eMedicine Specialties > Hematology > Stem Cells and Disorders

Acute Lymphoblastic Leukemia: Differential Diagnoses & Workup

Author: Karen Seiter, MD, Professor, Department of Internal Medicine, Division of Oncology/Hematology, New York Medical College
Contributor Information and Disclosures

Updated: Feb 3, 2009

Differential Diagnoses

Acute Myelogenous Leukemia
Lymphoma, B-Cell
Lymphoma, High-Grade Malignant Immunoblastic
Lymphoma, Mantle Cell
Lymphoma, Non-Hodgkin

Other Problems to Be Considered

Acute biphenotypic leukemia
NK-cell leukemia

Workup

Laboratory Studies

  • A complete blood cell (CBC) count with differential demonstrates anemia and thrombocytopenia to varying degrees in individuals with acute lymphoblastic leukemia (ALL). Patients with ALL can have a high, normal, or low WBC count, but they usually exhibit neutropenia.
  • Abnormalities in the prothrombin time (PT) / activated partial thromboplastin time (aPTT) / fibrinogen / fibrin degradation products may suggest concomitant DIC, which results in an elevated prothrombin time, decreased fibrinogen levels, and the presence of fibrin split products.
  • A review of the peripheral blood smear confirms the findings of the CBC count.
    • Circulating blasts are usually seen.
    • Schistocytes are sometimes seen if DIC is present.
  • A chemistry profile is recommended.
    • Most patients with acute lymphoblastic leukemia (ALL) have an elevated lactic dehydrogenase level (LDH), and they frequently have an elevated uric acid level.
    • Liver function tests and blood urea nitrogen (BUN)/creatinine determinations are necessary before the initiation of therapy.
  • Appropriate cultures, in particular blood cultures, should be obtained in patients with fever or with other signs of infection without fever.

Imaging Studies

  • Chest x-ray films may reveal signs of pneumonia and/or a prominent mediastinal mass in some cases of T-cell acute lymphoblastic leukemia (ALL).
  • Computed tomography (CT) scans can further define the degree of lymphadenopathy in some patients, including those with mediastinal masses.
  • Multiple-gated acquisition (MUGA) scans or electrocardiographs (ECGs) are needed when the diagnosis of acute lymphoblastic leukemia (ALL) is confirmed, because many chemotherapeutic agents used in the treatment of acute leukemia are cardiotoxic.

Other Tests

  • An ECG is recommended before the initiation of treatment.

Procedures

  • Bone marrow aspiration and biopsy are the definitive diagnostic tests to confirm the diagnosis of leukemia. Immunophenotyping helps elucidate the subtype.
    • Aspiration slides should be stained for morphology with either Wright or Giemsa stain. The diagnosis of acute lymphoblastic leukemia (ALL) is made when at least 30% lymphoblasts (French-American-British [FAB] classification) or 20% lymphoblasts (World Health Organization [WHO] classification) are present in the bone marrow and/or peripheral blood.
    • In addition, slides should be stained with myeloperoxidase (or Sudan black) and terminal deoxynucleotidyl transferase (TdT), unless another method is used, such as flow cytometry.
    • Bone marrow samples should also be sent for cytogenetics and flow cytometry. Approximately 15% of patients with acute lymphoblastic leukemia (ALL) have a t(9;22) translocation (ie, Philadelphia [Ph] chromosome), but other chromosomal abnormalities may also occur, such as t(4;11), t(2;8), and t(8;14).
  • A negative myeloperoxidase stain and a positive TdT is the hallmark of the diagnosis of most cases of acute lymphoblastic leukemia (ALL). However, positive confirmation of lymphoid (and not myeloid) lineage should be sought by flow cytometric demonstration of lymphoid antigens, such as CD3 (T-lineage ALL) or CD19 (B-lineage ALL), in order to avoid confusion with some types of myeloid leukemia (eg, M0), which also stain negative with myeloperoxidase.Although more than 95% of cases of the L1 or L2 subtype of acute lymphoblastic leukemia (ALL) are positive for TdT, TdT is not specific for ALL. TDT is absent in L3 (mature B-cell) ALL. TdT helps distinguish acute lymphoblastic leukemia (ALL) from malignancies of more mature lymphocytes (ie, non-Hodgkin lymphoma [NHL]).
  • In cases of acute leukemia that are MPO negative, TdT positive, the distinction between AML and acute lymphoblastic leukemia (ALL) is made based on the analysis of flow cytometry results. Patients with AML demonstrate myeloid markers such as CD33, whereas patients with ALL demonstrate lymphoid markers. Further confusion arises because some patients with acute lymphoblastic leukemia (ALL) have aberrant expression of myeloid markers, such as CD13. However, if the cells are TdT positive, myeloperoxidase negative, CD33 negative and demonstrate lymphoid markers, the leukemia is considered ALL.
  • Studies for bcr-abl analysis by polymerase chain reaction (PCR) or cytogenetics may help distinguish patients with Philadelphia chromosome–positive ALL from those with the lymphoid blastic phase of chronic myelogenous leukemia (CML). Most patients with Ph+ ALL have the p190 type of bcr-abl, whereas patients with lymphoid blastic CML have the p210 type of bcr-abl.
  • Newer studies are analyzing acute lymphoblastic leukemia (ALL) subtypes by gene expression profiling. In children with ALL, Bogni et al distinguished 3 groups of patients.1 Interestingly, one of these groups had a significantly increased risk of developing treatment-related AML following chemotherapy for their acute lymphoblastic leukemia (ALL).

