Pathogenesis and Morphology
The disease is based on the monoclonal proliferation of neoplastic myeloblasts. These cells lose the ability to differentiate, accumulate in the bone marrow, and enter the systemic circulation.
On microscopy (Romanovsky-Giemsa stain), blasts exhibit:
- Fine nuclear chromatin and 3–5 nucleoli.
- Azurophilic granules in the cytoplasm.
- Auer rods — specific inclusions most characteristic of promyelocytes.
Systemic Manifestations
Tumor cells actively infiltrate organs, causing dysfunction:
- Lymphoid organs: the liver, spleen, and lymph nodes enlarge, though they rarely reach giant sizes.
- Gastrointestinal tract: infiltration of mucosal membranes leads to necrotic processes and ulcerations in the oral cavity and stomach.
- Central nervous system and lungs: neuroleukemia (infiltration of the meninges) and leukemic pneumonitis may occur.
Clinical Significance
AML is more frequently diagnosed in adults (median age 50 years), although it occurs in all age groups. The primary causes of mortality are related to:
- Hemorrhagic syndrome: massive hemorrhages into vital organs, especially the brain.
- Infectious complications, including sepsis, developing against the background of suppressed normal hematopoiesis.