Acute Lymphoblastic and Acute Myeloid Leukemia

Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) begin when an immature hematopoietic precursor undergoes malignant transformation. The resulting blasts proliferate without maturing normally and displace healthy marrow cells. The clinical consequences come less from the number of blasts alone than from what the marrow can no longer produce. Reduced red-cell production causes fatigue, pallor, exertional dyspnea, and tachycardia. Reduced platelet production causes petechiae, bruising, mucosal bleeding, and potentially intracranial or gastrointestinal hemorrhage. Reduced functional neutrophil production leaves the patient vulnerable to serious infection, even when the total white-cell count is elevated. A high WBC does not mean the patient has adequate immunity when much of that count consists of immature, ineffective blasts. ALL arises from lymphoid precursors, usually B- or T-cell lineage. AML arises from myeloid precursors. The distinction is not made reliably from symptoms or the total WBC; it requires marrow or blood blast assessment, immunophenotyping, and genetic testing. Under current WHO criteria, ALL generally requires at least 20% lymphoblasts in bone marrow or peripheral blood. AML generally requires at least 20% myeloblasts, although certain defining genetic...