eMedicine Specialties > Hematology > Stem Cells and Disorders
Acute Myelogenous Leukemia: Differential Diagnoses & Workup
Updated: Nov 10, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Differential Diagnoses
Workup
Laboratory Studies
- A complete blood cell (CBC) count with differential demonstrates anemia and thrombocytopenia to varying degrees. Patients with acute myelogenous leukemia (AML) can have high, normal, or low WBC counts.
- Prothrombin time (PT) / activated partial thromboplastin time (aPTT) / fibrinogen / fibrin degradation products
- The most common abnormality is DIC, which results in an elevated prothrombin time, a decreasing fibrinogen level, and the presence of fibrin split products.
- Acute promyelocytic leukemia (APL), also known as M3, is the most common subtype of acute myelogenous leukemia (AML) associated with DIC.
- Peripheral blood smear
- Review of THE peripheral blood smear confirms the findings of the CBC count.
- Circulating blasts are usually seen.
- Schistocytes are occasionally seen if DIC is present.
- Chemistry profile
- Most patients with acute myelogenous leukemia (AML) have an elevated lactic dehydrogenase (LDH) level and, frequently, an elevated uric acid level.
- Liver function tests and blood urea nitrogen (BUN)/creatinine level tests are necessary before the initiation of therapy.
- Appropriate cultures should be obtained in patients with fever or signs of infection, even in the absence of fever.
- Perform human leukocyte antigen (HLA) or DNA typing in patients who are potential candidates for allogeneic transplantation.
- Bone marrow aspiration
- A blast count can be performed with bone marrow aspiration. Historically, by French-American-British (FAB) classification, acute myelogenous leukemia (AML) was defined by the presence of more than 30% blasts in the bone marrow. In the newer World Health Organization (WHO) classification, AML is defined as the presence of greater than 20% blasts in the marrow.1
- The bone marrow aspirate also allows evaluation of the degree of dysplasia in all cell lines.
- Bone marrow biopsy is useful to assess cellularity. Biopsy is most important in patients in whom an aspirate can not be obtained (dry tap).
- Flow cytometry (immunophenotyping) can be used to help distinguish acute myelogenous leukemia (AML) from acute lymphocytic leukemia (ALL) and further classify the subtype of AML. The immunophenotype correlates with prognosis in some instances.
- Cytogenetic studies performed on bone marrow provide important prognostic information and are useful to confirm a diagnosis of APL, which bears the t(15;17) chromosome abnormality and is treated differently.
- Fluorescence in situ hybridization (FISH) studies can be used to get a faster overview of cytogenetic abnormalities than traditional cytogenetic studies. FISH does not replace cytogenetics.
- Several molecular abnormalities that are not detected with routine cytogenetics have been shown to have prognostic importance in patients with acute myelogenous leukemia (AML). The bone marrow should be evaluated at least for the commercially available tests.
- Fms-like tyrosine kinase 3 (FLT3) is the most commonly mutated gene in persons with acute myelogenous leukemia (AML) and is constitutively activated in one third of AML cases.z8 Internal tandem duplications (ITDs) in the juxtamembrane domain of FLT3 exist in 25% of AML cases. In other cases, mutations exist in the activation loop of FLT3. Most studies demonstrate that patients with AML and FLT3 mutations have a poor prognosis. Analysis of FLT3 is commercially available.
- Mutations in nucleophosmin (NPM1) are associated with increased response to chemotherapy in patients with a normal karyotype. Thiede et al studied FLT3 and NPM1 in 1485 patients with acute myelogenous leukemia (AML).9 The analysis of the clinical impact in 4 groups (NPM1 and FLT3 -ITD single mutants, double mutants, and wild-type [wt] for both) revealed that patients having only an NPM1 mutation (without a FLT3 -ITD) had a significantly better overall and disease-free survival and a lower cumulative incidence of relapse.9 Analysis of NPM1 is commercially available.
- Mutations in CEBPA are detected in 15% of patients with normal cytogenetics findings and are associated with a longer remission duration and longer overall survival.
- ERG overexpression is an adverse predictor in cytogenetically normal acute myelogenous leukemia (AML).
- A study by the Cancer and Leukemia Group B (CALGB) found that high BAALC expression was associated with FLT3-ITD, wild-type NPM1, mutated CEBPA (P = 0.003), MLL-PTD (P = 0.009), absent FLT3-TKD and high ERG expression. In a multivariable analysis, high BAALC expression independently predicted lower complete remission rates when adjusting for ERG expression and age, and shorter survival when adjusting for FLT3-ITD, NPM1, CEBPA and WBC count.
- The clinical impact of MLL partial tandem duplication (MLL-PTD) was evaluated in 238 adults aged 18 to 59 years with cytogenetically normal de novo acute myeloid leukemia who were treated by CALGB. Of the patients with MLL-PTD, 92% achieved complete remission compared with 83% of patients without MLL-PTD (P = 0.39).< LI>
- Gene-expression profiling is a research tool that allows a comprehensive classification of acute myelogenous leukemia (AML) based on the expression pattern of thousands of genes.
