Color Atlas of Hematology - Practical Microscopic and Clinical ...

116Abnormalities of the White Cell SeriesCharacteristics of CMLAge of onset: Any age. Peak inicidence about 50 years.Clinical findings: Slowly developing fatigue, anemia; in some casespalpable splenomegaly; no fever.CBC: Leukocytosis and a left shift in the granulocyte series; possiblyHb , thrombocytes or .Advanced diagnostics: Bone marrow, cytogenetics, and moleculargenetics (Philadelphia chromosome and BCR-ABL rearrangement).Differential diagnosis: Reactive leukocytoses (alkaline phosphatase,trigger?); other myeloproliferative disorders (bone marrow, cytogenetics,alkaline phosphatase).Course, therapy: Chronic progression. Acute transformation afteryears. New, curative drugs are currently under development. Evaluatethe possibility of a bone marrow transplant (up to age approx. 60years).Steps in the Diagnosis of Chronic Myeloid LeukemiaLeft-shift leukocytosis in conjunction with usually low-grade anemia,thrombocytopenia or thrombocytosis (which often correlates with themigration of small megakaryocyte nuclei into the blood stream), and clinicalsplenomegaly is typical of CML. LDH and uric acid concentrations areelevated as a result of the increased cell turnover.The average “typical” cell composition is as follows (in a series analyzedby Spiers): about 2% myeloblasts, 3% promyelocytes, 24% myelocytes, 8%metamyelocytes, 57% band and segmented neutrophilic granulocytes, 3%basophils, 2% eosinophils, 3% lymphocytes, and 1% monocytes.In almost all cases of CML the hematopoietic cells display a markerchromosome, an anomalously configured chromosome 22 (Philadelphiachromosome). The translocation responsible for the Philadelphia chromosomecorresponds to a special fusion gene (BCR-ABL) that can be determinedby polymerase chain reaction (PCR) and fluorescence in situ hybridization(FISH).