. Blood. 2007 Dec 1. 110(12):4030-6. [Medline].\nRudzki Z, Sacha T, Stoj A. The gain-of-function JAK2 V617F mutation shifts the phenotype of essential thrombocythemia and chronic idiopathic myelofibrosis to more \"erythremic\" and less \"thrombocythemic\": a molecular, histologic, and clinical study. Int J Hematol. Aug 2007. 86(2):130-6. [Medline].\nAl-Assar O, Ul-Hassan A, Brown R. Gains on 9p are common genomic aberrations in idiopathic myelofibrosis: a comparative genomic hybridization study. Br J Haematol. 2005 Apr. 129(1):66-71. [Medline].\nHussein K, Van Dyke DL, Tefferi A. Conventional cytogenetics in myelofibrosis: literature review and discussion. Eur J Haematol. 2009. 82(5):329-38. [Medline].\nLivun A, Newberry KJ, Manshouri T, Kusec R, Verstovsek S. Genes Involved in Maintaining the Bone Marrow Stroma Are Dysregulated in Patients with Myelofibrosis: Lenalidomide Treatment Up-regulates SOCS3. Anticancer Res. 2015 Oct. 35 (10):5219-23. [Medline].\nFadilah SA, Raja-Zahratul-Azma RS, Leong CF. 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Myelofibrosis in visceral leishmaniasis. Br J Haematol. 1991 Aug. 78(4):573-4. [Medline].\nPolverelli N, Palumbo GA, Binotto G, et al. Epidemiology, outcome, and risk factors for infectious complications in myelofibrosis patients receiving ruxolitinib: A multicenter study on 446 patients. Hematol Oncol. 2018 Apr 6. [Medline].\nPaquette RL, Meshkinpour A, Rosen PJ. Autoimmune myelofibrosis. A steroid-responsive cause of bone marrow fibrosis associated with systemic lupus erythematosus. Medicine (Baltimore). 1994 May. 73(3):145-52. [Medline].\nRossbach HC. Familial infantile myelofibrosis as an autosomal recessive disorder: preponderance among children from Saudi Arabia. Pediatr Hematol Oncol. Jul 2006. 23(5):453-4. [Medline].\nSheikha A. Fatal familial infantile myelofibrosis. J Pediatr Hematol Oncol. 2004. 26(3):164-8. [Medline].\nMallouh AA, Sa'di AR. Agnogenic myeloid metaplasia in children. Am J Dis Child. 1992. 146(8):965-7. [Medline].\nIvanyi JL, Mahunka M, Papp A. Prognostic significance of bone marrow reticulin fibres in idiopathic myelofibrosis: evaluation of clinicopathological parameters in a scoring system. Haematologia (Budap). 1994. 26(2):75-86. [Medline].\nTefferi A, Huang J, Schwager S. Validation and comparison of contemporary prognostic models in primary myelofibrosis: analysis based on 334 patients from a single institution. Cancer. May 2007. 109(10):2083-8. [Medline].\nCervantes F, Dupriez B, Pereira A, et al. New prognostic scoring system for primary myelofibrosis based on a study of the International Working Group for Myelofibrosis Research and Treatment. Blood. 2009 Mar 26. 113(13):2895-901. [Medline].\nEl-Moneim AA, Kratz CP, Böll S, Rister M, Pahl HL, Niemeyer CM. Essential versus reactive thrombocythemia in children: retrospective analyses of 12 cases. Pediatr Blood Cancer. 2007. 49(1):52-5. [Medline].\nCohn SL, Cohn RA, Chou P. Infantile myelofibrosis with nephromegaly secondary to myeloid metaplasia. Clin Pediatr (Phila). 1991 Jan. 30(1):59-61. [Medline].\nFernbach SK, Feinstein KA. Extramedullary hematopoiesis in the kidneys in infant siblings with myelofibrosis. Pediatr Radiol. 1992. 22(3):211-2. [Medline].\nPilorget H, Bangui A, Adam M. [Myelofibrosis regressing under corticotherapy and intravenous immunoglobulins in an infant(in French)]. Arch Pediatr. 1996 Jan. 3(1):40-3. [Medline].\nOzsoylu S, Ruacan S. High-dose intravenous corticosteroid treatment in childhood idiopathic myelofibrosis. Acta Haematol. 