Imaging Studies
- Chest radiographs help assess for pneumonia and signs of cardiac disease in individuals with acute myelogenous leukemia (AML).
- Multiple gated acquisition (MUGA) scanning is needed once the diagnosis is of acute myelogenous leukemia (AML) is confirmed, because many chemotherapeutic agents used in treatment are cardiotoxic.
Other Tests
- Electrocardiography should be performed before treatment of acute myelogenous leukemia (AML).
Procedures
- Bone marrow aspiration and biopsy are the definitive diagnostic tests for acute myelogenous leukemia (AML).
- Aspiration slides are stained for morphology with either Wright or Giemsa stain.
- To determine the FAB type of the leukemia, slides are also stained with myeloperoxidase (or Sudan black), terminal deoxynucleotidyl transferase (TdT) (unless performed by another method [eg, flow cytometry]), and double esterase (see Histologic Findings).
- Bone marrow samples should also be sent for cytogenetics testing and flow cytometry.
- Patients with APL should have their marrow evaluated for the PML/RARa genetic rearrangement.
- When possible, the bone marrow should be evaluated for FLT3 and NPM1 mutations.
Histologic Findings
The older, more traditional, FAB classification of acute myelogenous leukemia (AML) is as follows:- M0 - Undifferentiated leukemia
- M1 - Myeloblastic without differentiation
- M2 - Myeloblastic with differentiation
- M3 - Promyelocytic
- M4 - Myelomonocytic
- M4eo - Myelomonocytic with eosinophilia
- M5 - Monoblastic leukemia
- M5a - Monoblastic without differentiation
- M5b - Monocytic with differentiation
- M6 - Erythroleukemia
- M7 - Megakaryoblastic leukemia
The newer WHO classification is as follows1 :
- Acute myelogenous leukemia (AML) with recurrent genetic abnormalities
- AML with t(8;21)(q22;q22), (AML1/ETO)
- AML with abnormal bone marrow eosinophils and inv(16)(p13q22) or t(16;16)(p13)(q22), (CBFB/MYH11)
- APL with t(15;17)(q22;q12), (PML/RARa) and variants
- AML with 11q23 (MLL) abnormalities
- AML with multilineage dysplasia
- Following MDS or MDS/myeloproliferative disease (MPD)
- Without antecedent MDS or MDS/myeloproliferative disease (MPD) but with dysplasia in at least 50% of cells in 2 or more lineages
- AML and MDS, therapy related
- Alkylating agent or radiation-related type
- Topoisomerase II inhibitor type
- Others
- AML, not otherwise classified
- AML, minimally differentiated
- AML, without maturation
- AML, with maturation
- Acute myelomonocytic leukemia
- Acute monoblastic or monocytic leukemia
- Acute erythroid leukemia
- Acute megakaryoblastic leukemia
- Acute basophilic leukemia
- Acute panmyelosis and myelofibrosis
- Myeloid sarcoma
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Table
Abnormality | Genes Involved | Morphology | Response |
| t(8;21)(q22;q22) | AML/ETO | M2 | Good |
| inv(16)(p13;q22) | CBFb/MYH11 | M4eo | Good |
| Normal | Multiple | Varies | Intermediate |
| -7 | Multiple | Varies | Poor |
| -5 | Multiple | Varies | Poor |
| +8 | Multiple | Varies | Intermediate-poor |
| 11q23 | MLL | Varies | Intermediate-poor |
| Miscellaneous | Multiple | Varies | Intermediate-poor |
| Multiple complex* | Multiple | Varies | Poor |
Abnormality | Genes Involved | Morphology | Response |
| t(8;21)(q22;q22) | AML/ETO | M2 | Good |
| inv(16)(p13;q22) | CBFb/MYH11 | M4eo | Good |
| Normal | Multiple | Varies | Intermediate |
| -7 | Multiple | Varies | Poor |
| -5 | Multiple | Varies | Poor |
| +8 | Multiple | Varies | Intermediate-poor |
| 11q23 | MLL | Varies | Intermediate-poor |
| Miscellaneous | Multiple | Varies | Intermediate-poor |
| Multiple complex* | Multiple | Varies | Poor |
* Refers to 3-5 different cytogenetic abnormalities, depending on the classification used.