Histologic Findings

The older, traditional classification of acute lymphoblastic leukemia (ALL) is the FAB classification. This has now been replaced by the newer WHO classification but the FAB system is listed below for historical purposes: 

  • L1 – Small cells with homogeneous chromatin, regular nuclear shape, small or absent nucleolus, and scanty cytoplasm; subtype represents 25-30% of adult cases
  • L2 – Large and heterogeneous cells, heterogeneous chromatin, irregular nuclear shape, and nucleolus often large; subtype represents 70% of cases (most common)
  • L3 – Large and homogeneous cells with multiple nucleoli, moderate deep blue cytoplasm, and cytoplasmic vacuolization that often overlies the nucleus (most prominent feature); subtype represents 1-2% of adult cases

The WHO classifies the L1 and L2 subtypes of acute lymphoblastic leukemia (ALL) as either precursor B lymphoblastic leukemia/lymphoblastic lymphoma or precursor T lymphoblastic leukemia/lymphoblastic lymphoma depending on the cell of origin. The L3 subtype of ALL is included in the group of mature B-cell neoplasms, as the subtype Burkitt lymphoma/leukemia.

Cytogenetic abnormalities occur in approximately 70% of cases of acute lymphoblastic leukemia (ALL) in adults. These abnormalities include balanced translocations as occur in cases of AML. However, abnormalities of chromosome number (hypodiploidy, hyperdiploidy) are more common in ALL than in AML.

Table 1. Common Cytogenetic Abnormalities in ALL

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Table
AbnormalityGenes Involved3-Year Event-Free Survival

t(10;14)(q24;q11)

HOX11/TCRA

75%

6qUnknown47%
14q11TCRA/TCRD 42%
11q23MLL18-26%
9pUnknown22%
12TEL20%

t(1;19)(q23;p13)

PBX1/E2A

20%

t(8;14)(q24;q32)
t(2;8)(p12;q24)
t(8;22)(q24;q11)

c-myc/IGH

IGK/c-myc

c-myc/IGL

17%*
80%†
t(9;22)(q34;q11)
bcr-abl

5-10%*

66%‡
t(4;11)(q21;q23)AF4-MLL

0-10%

AbnormalityGenes Involved3-Year Event-Free Survival

t(10;14)(q24;q11)

HOX11/TCRA

75%

6qUnknown47%
14q11TCRA/TCRD 42%
11q23MLL18-26%
9pUnknown22%
12TEL20%

t(1;19)(q23;p13)

PBX1/E2A

20%

t(8;14)(q24;q32)
t(2;8)(p12;q24)
t(8;22)(q24;q11)

c-myc/IGH

IGK/c-myc

c-myc/IGL

17%*
80%†
t(9;22)(q34;q11)
bcr-abl

5-10%*

66%‡
t(4;11)(q21;q23)AF4-MLL

0-10%

* Traditional regimens.
†Hyper-CVAD (cyclophosphamide, vincristine, doxorubicin [Adriamycin], dexamethasone) with rituxan.
‡Hyper-CVAD with imatinib.

