Myelofibrosis natural history, complications and prognosis

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

Overview

The development of myelofibrosis is a a slow process and it does not cause early symptoms. A significant proportion of the patients can be asymptomatic and the diagnosis is usually made in the setting of an unrelated condition. The most overlapping and common findings encountered are anemia and splenomegaly presenting as weakness, easy fatigability, palpitations, and dyspnea in the case of anemia and early satiety with possible accompanying left upper quadrant discomfort if splenomegaly is present. The disease has a progressive course and can result in pancytopenia as the bone marrow failure ensues. This can result in bleeding complications, easy bruising, increase in the susceptibility to infections, and worsening anemia. The bone marrow failure paves the way for extramedullary hematopoiesis (EMH) which mainly occurs in the reticuloendothelial tissues. If left untreated, myelofibrosis can lead to severe complications, the most feared of which are acute leukemia, heart failure, and portal hypertension.

Natural History, Complications, and Prognosis

Natural History

Complications

Common complications of myelofibrosis include:

Hematologic
Gastroentistinal
Urological
Cardiopulmonary
Neurological
Musculoskeletal
Other

Prognosis

  • The Dynamic International Prognostic Scoring System (DIPSS)‐plus currently provides the most comprehensive prognostic tool for primary myelofibrosis (PMF). This scoring system comprises of eight risk variables:[75][4][76]
  • The presence of 0, 1, 2 or 3, and ≥4 adverse factors defines low, intermediate-1, intermediate-2 and high-risk disease with median survivals of approximately 15.4, 6.5, 2.9 and 1.3 years, respectively.
DIPSS Plus Score Calculator for Prognosis in Myelofibrosis

References

  1. ↑ Hoffman, Ronald (2018). Hematology : basic principles and practice. Philadelphia, PA: Elsevier. ISBN 9780323357623.
  2. ↑ 2.0 2.1 Cervantes F, Pereira A, Esteve J, Cobo F, Rozman C, Montserrat E (November 1997). "[Idiopathic myelofibrosis: initial features, evolutive patterns and survival in a series of 106 patients]". Med Clin (Barc) (in Spanish; Castilian). 109 (17): 651–5. PMID 9488952.
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  4. ↑ 4.0 4.1 4.2 Tefferi A (December 2016). "Primary myelofibrosis: 2017 update on diagnosis, risk-stratification, and management". Am. J. Hematol. 91 (12): 1262–1271. doi:10.1002/ajh.24592. PMID 27870387.
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  12. ↑ Birgegard G, Samuelsson J, Ahlstrand E, Ejerblad E, Enevold C, Ghanima W, Hasselbalch H, Nielsen CH, Knutsen H, Pedersen OB, Sørensen A, Andreasson B (November 2018). "Inflammatory functional iron deficiency common in myelofibrosis, contributes to anaemia and impairs quality of life. From the Nordic MPN study Group". Eur. J. Haematol. doi:10.1111/ejh.13198. PMID 30472746.
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  18. ↑ Pizzi M, Gergis U, Chaviano F, Orazi A (September 2016). "The effects of hematopoietic stem cell transplant on splenic extramedullary hematopoiesis in patients with myeloproliferative neoplasm-associated myelofibrosis". Hematol Oncol Stem Cell Ther. 9 (3): 96–104. doi:10.1016/j.hemonc.2016.07.002. PMID 27521149.
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  73. ↑ Kundranda MN, Tibes R, Mesa RA (March 2012). "Transformation of a chronic myeloproliferative neoplasm to acute myelogenous leukemia: does anything work?". Curr Hematol Malig Rep. 7 (1): 78–86. doi:10.1007/s11899-011-0107-9. PMID 22170483.
  74. ↑ Theocharides AP, Lundberg P, Lakkaraju AK, Lysenko V, Myburgh R, Aguzzi A, Skoda RC, Manz MG (June 2016). "Homozygous calreticulin mutations in patients with myelofibrosis lead to acquired myeloperoxidase deficiency". Blood. 127 (25): 3253–9. doi:10.1182/blood-2016-02-696310. PMID 27013444.
  75. ↑ Gangat N, Caramazza D, Vaidya R, George G, Begna K, Schwager S, Van Dyke D, Hanson C, Wu W, Pardanani A, Cervantes F, Passamonti F, Tefferi A (February 2011). "DIPSS plus: a refined Dynamic International Prognostic Scoring System for primary myelofibrosis that incorporates prognostic information from karyotype, platelet count, and transfusion status". J. Clin. Oncol. 29 (4): 392–7. doi:10.1200/JCO.2010.32.2446. PMID 21149668.
  76. ↑ Bose P, Verstovsek S (August 2016). "Prognosis of Primary Myelofibrosis in the Genomic Era". Clin Lymphoma Myeloma Leuk. 16 Suppl: S105–13. doi:10.1016/j.clml.2016.02.031. PMC 4987499. PMID 27521306.
  77. ↑ Kuykendall AT, Talati C, Padron E, Sweet K, Sallman D, List AF, Lancet JE, Komrokji RS (November 2018). "Genetically inspired prognostic scoring system (GIPSS) outperforms dynamic international prognostic scoring system (DIPSS) in myelofibrosis patients". Am. J. Hematol. doi:10.1002/ajh.25335. PMID 30390311.
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  81. ↑ Tefferi A, Nicolosi M, Mudireddy M, Szuber N, Finke CM, Lasho TL, Hanson CA, Ketterling RP, Pardanani A, Gangat N, Mannarelli C, Fanelli T, Guglielmelli P, Vannucchi AM (March 2018). "Driver mutations and prognosis in primary myelofibrosis: Mayo-Careggi MPN alliance study of 1,095 patients". Am. J. Hematol. 93 (3): 348–355. doi:10.1002/ajh.24978. PMID 29164670.


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