Table 2. Cytogenetic Abnormalities in APL
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Table
| Translocation | Genes Involved | All-Trans-Retinoic Acid Response |
| t(15;17)(q21;q11) | PML/RARa | Yes |
| t(11;17)(q23;q11) | PLZF/RARa | No |
| t(11;17)(q13;q11) | NuMA/RARa | Yes |
| t(5;17)(q31;q11) | NPM/RARa | Yes |
| t(17;17) | stat5b/RARa | Unknown |
| Translocation | Genes Involved | All-Trans-Retinoic Acid Response |
| t(15;17)(q21;q11) | PML/RARa | Yes |
| t(11;17)(q23;q11) | PLZF/RARa | No |
| t(11;17)(q13;q11) | NuMA/RARa | Yes |
| t(5;17)(q31;q11) | NPM/RARa | Yes |
| t(17;17) | stat5b/RARa | Unknown |
Table 3. Immunophenotyping of AML Cells
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Table
Marker | Lineage |
| CD13 | Myeloid |
| CD33 | Myeloid |
| CD34 | Early precursor |
| HLA-DR | Positive in most AML, negative in APL |
| CD11b | Mature monocytes |
| CD14 | Monocytes |
| CD41 | Platelet glycoprotein IIb/IIIa complex |
| CD42a | Platelet glycoprotein IX |
| CD42b | Platelet glycoprotein Ib |
| CD61 | Platelet glycoprotein IIIa |
| Glycophorin A | Erythroid |
| TdT | Usually indicates acute lymphocytic leukemia, however, may be positive in M0 or M1 |
| CD11c | Myeloid |
| CD117 (c-kit) | Myeloid/stem cell |
Marker | Lineage |
| CD13 | Myeloid |
| CD33 | Myeloid |
| CD34 | Early precursor |
| HLA-DR | Positive in most AML, negative in APL |
| CD11b | Mature monocytes |
| CD14 | Monocytes |
| CD41 | Platelet glycoprotein IIb/IIIa complex |
| CD42a | Platelet glycoprotein IX |
| CD42b | Platelet glycoprotein Ib |
| CD61 | Platelet glycoprotein IIIa |
| Glycophorin A | Erythroid |
| TdT | Usually indicates acute lymphocytic leukemia, however, may be positive in M0 or M1 |
| CD11c | Myeloid |
| CD117 (c-kit) | Myeloid/stem cell |
More on Acute Myelogenous Leukemia |
| Overview: Acute Myelogenous Leukemia |
 Differential Diagnoses & Workup: Acute Myelogenous Leukemia |
| Treatment & Medication: Acute Myelogenous Leukemia |
| Follow-up: Acute Myelogenous Leukemia |
| References |
| Further Reading |
| « Previous Page | Next Page » |
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Further Reading
Related eMedicine Topics
- Acute Myelocytic Leukemia [in the Pediatrics: General Medicine section]
- Acute Myeloid Leukemia With Myelodysplasia-Related Features [in the Pathology section]
- Alloimmunization From Transfusions [in the Allergy and Immunology section]
- Erythroleukemia
Clinical Trials
- Efficacy of 5-azacytidine Added to Standard Primary Therapy in Elderly Patients With Newly Diagnosed Acute Myeloid Leukemia (AML)
- Lentivirus Transduced Acute Myeloid Leukaemia Blasts Expressing B7.1 (CD80) and IL-2
- Standard Idarubicin and Cytarabine for the Treatment of Acute Myeloid Leukemia (AML)
- Study to Investigate the Efficacy, Safety and Tolerability of AZD1152 Alone and in Combination With Low Dose Cytosine Arabinoside (LDAC)in Acute Myeloid Leukaemia (AML) Patients
- Study to Assess the Safety, Tolerability, and Efficacy of Tipifarnib Plus Bortezomib in the Treatment of Acute Myeloid Leukemia
Clinical Guideline
- Guidelines on the management of acute myeloid leukaemia in adults. British Committee for Standards in Haematology - Professional Association. 2006 Nov. 25 pages. NGC:006225
Keywords
acute myelogenous leukemia, acute myeloid leukemia, AML, acute nonlymphoblastic leukemia, acute nonlymphocytic leukemia, acute non-lymphoblastic leukemia, acute non-lymphocytic leukemia, nonlymphoblastic leukemia, nonlymphocytic leukemia, non-lymphoblastic leukemia, non-lymphocytic leukemia, leukemia, cancer, bone marrow cancer, bone marrow failure,
radiation exposure, Bloom syndrome, Down syndrome, trisomy 21, congenital neutropenia, Fanconi anemia, neurofibromatosis, acute promyelocytic leukemia, APL, M3, promyelocytic leukemia, immature bone marrow cells, chromosomal translocation, genetic abnormality, cytogenetic abnormalities, anemia, thrombocytopenia, neutropenia, myelodysplastic syndrome, MDS, antecedent hematologic disorder, AHD, disseminated intravascular coagulation, DIC,
organ infiltration with leukemic cells, leukostasis, familial erythroleukemia, bone marrow transplantation, bone marrow transplant, BMT, allogeneic BMT, autologous BMT, alkylating agents, topoisomerase-II inhibitors, acute monocytic leukemia, M5, acute myelomonocytic leukemia, M4, blast count, acute undifferentiated leukemia, M0, acute megakaryocytic leukemia, M7, bone marrow aspiration, arabinosylcytosine, araC, ara-C, fibrinolysis,
all-trans-retinoic acid, ATRA, retinoic acid syndrome, malignant disease of bone marrow, bleeding gums, multiple ecchymoses, gingivitis, petechiae, leukemia cutis, chloromata, soft-tissue chloroma, granulocytic sarcoma, Li-Fraumeni syndrome, aplastic anemia, pancytopenia, myelofibrosis, paroxysmal nocturnal hemoglobinuria, polycythemia vera
