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Pathophysiology. Polycythemia vera (PV), being a primary polycythemia (increase in the fraction of volume occupied by red cells in the blood), is caused by neoplastic proliferation and maturation of erythroid, megakaryocytic and granulocytic elements to produce what is referred to as panmyelosis.
Polycythemia vera (PCV) (a.k.a. polycythemia rubra vera (PRV)) occurs when excess red blood cells are produced as a result of an abnormality of the bone marrow. Often, excess white blood cells and platelets are also produced. A hallmark of polycythemia vera is an elevated hematocrit, with Hct > 55% seen in 83% of cases.
Polycythemia vera (PV) is associated most often with the JAK2 V617F mutation greater than 95% of cases, whereas the remainder has a JAK2 exon 12 mutations. High hemoglobin or hematocrit counts are required, as is a bone marrow examination showing "prominent erythroid , granulocytic and megakaryocytic proliferation with pleomorphic, mature ...
Once the reactive causes of thrombocythemia are ruled out, clonal thrombocythemia should be considered. The most common cause of clonal thrombocythemia is a myeloproliferative neoplasm . These include: essential thrombocythemia , chronic myelogenous leukemia , polycythemia vera , and primary myelofibrosis .
Secondary erythromelalgia can result from small fiber peripheral neuropathy of any cause, polycythemia vera, essential thrombocythemia, hypercholesterolemia, mushroom or mercury poisoning, and some autoimmune disorders. Primary erythromelalgia is caused by mutation of the voltage-gated sodium channel α-subunit gene SCN9A.
Causes: Overproduction of hematopoietic cells, genetic mutations. Diagnostic method: Clinical criteria. Differential diagnosis: Chronic myelogenous leukemia, myelodysplastic syndrome, polycythemia vera, primary myelofibrosis, secondary thrombocytosis. Treatment: Low-dose aspirin, plateletpheresis, cytoreductive therapy. Prognosis
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