Table 2. Effect of Chromosome Number on Prognosis

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Table
Chromosome Number3-Year Event-Free Survival
Near tetraploidy46-56%
Normal karyotype34-44%
Hyperdiploidy >5032-59%
Hyperdiploidy 47-5021-53%
Pseudodiploidy12-25%
Hypodiploidy11%
Chromosome Number3-Year Event-Free Survival
Near tetraploidy46-56%
Normal karyotype34-44%
Hyperdiploidy >5032-59%
Hyperdiploidy 47-5021-53%
Pseudodiploidy12-25%
Hypodiploidy11%

Eighty-five percent of cases of ALL are derived from B cells. The primary distinction is between (1) early (pro-B) ALL, which is TDT positive, CD10 (CALLA) negative, surface Ig negative; (2) precursor B ALL, which is TDT positive, CD10 (CALLA) positive, surface Ig negative; and (3) mature B cell (Burkitt) ALL, which is TdT negative, surface Ig positive. Fifteen percent of cases are derived from T cells. These cases are subclassified into different stages corresponding to the phases of normal thymocyte development. The early subtype is surface CD3 negative, cytoplasmic CD3 positive, and either double negative (CD4-, CD8-) or double positive (CD4+, CD8+). The latter subtype is surface CD3 positive, CD1a negative, and positive for either CD4 or CD8, but not both.

Table 3. Immunophenotyping of ALL Cells – ALL of B-Cell Lineage (85% of cases of adult ALL)

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Table
ALL CellsTdTCD19CD10CyIg§ SIg||
Early B-precursor ALL++---
Pre–B-cell ALL ++++-
B-cell ALL-++/-+/-+
ALL CellsTdTCD19CD10CyIg§ SIg||
Early B-precursor ALL++---
Pre–B-cell ALL ++++-
B-cell ALL-++/-+/-+

§ Cytoplasmic immunoglobulin.
|| Surface immunoglobulin.
See image below.

Diagnostic workup of a patient with pre–B-c...

Diagnostic workup of a patient with pre–B-cell acute lymphoblastic leukemia. Bone marrow aspiration revealed French-American-British L2 morphology.

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Diagnostic workup of a patient with pre–B-c...

Diagnostic workup of a patient with pre–B-cell acute lymphoblastic leukemia. Bone marrow aspiration revealed French-American-British L2 morphology.


Table 4. Immunophenotyping of ALL Cells – ALL of T-Cell Lineage (15% of cases of adult ALL)

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Table
ALL CellsTdTSurface CD3CD4/CD8
Early T-precursor ALL+-+/+ or -/-
T-cell ALL+++/- or -/+
ALL CellsTdTSurface CD3CD4/CD8
Early T-precursor ALL+-+/+ or -/-
T-cell ALL+++/- or -/+

More on Acute Lymphoblastic Leukemia

Overview: Acute Lymphoblastic Leukemia
Differential Diagnoses & Workup: Acute Lymphoblastic Leukemia
Treatment & Medication: Acute Lymphoblastic Leukemia
Follow-up: Acute Lymphoblastic Leukemia
Multimedia: Acute Lymphoblastic Leukemia
References
Further Reading
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Further Reading

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Keywords

acute lymphoblastic leukemia, ALL, lymphoid precursor cells, lymphoblasts, malignant lymphoid disorder, cancer, bone marrow malignancy, bone marrow cancer, leukemia, bone marrow failure, lymphoma, bone marrow carcinoma, anemia, thrombocytopenia, neutropenia, leukemia in children,

bone pain, splenomegaly, mediastinal mass, leukostasis, dizziness, palpitations, dyspnea, disseminated intravascular coagulation, DIC, pneumonia, petechiae, ecchymoses, hepatosplenomegaly, lymphadenopathy, Philadelphia chromosome, Ph chromosome, myeloproliferative disorder

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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; Schering Honoraria Speaking and teaching; Cephalon Honoraria Speaking and teaching

Medical Editor

Clarence Sarkodee-Adoo, MD, Consulting Staff, Department of Bone Marrow Transplantation, City of Hope Samaritan BMT Program
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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

CME Editor

Rajalaxmi McKenna, MD, FACP, Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Chief Editor

Emmanuel C Besa, MD, Professor, Department of Medicine, Division of Hematologic Malignancies, Kimmel Cancer Center, 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 Hematology, and New York Academy of Sciences
Disclosure: Nothing to disclose.

 
 
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