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Etiology

• No evidence of cytotoxic drugs or a viral etiology. 
• Cigarette smoking accelerated the progression to blast crisis 
• Atomic bomb survivors had an increased incidence;  only large doses of radiation can induce CML.

Three phases

• Chronic phase
• Accelerated  phase
• Blast crisis phase

Clinical Presentation


Signs and Symptoms
 
Fatigue, malaise, and weight loss or  splenic enlargement and symptoms, such as early satiety and left               upper quadrant pain or mass.
 
Granulocyte or platelet dysfunction, such as infections, thrombosis, or bleeding.
 
Severe leukocytosis or thrombosis such as vasoocclusive disease, cerebrovascular accidents, myocardial infarction, venous thrombosis, priapism, visual disturbances, and pulmonary insufficiency.

Unexplained fever, significant weight loss, increasing dose requirement of the drugs controlling the disease, bone and joint pain, bleeding, thrombosis, and infections suggest transformation into accelerated or blastic phases.


Physical Findings

Minimal to moderate splenomegaly; mild hepatomegaly
Lymphadenopathy and myeloid sarcomas are unusual except late in the course of the disease; poor prognosis


Hematologic Findings in chronic phase

Elevated white blood cell counts (WBCs), with increases in both immature and mature granulocytes, are present at diagnosis; 16,000 to 200,00/cmm
Usually less than 5% circulating blasts
Platelet counts elevated or decreased, a mild degree of normocytic normochromic anemia .

Leukocyte alkaline phosphatase is low in CML cells.
Histamine production secondary to basophila is increased in later stages, causing pruritus, diarrhea, and flushing.


Marrow or blood basophilia, eosinophilia, and monocytosis

Disease acceleration: the development of increasing degrees of anemia or blood or marrow blasts between 10 and 20%, blood or marrow basophils 20%, or platelet count less than 100,000/L.
Blast crisis: Acute leukemia, with blood or marrow blasts 20%.

Chromosomal Findings

The cytogenetic hallmark of CML, is the t(9;22)

 Recognized by the presence of a shortened chromosome 22 (22q-), designated as the Philadelphia chromosome, that arises from the reciprocal t(9;22). Some patients may have complex translocations (designated as variant translocations) involving three, four, or five chromosomes (usually including chromosomes 9 and 22).


Imatinib mesylate tyrosine kinase inhibitorinduces apoptosis in cells expressing Bcr/Abl.