Pathogenesis and morphology
The disease is based on the monoclonal proliferation of tumor myeloblasts. These cells lose the capacity for differentiation, accumulate in the bone marrow, and enter the systemic circulation.
Upon microscopy (Romanovsky-Giemsa stain), blasts exhibit:
- Fine nuclear chromatin and 3–5 nucleoli.
- Azurophilic granularity in the cytoplasm.
- Auer rods — specific inclusions most characteristic of promyelocytes.
Systemic changes
Tumor cells actively infiltrate organs, causing dysfunction:
- Lymphoid organs: the liver, spleen, and lymph nodes enlarge, but rarely reach giant proportions.
- Gastrointestinal tract: infiltration of mucous membranes leads to necrotic processes and ulceration in the oral cavity and stomach.
- Central nervous system and lungs: neuroleukemia (infiltration of the meninges) and leukemic pneumonitis are possible.
Clinical significance
AML is more frequently diagnosed in adults (median age 50 years), though it occurs in all age groups. The main causes of mortality are associated with:
- Hemorrhagic syndrome: massive hemorrhages into vital organs, especially the brain.
- Infectious complications, including sepsis, developing against the background of suppressed normal hematopoiesis.
Briefly: answers to topical questions
How does acute myeloid leukemia differ morphologically and cytochemically from acute lymphoblastic leukemia?
Acute myeloid leukemia and acute lymphoblastic leukemia differ in the type of proliferating precursor cells, as well as specific cytologic and cytochemical markers.
| Sign | Acute myeloid leukemia | Acute lymphoblastic leukemia |
|---|---|---|
| Substrate | Myeloblasts | Low-differentiated lymphocyte precursors |
| Morphology | Fine chromatin, 3–5 nucleoli, small azurophilic granules, Auer rods (J. Auer) | Not described in sources |
| Cytochemistry | In myeloid differentiation — positive myeloperoxidase reaction; in monocytic differentiation — positive reaction for nonspecific lysosomal esterases | Not described in sources |
In which specific variant of acute myeloid leukemia is severe DIC syndrome most frequently developed?
Severe DIC syndrome is characteristic of acute promyelocytic leukemia, a distinct variant of acute myeloid leukemia. It is characterized by coagulopathy with excessively activated fibrinolysis and DIC syndrome.
Morphologically, this disease is dominated by abnormal promyelocytes. Genetically, recombination of the RARA gene with the PML gene and the specific translocation t(15;17)(q22;q11-12) are detected.
What is a chloroma (granulocytic sarcoma) and what is its morphological substrate?
A chloroma (granulocytic sarcoma) is a specific focal process representing a growing tumor formed by an accumulation of leukemic cells.
The morphological substrate of the lesion consists of leukemic cells in myeloid leukemia. The pathology got its name from its characteristic green color. Manifestation variants:
- Granulocytic sarcoma (granulocytic sarcoma) — pleural thickening due to the accumulation of leukemic cells.
- Myeloid sarcoma (chloroma) — a focal bone process (usually localized in the skull, spine, ribs, or sternum in children).
"Auer is a myeloid example": the presence of Auer rods and myeloperoxidase is the "gold standard" for AML diagnosis.
Class and exam questions
What is "pyoid bone marrow"?
This is a macroscopic description of the bone marrow in AML, which acquires a gray or greenish tint due to massive leukemic infiltration.
Which organs are most commonly affected in AML?
Blasts infiltrate the spleen, liver, kidneys, gastrointestinal mucosa, and less commonly the skin and lymph nodes.
Why do bleeding episodes occur in AML?
Tumor cells crowd out normal hematopoietic lineages, leading to platelet deficiency and the development of pronounced hemorrhagic syndrome.
What else to study on this topic
- Differential diagnosis of AML and acute lymphoblastic leukemias.
- Classification of AML variants according to the FAB system.
- The role of cytochemical reactions in leukemia typing.
- Mechanisms of secondary infection development in leukemias.
- Genetic markers and their prognostic significance.
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