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Essential thrombocytosis is an indolent disorder and allows long-term survival Average survival is longer than 15 years from diagnosis, and the survival of patients younger than 50 years does not appear different from matched controls The major source of morbidity thrombosis can be reduced by appropriate platelet control Late in the course of the disease, the bone marrow may become fibrotic, and massive splenomegaly may occur, sometimes with splenic infarction There is a 10 15% risk of progression to myelofibrosis after 15 years, and a 1 5% risk of transformation to acute leukemia over 20 years
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Barbui T et al Practice guidelines for the therapy of essential thrombocythemia A statement from the Italian Society of Hematology, the Italian Society of Experimental Hematology and the Italian Group for Bone Marrow Transplantation Haematologica 2004 Feb;89(2):215 32 [PMID: 15003898]
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Patients are almost invariably anemic at presentation The white blood count is variable either low, normal, or
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elevated and may be increased to 50,000/mcL The platelet count is variable The peripheral blood smear is dramatic, with significant poikilocytosis and numerous teardrop forms in the red cell line Nucleated red blood cells are present and the myeloid series is shifted, with immature forms including a small percentage of promyelocytes or myeloblasts Platelet morphology may be bizarre, and giant degranulated platelet forms (megakaryocyte fragments) may be seen The triad of teardrop poikilocytosis, leukoerythroblastic blood, and giant abnormal platelets is highly suggestive of myelofibrosis The bone marrow usually cannot be aspirated (dry tap), though early in the course of the disease it is hypercellular, with a marked increase in megakaryocytes Fibrosis at this stage is detected by a silver stain demonstrating increased reticulin fibers Later, biopsy reveals more severe fibrosis, with eventual replacement of hematopoietic precursors by collagen There is no characteristic chromosomal abnormality
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intensity allogeneic stem cell transplantation now appear to offer the possibility of improving the outcome for many patients End-stage myelofibrosis is characterized by generalized debility, liver failure, and bleeding from thrombocytopenia, with some cases terminating in acute myelogenous leukemia
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Dingli D et al Myelofibrosis with myeloid metaplasia: new developments in pathogenesis and treatment Intern Med 2004 Jul;43(7):540 7 [PMID: 15335177] Kralovics R et al A gain-of-function mutation of JAK2 in myeloproliferative disorders N Engl J Med 2005 Apr 28;352 (17):1779 90 [PMID: 15858187] Mesa RA et al Durable responses to thalidomide-based drug therapy for myelofibrosis with myeloid metaplasia Mayo Clin Proc 2004 Jul;79(7):883 9 [PMID: 15244384]
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CHRONIC MYELOGENOUS LEUKEMIA
Differential Diagnosis
A leukoerythroblastic blood picture from other causes may be seen in response to severe infection, inflammation, or infiltrative bone marrow processes However, teardrop poikilocytosis and giant abnormal platelet forms will not be present Bone marrow fibrosis may be seen in metastatic carcinoma, Hodgkin s disease, and hairy cell leukemia These disorders are diagnosed by characteristic morphology of involved tissues Concerning other myeloproliferative disorders, chronic myelogenous leukemia is diagnosed when there is marked leukocytosis, normal red blood cell morphology, and the presence of the bcr/abl fusion gene Polycythemia vera is characterized by an elevated hematocrit Essential thrombocytosis shows predominant platelet count elevations
ESSENTIALS OF DIAGNOSIS
Strikingly elevated white blood count Markedly left-shifted myeloid series but with a low percentage of promyelocytes and blasts Presence of Philadelphia chromosome or bcr/abl gene
General Considerations
Chronic myelogenous leukemia (CML) is a myeloproliferative disorder characterized by overproduction of myeloid cells These myeloid cells retain the capacity for differentiation, and normal bone marrow function is retained during the early phases The disease usually remains stable for years and then transforms to a more overtly malignant disease CML is characterized by a specific chromosomal abnormality, the Philadelphia chromosome, a reciprocal translocation between the long arms of chromosomes 9 and 22 A large portion of 22q is translocated to 9q, and a smaller piece of 9q is moved to 22q The portion of 9q that is translocated contains abl, a protooncogene that is the cellular homolog of the Ableson murine leukemia virus The abl gene is received at a specific site on 22q, the break point cluster (bcr) The fusion gene bcr/abl produces a novel protein that differs from the normal transcript of the abl gene in that it possesses tyrosine kinase activity (a characteristic activity of transforming genes) Evidence that the bcr/abl fusion gene is pathogenic is provided by transgenic mouse models in which introduction of the gene almost invariably leads to leukemia Early CML ( chronic phase ) does not behave like a malignant disease Normal bone marrow function is retained, white blood cells differentiate and, despite some qualitative abnormalities, the neutrophils combat infection normally However, CML is inherently unstable, and without treatment the disease progresses to an accelerated and then acute blast phase, which is morphologically indistinguishable from acute leukemia
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