1986. 75(1):49-51. [Medline].\nSchwartz CL, Cohen H. Myeloproliferative and myelodysplastic syndromes. Pizzo PA, Poplack DG, eds. Principles and Practice of Pediatric Oncology. 3rd ed. Philadelphia, PA: JB Lippincott Company; 1997. 512-4.\nDomingues MA, Haepers AT, Massaut IH, Vassallo J, Lorand-Metze I. Reversal of bone marrow fibrosis in idiopathic myelofibrosis after treatment with alpha-interferon. Haematologica. 1998 Dec. 83(12):1124-5. [Medline].\nRambaldi A, Barbui T, Barosi G. From palliation to epigenetic therapy in myelofibrosis. 2008. Available at http://asheducationbook.hematologylibrary.org/cgi/content/full/2008/1/39.\nTefferi A. Treatment approaches in myelofibrosis with myeloid metaplasia: the old and the new. Semin Hematol. 2003 Jan. 40(1 Suppl 1):18-21. [Medline].\nTefferi A, Cortes J, Verstovsek S, et al. Lenalidomide therapy in myelofibrosis with myeloid metaplasia. Blood. 2006. 108(4):1158-64. [Medline].\nArlet P, Nicodeme R, Adoue D. Clinical evidence for 1,25-dihydroxycholecalciferol action in myelofibrosis. Lancet. 1984 May 5. 1(8384):1013-4. [Medline].\nRichard C, Mazorra F, Iriondo A. The usefulness of 1,25-dihydroxy-vitamin D3(1,25(OH)2vitD3) in the treatment of idiopathic myelofibrosis. Br J Haematol. 1986 Feb. 62(2):399-400. [Medline].\nDanilov AV, Relias V, Feeney DM, Miller KB. Decitabine is an effective treatment of idiopathic myelofibrosis. Br J Haematol. 2009. 145(1):131-2. [Medline].\nOstojic A, Vrhovac R, Verstovsek S. Ruxolitinib for the treatment of myelofibrosis: its clinical potential. Ther Clin Risk Manag. 2012. 8:95-103. [Medline]. [Full Text].\nMulcahy N. New dosing, safety guidance for myelofibrosis drug. Medscape Medical News [serial online]. June 14, 2013. Available at http://www.medscape.com/viewarticle/806310. Accessed: June 24, 2013.\nChustecka Z. Pacritinib: New Myelofibrosis Drug, Even With Thrombocytopenia. Medscape Medical News. May 30, 2015. [Full Text].\nBeauverd Y, McLornan DP, Harrison CN. Pacritinib: a new agent for the management of myelofibrosis?. Expert Opin Pharmacother. 2015 Oct. 16 (15):2381-90. [Medline].\nDomm J, Calder C, Manes B, Crossno C, Correa H, Frangoul H. Unrelated stem cell transplant for infantile idiopathic myelofibrosis. Pediatr Blood Cancer. 2009. 52(7):893-5. [Medline].\nSoll E, Massumoto C, Clift RA. Relevance of marrow fibrosis in bone marrow transplantation: a retrospective analysis of engraftment. Blood. 1995 Dec 15. 86(12):4667-73. [Medline].\nKerbauy DM, Gooley TA, Sale GE. Hematopoietic cell transplantation as curative therapy for idiopathic myelofibrosis, advanced polycythemia vera, and essential thrombocythemia. Biol Blood Marrow Transplant. Mar 2007. 13(3):355-65. [Medline].\nAnderson JE, Sale G, Appelbaum FR. Allogeneic marrow transplantation for primary myelofibrosis and myelofibrosis secondary to polycythaemia vera or essential thrombocytosis. Br J Haematol. 1997 Sep. 98(4):1010-6. [Medline].\nMerup M, Lazarevic V, Nahi H. Different outcomes of allogeneic transplantation in myelofibrosis using conventional or reduced-intensity conditioning regimens. Br J Haematol. Nov 2006. 135(3):367-73. [Medline].\nPlatzbecker U, Ehninger G, Schmitz N, Bornhauser M. Reduced-intensity conditioning followed by allogeneic hematopoietic cell transplantation in myeloid diseases. Ann Hematol. 2003. 82(8):463-8. [Medline].\nMesa RA, Nagorney DS, Schwager S. Palliative goals, patient selection, and perioperative platelet management: outcomes and lessons from 3 decades of splenectomy for myelofibrosis with myeloid metaplasia at the Mayo Clinic. Cancer. Jul 2006. 