Acute myeloid leukemia

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Acute myeloid leukemia Acute myeloid leukemia

Classification Classification

FAB:

M0, M1, M2, M3, M4, M5, M6 and M7M0, M1, M2, M3, M4, M5, M6 and M7

Clinical features Clinical features

Routine Laboratory diagnosis Routine Laboratory diagnosis

Slides Slides

Surface marker analysis Surface marker analysis

Molecular laboratory diagnosis Molecular laboratory diagnosis

Treatment Treatment

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www.kau.edu.sa/mgari www.kau.edu.sa/mgari

AML AML

Classification Classification

FAB classification was proposed in FAB classification was proposed in 1976.

1976.

Based on standard morphology of the Based on standard morphology of the PB smear and

PB smear and cytochemical cytochemical stains. stains.

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Characteristics Characteristics Type Type

Myeloid cells without morphological and Myeloid cells without morphological and cytochemical

cytochemical maturation.maturation.

M0M0

Myeloid cells with minimal morphological and Myeloid cells with minimal morphological and cytochemical

cytochemical maturation. maturation.

M1M1

Myeloid cells with maturation.

M2M2

Acute

Acute promyelocyticpromyelocytic maturation.maturation.

M3M3

Grnulocytic

Grnulocytic and monocticand monoctic maturation.maturation.

M4M4

Moncytic

Moncytic with well or poorly differentiation.with well or poorly differentiation.

M5M5

Erythroid

Erythroid maturation (erythroleukemiamaturation (erythroleukemia).).

M6M6

Megakaryoblastic

Megakaryoblastic leukemia.leukemia.

M7M7

FAB classification of AML

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Clinical features:

1. Due to bone marrow failure

• Pallor from anemia.

• Fever, features of mouth, throat, skin, respiratory or other infections (septicemia).

• Spontanous bruises, purpura, bleeding gums or bleeding from venepuncture sites due to

thrombocytopenia.

• Occasionally there is a major internal hemorrhage. A bleeding tendency due to therombocytopenia and

DIC.

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2. Due to organ infiltration

• Gum hypertrophy and infiltration.

• Skin involvement (M4 and M5).

• Mild spleenomegaly and hepatomegaly.

• Lysosyme released by blast cells may cause renal damage with K+ leakage and hypokalemia (M5).

• Rare meningeal syndrome, headache, nausea and

vomiting.

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Laboratory diagnosis

1. CBC and differential count reveal the following:

• A normochrmic normocytic anaemia.

• Total WBC is highly variable, decreased to markedly elevated.

• Low platelet count (thrombocytopenia)

2. Blood film examination reveal the following:

• Variable number of blast cells with Auer rods and other abnormal cells (promyelocytes, myelocytes, agranular neutrophils, pseudo- pleger cells or myelomonocytes.

3. Bone marrow eamination:

• Hypercellular with >30% blasts and marked proliferation of these leukemic cells.

• Normal erythroid and megakaroycyte precursors are reduced.

• Cytochemical stains demonstrate most of AML subtypes are peroxidase and Sudan black positive.

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Normal BM

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AML0

No azurophil granules

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AML M1

A few azurophilic granules or Auer rods

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AML M2

Some maturation beyond promyelocytes; Auer rods

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AML M3

Hypergranular promyelocytes;

Auer rods

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AML M4

>=20% monocytes;

monocytoid cells in blood

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AML M5 M5a & M5b

Monoblastic (M5A)

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AML M6

Predominance of erythroblasts;

dyserythropoiesis

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AML M7

"Dry" aspirate; biopsy with blasts and dysplastic