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Primary Myelofibrosis

Myeloproliferative neoplasm characterized by clonal stem cell proliferation, megakaryocyte abnormalities, bone marrow fibrosis, extramedullary hematopoiesis, splenomegaly, anemia, and constitutional symptoms, with driver mutations in JAK2, CALR, or MPL, risk-stratified by DIPSS-Plus or MIPSS70/MIPSS70+v2.0, treated with JAK inhibitors (ruxolitinib, fedratinib, momelotinib, pacritinib) and allogeneic stem cell transplantation.

Written by: Saygı Hospital Health Guide Editorial Board
Last updated:

This content has been compiled by the Saygı Hospital Health Guide Editorial Board and is periodically reviewed by a specialist physician.

References (5)

This content is for informational purposes only and does not constitute medical advice. You can book an appointment at our Hematoloji department. Book Appointment →

What is Primary Myelofibrosis?

Primary myelofibrosis (PMF) is a chronic myeloproliferative neoplasm characterized by clonal proliferation of bone marrow stem cells with abnormal megakaryocyte morphology and proliferation, leading to release of cytokines (PDGF, TGF-beta, FGF) that stimulate fibroblasts and produce reticulin and collagen fibrosis. The disease progresses from prefibrotic/early stage (hypercellular marrow with megakaryocytic abnormalities, minimal fibrosis) to overt fibrotic stage (extensive marrow fibrosis with osteosclerosis, leukoerythroblastic peripheral blood, extramedullary hematopoiesis with hepatosplenomegaly). Annual incidence is 0.5-1.5 per 100,000 with median age 65 years.

WHO 2022 classification distinguishes prefibrotic/early PMF and overt fibrotic PMF, both requiring driver mutation (JAK2 V617F in 60%, CALR exon 9 in 25%, MPL W515 in 8%, or triple-negative in 10%) plus characteristic bone marrow morphology and exclusion of other myeloid neoplasms. High molecular risk mutations include ASXL1 (most common, ~30%), EZH2, IDH1/2, SRSF2, U2AF1 Q157 - presence of any associated with shorter survival and increased blast transformation risk. Risk stratification: DIPSS-Plus integrates age >65, hemoglobin <10, leukocytes >25,000, peripheral blasts >=1%, constitutional symptoms, transfusion need, platelets <100,000, unfavorable karyotype. MIPSS70 and MIPSS70+v2.0 add high molecular risk mutations and additional cytogenetic categories for younger patients (<70 years) eligible for allogeneic stem cell transplantation.

JAK inhibitors are mainstay of treatment for symptomatic patients: ruxolitinib (JAK1/2 inhibitor) is first-line, providing >35% spleen volume reduction at 24 weeks in COMFORT-I/II trials and significant symptom improvement, with prolonged overall survival; main toxicities are anemia and thrombocytopenia. Fedratinib (JAK2 selective) approved for ruxolitinib-resistant or intolerant patients; FDA black box warning for Wernicke encephalopathy requires thiamine supplementation. Momelotinib (JAK1/JAK2/ACVR1 inhibitor) approved 2023 for myelofibrosis with anemia, additionally improving anemia by inhibiting hepcidin via ACVR1 inhibition. Pacritinib (JAK2/IRAK1 inhibitor) approved for severe thrombocytopenia (<50,000/microL). Allogeneic stem cell transplantation is the only curative therapy, indicated for intermediate-2 or high-risk disease in patients <70 years with adequate performance status; reduced-intensity conditioning preferred. Supportive care includes red blood cell transfusions for anemia, danazol or luspatercept for transfusion-dependent anemia, hydroxyurea for symptomatic leukocytosis or thrombocytosis, and splenectomy in select cases (high morbidity, last resort).

Symptoms

Massive splenomegaly causing abdominal fullness, early satiety
Fatigue from anemia
Constitutional symptoms (fevers, night sweats, weight loss, pruritus)
Bone pain from medullary expansion
Hepatomegaly
Easy bruising or bleeding from thrombocytopenia
Recurrent infections from neutropenia
Extramedullary hematopoiesis (paraspinal masses, pulmonary hypertension)
Cachexia in advanced disease
Symptoms of leukemic transformation (rapid clinical decline)

Risk Factors

Age over 65 years
Driver mutations (JAK2, CALR, MPL)
High molecular risk mutations (ASXL1, EZH2, IDH1/2, SRSF2, U2AF1)
Unfavorable karyotype (complex, monosomal, +8, -7/7q-, i(17q))
Unmutated CALR or triple-negative phenotype (worse prognosis)
Ionizing radiation exposure
Prior MPN (post-PV or post-ET myelofibrosis)
Male sex (slightly higher)

When to See a Doctor?

If you experience any of the following symptoms, seek medical attention promptly:

  • Massive splenomegaly with abdominal symptoms
  • Constitutional symptoms with anemia
  • Leukoerythroblastic smear with teardrop red cells
  • Cytopenias with hypercellular bone marrow on biopsy
  • Known PV or ET with worsening cytopenias and splenomegaly
  • Bone pain with hematologic abnormalities
  • Pulmonary hypertension with extramedullary hematopoiesis
  • Pre-transplant evaluation for high-risk patient
  • Rapid clinical decline (concern for leukemic transformation)

Treatment Methods

01
Bone marrow biopsy with reticulin/trichrome staining and cytogenetics
02
Driver mutation testing (JAK2, CALR, MPL) and NGS panel
03
Risk stratification with DIPSS-Plus, MIPSS70, MIPSS70+v2.0
04
Ruxolitinib (JAK1/2 inhibitor) first-line for symptoms and splenomegaly
05
Fedratinib for ruxolitinib-resistant/intolerant
06
Momelotinib for myelofibrosis with anemia
07
Pacritinib for severe thrombocytopenia (<50,000)
08
Allogeneic stem cell transplantation for intermediate-2/high-risk patients <70
09
Transfusion support for anemia, danazol or luspatercept
10
Hydroxyurea for symptomatic leukocytosis/thrombocytosis
11
Splenectomy or splenic radiation in select refractory cases
12
Surveillance for blast transformation

Which Department to Visit?

You can visit our Hematoloji department for these complaints. Our specialist physicians will create the most suitable treatment plan for you.

Learn About Hematoloji Department

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Health Disclaimer: The information on this page is prepared for general informational purposes only. It does not replace medical diagnosis and treatment. Please consult your physician for your complaints. Saygı Hospital does not accept responsibility for actions taken based on the information on this page.