107(2):361-70. [Medline].\nTefferi A, Mesa RA, Nagorney DM. Splenectomy in myelofibrosis with myeloid metaplasia: a single-institution experience with 223 patients. Blood. 2000 Apr 1. 95(7):2226-33. [Medline].\nTrisha Simone Tavares, MD, FAAP Attending Physician, Department of Pediatrics, Section of Hematology/Oncology, Cardon Children's Medical Center\nTrisha Simone Tavares, MD, FAAP is a member of the following medical societies: Children's Oncology Group\nCoauthor(s)\nJ Martin Johnston, MD Associate Professor of Pediatrics, Mercer University School of Medicine; Director of Hematology/Oncology, The Children's Hospital at Memorial University Medical Center; Consulting Oncologist/Hematologist, St Damien's Pediatric Hospital\nJ Martin Johnston, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Pediatric Hematology/Oncology, International Society of Paediatric Oncology\nRobert J Arceci, MD, PhD Director, Children’s Center for Cancer and Blood Disorders, Department of Hematology/Oncology, Co-Director of the Ron Matricaria Institute of Molecular Medicine, Phoenix Children’s Hospital; Editor-in-Chief, Pediatric Blood and Cancer; Professor, Department of Child Health, University of Arizona College of Medicine\nRobert J Arceci, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American Association for Cancer Research, American Pediatric Society, American Society of Hematology, American Society of Pediatric Hematology/Oncology\nJames L Harper, MD Associate Professor, Department of Pediatrics, Division of Hematology/Oncology and Bone Marrow Transplantation, Associate Chairman for Education, Department of Pediatrics, University of Nebraska Medical Center; Assistant Clinical Professor, Department of Pediatrics, Creighton University School of Medicine; Director, Continuing Medical Education, Children's Memorial Hospital; Pediatric Director, Nebraska Regional Hemophilia Treatment Center\nJames L Harper, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for Cancer Research, American Federation for Clinical Research, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Council on Medical Student Education in Pediatrics, and Hemophilia and Thrombosis Research Society\nSharada A Sarnaik, MBBS Professor of Pediatrics, Wayne State University School of Medicine; Director, Sickle Cell Center, Attending Hematologist/Oncologist, Children's Hospital of Michigan\nSharada A Sarnaik, MBBS is a member of the following medical societies: American Association of Blood Banks, American Association of University Professors, American Society of Hematology, American Society of Pediatric Hematology/Oncology, New York Academy of Sciences, and Society for Pediatric Research\nMary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference\nencoded search term (Pediatric Myelofibrosis) and Pediatric Myelofibrosis\nMyeloproliferative Disease\nEssential Thrombocytosis\nMyelophthisic Anemia\nPathology of Acute Myeloid Leukemia Not Otherwise Specified\n'Impressive' Results After Change of HSCT Conditioning Regimen in Myelofibrosis Patients\nWeight Gain, Blood Pressure Rise Seen With JAK Inhibitor Therapy\nAnother JAK Inhibitor Shows Promise for Alopecia Areata\nTop News From ASH 2013: Slideshow\n2002 197954-overview Diseases & Conditions\nDiseases & Conditions Primary Myelofibrosis\n2010 fedratinib-1000346 Drugs\nDrugs fedratinib\n2010 pacritinib-1000150 Drugs\nDrugs pacritinib\nDiseases & Conditions Pediatric Myelofibrosis"