Acute Myelogenous Leukemia Clinical Presentation

  • Author: Karen Seiter, MD; Chief Editor: Emmanuel C Besa, MD   more...
 
Updated: Mar 9, 2012
 

History

Patients with acute myelogenous leukemia (AML) present with symptoms resulting from bone marrow failure, symptoms resulting from organ infiltration with leukemic cells, or both. The time course is variable. Some patients, particularly younger ones, present with acute symptoms over a few days to 1-2 weeks. Others have a longer course, with fatigue or other symptoms lasting from weeks to months. A longer course may suggest an antecedent hematologic disorder, such as myelodysplastic syndrome (MDS).

Symptoms of bone marrow failure

Symptoms of bone marrow failure are related to anemia, neutropenia, and thrombocytopenia. The most common symptom of anemia is fatigue. Patients often retrospectively note a decreased energy level over past weeks. Other symptoms of anemia include dyspnea upon exertion, dizziness, and, in patients with coronary artery disease, anginal chest pain. In fact, myocardial infarction may be the first presenting symptom of acute leukemia in an older patient.

Patients with AML often have decreased neutrophil levels despite an increased total white blood cell (WBC) count. Patients generally present with fever, which may occur with or without specific documentation of an infection. Patients with the lowest absolute neutrophil counts (ANCs) (ie, < 500 cells/µL, especially < 100 cells/µL) have the highest risk of infection.

Patients often have a history of upper respiratory infection symptoms that have not improved despite empiric treatment with oral antibiotics.

Patients present with bleeding gums and multiple ecchymoses. Bleeding may be caused by thrombocytopenia, coagulopathy that results from disseminated intravascular coagulation (DIC), or both. Potentially life-threatening sites of bleeding include the lungs, gastrointestinal (GI) tract, and the central nervous system.

Symptoms of organ infiltration with leukemic cells

Alternatively, symptoms may be the result of organ infiltration with leukemic cells. The most common sites of infiltration include the spleen, liver, gums, and skin. Infiltration occurs most commonly in patients with the monocytic subtypes of AML. Patients with splenomegaly note fullness in the left upper quadrant and early satiety. Patients with gum infiltration often present to their dentist first. Gingivitis due to neutropenia can cause swollen gums, and thrombocytopenia can cause the gums to bleed.

Patients with markedly elevated WBC counts (>100,000 cells/µL) can present with symptoms of leukostasis (ie, respiratory distress and altered mental status). Leukostasis is a medical emergency that calls for immediate intervention. Patients with a high leukemic cell burden may present with bone pain caused by increased pressure in the bone marrow.

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Physical Examination

Physical signs of anemia, including pallor and a cardiac flow murmur, are frequently present in AML patients. Fever and other signs of infection can occur, including lung findings of pneumonia.

Patients with thrombocytopenia usually demonstrate petechiae, particularly on the lower extremities. The petechiae are small, often punctate, hemorrhagic rashes that are not palpable. Areas of dermal bleeding or bruises (ie, ecchymoses) that are large or present in several areas may indicate a coexistent coagulation disorder (eg, DIC). Purpura is characterized by flat bruises that are larger than petechiae but smaller than ecchymoses.

Signs relating to organ infiltration with leukemic cells include hepatosplenomegaly and, to a lesser degree, lymphadenopathy. Occasionally, patients have skin rashes due to infiltration of the skin with leukemic cells (leukemia cutis). Chloromata are extramedullary deposits of leukemia. Rarely, a bony or soft-tissue chloroma may precede the development of marrow infiltration by AML (granulocytic sarcoma).

Signs relating to leukostasis include respiratory distress and altered mental status.

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Complications

Death may occur in patients with AML as a consequence of uncontrolled infection or hemorrhage. This may happen even after use of appropriate blood product and antibiotic support.

The most common complication in AML patients is failure of the leukemia to respond to chemotherapy. The prognosis for these patients is poor because their disease usually does not respond to other chemotherapy regimens.

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Contributor Information and Disclosures
Author

Karen Seiter, MD  Professor, Department of Internal Medicine, Division of Oncology/Hematology, New York Medical College

Karen Seiter, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, and American Society of Hematology

Disclosure: Novartis Honoraria Speaking and teaching; Novartis Consulting fee Speaking and teaching; Eisai Honoraria Speaking and teaching; Celgene Honoraria Speaking and teaching

Specialty Editor Board

Clarence Sarkodee-Adoo, MD  Consulting Staff, Department of Bone Marrow Transplantation, City of Hope Samaritan BMT Program

Disclosure: Takeda Millenium Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Ronald A Sacher, MB, BCh, MD, FRCPC  Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center

Ronald A Sacher, MB, BCh, MD, FRCPC is a member of the following medical societies: American Association for the Advancement of Science, American Association of Blood Banks, American Clinical and Climatological Association, American Society for Clinical Pathology, American Society of Hematology, College of American Pathologists, International Society of Blood Transfusion, International Society on Thrombosis and Haemostasis, and Royal College of Physicians and Surgeons of Canada

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; Talecris Honoraria Board membership

Chief Editor

Emmanuel C Besa, MD  Professor, Department of Medicine, Division of Hematologic Malignancies, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University

Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Clinical Oncology, American Society of Hematology, and New York Academy of Sciences

Disclosure: Nothing to disclose.

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Table 1. Immunophenotyping of AML Cells
MarkerLineage
CD13Myeloid
CD33Myeloid
CD34Early precursor
HLA-DRPositive in most AML, negative in APL
CD11bMature monocytes
CD14Monocytes
CD41Platelet glycoprotein IIb/IIIa complex
CD42aPlatelet glycoprotein IX
CD42bPlatelet glycoprotein Ib
CD61Platelet glycoprotein IIIa
Glycophorin AErythroid
TdTUsually indicates acute lymphocytic leukemia, however, may be positive in M0 or M1
CD11cMyeloid
CD117 (c-kit)Myeloid/stem cell
Table 2. Common Cytogenetic Abnormalities in AML
AbnormalityGenes InvolvedMorphologyResponse
t(8;21)(q22;q22)AML/ETOM2Good
inv(16)(p13;q22)CBFb/MYH11M4eoGood
NormalMultipleVariesIntermediate
-7MultipleVariesPoor
-5MultipleVariesPoor
+8MultipleVariesIntermediate-poor
11q23MLLVariesIntermediate-poor
MiscellaneousMultipleVariesIntermediate-poor
Multiple complex*MultipleVariesPoor
* Refers to 3-5 different cytogenetic abnormalities, depending on the classification used.
Table 3. Cytogenetic Abnormalities in APL
TranslocationGenes InvolvedAll-Trans-Retinoic Acid Response
t(15;17)(q21;q11)PML/RARaYes
t(11;17)(q23;q11)PLZF/RARaNo
t(11;17)(q13;q11)NuMA/RARaYes
t(5;17)(q31;q11)NPM/RARaYes
t(17;17)stat5b/RARaUnknown
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