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Chronic Myelogenous Leukemia Treatment (PDQ®): Treatment - Health Professional Information [NCI] - Stage Information for Chronic Myelogenous Leukemia

Bone marrow sampling is done to assess cellularity, fibrosis, and cytogenetics. The Philadelphia chromosome (Ph1) is usually more readily apparent in marrow metaphases than in peripheral blood metaphases; in some cases, it may be mashed and reverse transcriptase–polymerase chain reaction (RT–PCR) or fluorescent in situ hybridization analyses on blood or marrow aspirates may be necessary to demonstrate the 9;22 translocation.

Histopathologic examination of bone marrow aspirate demonstrates a shift in the myeloid series to immature forms that increase in number as patients progress to the blastic phase of the disease. The marrow is hypercellular, and differential counts of both marrow and blood show a spectrum of mature and immature granulocytes similar to that found in normal marrow. Increased numbers of eosinophils or basophils are often present, and sometimes monocytosis is seen. Increased megakaryocytes are often found in the marrow, and sometimes fragments of megakaryocytic nuclei are present in the blood, especially when the platelet count is very high. The percentage of lymphocytes is reduced in both the marrow and blood in comparison with normal subjects, and the myeloid/erythroid ratio in the marrow is usually greatly elevated. The leukocyte alkaline phosphatase enzyme is either absent or markedly reduced in the neutrophils of patients with chronic myelogenous leukemia (CML).[1]

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Transition from the chronic phase to the accelerated phase and later the blastic phase may occur gradually over a period of 1 year or more, or it may appear abruptly (blast crisis). The annual rate of progression from chronic phase to blast crisis is 5% to 10% in the first 2 years and 20% in subsequent years.[2,3] Signs and symptoms commonly indicating such a change include the following:

  • Progressive leukocytosis.
  • Thrombocytosis or thrombocytopenia.
  • Anemia. (Refer to the PDQ summary on Fatigue for more information on anemia.)
  • Increasing and painful splenomegaly or hepatomegaly.
  • Fever. (Refer to the PDQ summary on Fever, Sweats, and Hot Flashes for more information.)
  • Bone pain. (Refer to the PDQ summary on Pain for more information.)
  • Development of destructive bone lesions.
  • Thrombotic or bleeding complications.

In the accelerated phase, differentiated cells persist, though they often show increasing morphologic abnormalities, and increasing anemia and thrombocytopenia and marrow fibrosis are apparent.[1]

Studies have suggested that certain presenting features have prognostic significance. The following are predictive of a shorter chronic phase:

  • Increased splenomegaly.
  • Older age.
  • Male gender.
  • Elevated serum lactate dehydrogenase.
  • Cytogenetic abnormalities in addition to the Ph1.
  • A higher proportion of marrow or peripheral blood blasts.
  • Basophilia.
  • Eosinophilia.
  • Thrombocytosis.
  • Anemia.

Predictive models using multivariate analysis have been derived.[2,3,4,5,6,7]

Chronic-phase CML

Chronic-phase CML is characterized by bone marrow and cytogenetic findings as described above with less than 10% blasts and promyelocytes in the peripheral blood and bone marrow.[8]

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