Leukemia, Acute Myeloid
- Acute myeloid leukemia (AML) is characterized by proliferation of abnormal immature myeloid progenitors (blasts) with reduced capacity to differentiate leading to bone marrow failure and a variety of systemic symptoms.
- Historically, the French–American–British (FAB) classification system divided AML based on the cell morphology with the addition of cytogenetics (subtypes M0 to M7).
- The World Health Organization (WHO) classification attempts to provide more meaningful prognostic information.
- AML with characteristic genetic abnormalities: translocation t(8;21), t(15;17), and inversion in chromosome 16 inv(16)
- AML with multilineage dysplasia: presence of a prior myelodysplastic syndrome (MDS) or myeloproliferative neoplasm (MPN) that transformed into AML
- AML and MDS, therapy related
- AML not otherwise categorized
- Acute leukemias of ambiguous lineage (biphenotypic acute leukemia)
- ~19,940 cases estimated in 2020, making it the most common type of leukemia in adults
- Predominant sex: male ≥ female
The incidence of AML increases with age, and median age is 67 years.
Etiology and Pathophysiology
Precise causes unknown, but some risk factors have been identified (see “Risk Factors”).
- Three risk groups
- Good risk: inv(16), t(8;21), t(15;17)
- Standard risk: normal karyotype
- Poor risk: monosomy 5 and 7 (typically secondary AML), deletion 5q, abnormalities of 11q23, or complex karyotype
- FLT3 gene mutations, especially internal tandem duplications (FLT3-ITD), have been associated with poor survival in AML. These and growing list of (onco)gene (e.g., NPM1, IDH1/2, DNMT3A, and P53) mutations have been studied to further risk-stratify patients (1).
- Genetic predisposition (e.g., Down syndrome); Bloom syndrome (~25% develop AML), Fanconi anemia (52%), neurofibromatosis, Li-Fraumeni syndrome, Wiskott-Aldrich syndrome, Kostmann syndrome, and Diamond-Blackfan anemia
- Radiation exposure
- Immunodeficiency states
- Chemical and drug exposure (nitrogen mustard and alkylating agents; benzene)
- Cigarette smoking
None currently identified, but treatment of high-risk MDS with hypomethylating agents (5-azacitidine [Vidaza]) has been shown to prolong time to transformation from MDS into AML
Commonly Associated Conditions
- Disseminated intravascular coagulopathy (DIC) especially in acute promyelocytic leukemia (APL) but may be seen in any AML
- Leukostasis (high blast number and increased adhesive ability of blasts)
- Tumor lysis syndrome (TLS): spontaneous or in response to chemotherapy
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Domino, Frank J., et al., editors. "Leukemia, Acute Myeloid." 5-Minute Clinical Consult, 27th ed., Wolters Kluwer, 2020. Medicine Central, im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/117516/all/Leukemia__Acute_Myeloid.
Leukemia, Acute Myeloid. In: Domino FJF, Baldor RAR, Golding JJ, et al, eds. 5-Minute Clinical Consult. Wolters Kluwer; 2020. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/117516/all/Leukemia__Acute_Myeloid. Accessed May 29, 2023.
Leukemia, Acute Myeloid. (2020). In Domino, F. J., Baldor, R. A., Golding, J., & Stephens, M. B. (Eds.), 5-Minute Clinical Consult (27th ed.). Wolters Kluwer. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/117516/all/Leukemia__Acute_Myeloid
Leukemia, Acute Myeloid [Internet]. In: Domino FJF, Baldor RAR, Golding JJ, Stephens MBM, editors. 5-Minute Clinical Consult. Wolters Kluwer; 2020. [cited 2023 May 29]. Available from: https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/117516/all/Leukemia__Acute_Myeloid.
* Article titles in AMA citation format should be in sentence-case
TY - ELEC T1 - Leukemia, Acute Myeloid ID - 117516 ED - Domino,Frank J, ED - Baldor,Robert A, ED - Golding,Jeremy, ED - Stephens,Mark B, BT - 5-Minute Clinical Consult, Updating UR - https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/117516/all/Leukemia__Acute_Myeloid PB - Wolters Kluwer ET - 27 DB - Medicine Central DP - Unbound Medicine ER -