Why thrombocytosis in cml

Upon EMS arrival, the patient was conscious but confused and somnolent. She did, however, report lightheadedness and chest pain prior to the event. The patient was admitted to the hospital for further evaluation. Laboratory studies again showed a platelet count of 2. Computed tomography CT of the brain was unremarkable and CT of the abdomen and pelvis did not display any lymphadenopathy. She denied any recent weight loss or fevers. Due to the chest discomfort preceding the episode, a troponin was ordered and was elevated; the patient subsequently was transferred to the intensive care unit with a heparin infusion and a cardiology consultation.

A transthoracic echocardiogram was unremarkable, as was a CT angiogram of the chest. Electroencephalogram and magnetic resonance imaging of the brain were negative as well.

Hospital Course: Given the negative neurologic and cardiac evaluation, the hematologist suspected that a complication of a myeloproliferative disorder was causing the symptoms.

He elected to perform a mechanical removal of platelets via apheresis. After the reduction in platelet number, troponin level normalized and there were no further occurrences of chest discomfort or neurologic episodes. A search for the suspected myeloproliferative disorder was conducted, which was initially believed to be essential thrombocytosis. This established the diagnosis of chronic myeloid leukemia. The differential reveals the predominant cells as descending from the neutrophil lineage, present in various stages of development and best visualized on bone marrow biopsy.

Additionally, the splenomegaly that can be present on physical and radiographic findings was not present in our patient who was surgically asplenic. In addition, she presented with vasomotor instability and NSTEMI, which have been reported in the literature for essential thrombocytosis but not well described for CML [ 8 ]. The mechanism by which thrombocytosis causes symptoms is not fully delineated, but may be related to increased viscosity of circulating blood from transient sludging or aggregation of platelets via a thromboxane-mediated mechanism; this is the rationale for utilizing aspirin as initial medical therapy in thrombocytosis [ 9 ].

Two case reports have described digital ischemia due to thrombocytosis in patients with chronic myeloid leukemia [ 3 - 4 ]. One patient was known to have CML and thrombocytosis; she presented with cyanosis in the left hand, in addition to vague neurologic symptoms such as giddiness and headache [ 3 ]. A second patient presented with cyanosis of a solitary toe and was diagnosed with CML as a result of a full hematologic investigation, similar to our patient [ 4 ].

In both instances, patients were treated initially with medical therapy in the form of hydroxyurea [ 3 ], or hydroxyurea in combination with aspirin and allopurinol [ 4 ]. Nonetheless, both patients failed medical therapy and continued to remain symptomatic, at which point mechanical removal of platelets via apheresis was successful in alleviating their conditions [ 3 - 4 ].

Plateletpheresis also achieved success in our patient, who demonstrated full resolution of neurologic symptoms and chest pain after reduction in platelet numbers was achieved.

Although symptomatic thrombocytosis is not a common occurrence in chronic myeloid leukemia, it has been described in case reports and successfully treated with platelet apheresis.

Once achieved, reduction in platelet numbers resulted in the cessation of symptoms. There has been no evidence to date, however, that plateletpheresis should be used in patients with thrombocytosis who are not experiencing complications [ 4 ]. Symptomatic thrombocytosis caused by chronic myeloid leukemia can have significant consequences that may require urgent hematologic intervention. Plateletpheresis should be considered in these patients. Furthermore, CML should be high on the differential diagnosis for cases of significant thrombocytosis, even when only a modest leukocytosis or neutrophilia is present.

Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. It can cause weakness, tiredness, and shortness of breath.

Leukopenia The shortage of normal white blood cells. This particular shortage can heighten the risk of infection. Neutropenia The shortage of a particular kind of white blood cell, the neutrophil. These cells are important in the fight of infection from bacteria. Those who are neutropenic are at high risk of getting serious bacterial infections.

Thrombocytopenia The shortage of platelets, which can lead to excess bruising or bleeding. The opposite condition, thrombocytosis, is the production of too many platelets — but bruising and bleeding are an issue, as well, because the platelets do not function as they should. How is CML treated? Bone aspiration and biopsy The bone marrow aspiration and biopsy are done at the same time.

These samples are sent to a lab where they examined for leukemia cells. Lab tests There are several lab tests that may be used to determine whether you have CML or how advanced the disease may be.

How is CML staged? Chronic phase These patients have a small amount—generally less than 10 percent—of myeloblasts in their blood or bone marrow, have fairly mild symptoms, and usually respond to standard treatments. Blast phase Patients in this phase typically have more than 20 percent myeloblasts. How is prognosis determined? There are few risk factors with CML , but they include: Radiation exposure Being exposed to high-dose radiation such as being a survivor of a nuclear reactor accident.

Age The risk of getting CML increases with age. Should I get screened for CML? Last reviewed:. December Alternative Names:. Keywords : Chronic myeloid leukemia, Philadelphia chromosome, Essential thrombocythemia. Chronic myeloid leukemia. N Engl J Med, ;; Proposals and rationale for revision of the World Health Organization diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis: recommendations from an ad hoc international expert panel.

Blood, ;; Cancer Genet Cytogenet, ;89; Clinical presentation and natural history of patients with essential thrombocythemia and the Philadelphia chromosome.

Am J Hematol, ;27; Blood, ;97; Philadelphia Ph chromosome-positive thrombocythemia without features of chronic myeloid leukemia in peripheral blood: natural history and diagnostic differentiation from Ph-negative essential thrombocythemia.

Ann Hematol, ;83; Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. Typical essential thrombocythaemia does not express bcr-abelson fusion transcript.

Br J Haematol, ;; Imatinib mesylate-a new oral targeted therapy. Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. Search for. Current Issue.