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Acute Myeloid Leukemia

*Leucosis myeloides acuta*

For medical students2 min readUpdated 2026-10-10

Acute myeloid leukemia (AML) is a group of malignant neoplasms of the hematopoietic system that develop from a bone marrow stem cell mutation. The disease is characterized by the uncontrolled proliferation of blast cells that crowd out normal hematopoietic lineages and infiltrate internal organs.

Key featureAuer rods in the cytoplasm of blasts are a pathognomonic marker of AML.
CytochemistryA positive reaction for myeloperoxidase confirms myeloid origin.
Bone marrowAcquires a characteristic pyoid (gray-greenish) appearance.
Main dangerSevere hemorrhagic syndrome and the risk of fatal central nervous system hemorrhage.

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:

Systemic Manifestations

Tumor cells actively infiltrate organs, causing dysfunction:

  1. Lymphoid organs: the liver, spleen, and lymph nodes enlarge, though they rarely reach giant sizes.
  2. Gastrointestinal tract: infiltration of mucosal membranes leads to necrotic processes and ulcerations in the oral cavity and stomach.
  3. 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:

Mnemonic

"Auer is a myeloid example": the presence of Auer rods and myeloperoxidase is the "gold standard" for AML diagnosis.

Frequently asked questions

How do acute myeloid leukemia and acute lymphoblastic leukemia differ morphologically and cytochemically?

Acute myeloid leukemia and acute lymphoblastic leukemia differ in the type of proliferating precursor cells, as well as specific cytologic and cytochemical markers.

FeatureAcute Myeloid LeukemiaAcute Lymphoblastic Leukemia
SubstrateMyeloblastsUndifferentiated lymphocyte precursors
MorphologyFine chromatin, 3–5 nucleoli, small azurophilic granules, Auer rods (J. Auer)Not specified in sources
CytochemistryIn myeloid differentiation — positive myeloperoxidase reaction; in monocytic differentiation — positive reaction for non-specific lysosomal esterasesNot specified in sources
In which specific variant of acute myeloid leukemia does severe disseminated intravascular coagulation (DIC) most frequently develop?

Severe DIC is characteristic of acute promyelocytic leukemia, a distinct variant of acute myeloid leukemia. It features coagulopathy with overly activated fibrinolysis and DIC.

Morphologically, abnormal promyelocytes predominate in this condition. Genetically, it reveals the RARA gene recombination with the PML gene and the specific translocation t(15;17)(q22;q11-12).

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 composed of an accumulation of leukemic cells.

The morphological substrate of the formation is leukemic cells in myeloid leukemia. The pathology received its name due to its characteristic green color. Manifestation variants:

  • Granulocytic sarcoma (granulocytic sarcoma) — pleural thickening due to leukemic cell accumulation.
  • Myeloid sarcoma (chloroma) — a focal bone process (typically localized in the skull, spine, ribs, or sternum in children).
What is "pyoid bone marrow"?

This is the macroscopic description of the bone marrow in AML, which takes on a grayish or greenish tint due to massive leukemic infiltration.

Which organs are most frequently affected in AML?

Blasts infiltrate the spleen, liver, kidneys, gastrointestinal mucosa, and less commonly the skin and lymph nodes.

Why do bleeding disorders occur in AML?

Tumor cells crowd out normal hematopoietic elements, leading to platelet deficiency and the development of a pronounced hemorrhagic syndrome.

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