eMedicine Specialties > Pediatrics: General Medicine > Oncology

Non-Hodgkin Lymphoma: Differential Diagnoses & Workup

Author: J Martin Johnston, MD, Associate Professor of Pediatrics, Mercer University School of Medicine; Director of Pediatric Hematology/Oncology, Backus Children's Hospital; Consulting Oncologist/Hematologist, St Damien's Pediatric Hospital
Contributor Information and Disclosures

Updated: Dec 5, 2008

Differential Diagnoses

Acute Lymphoblastic Leukemia
Lymphoproliferative Disorders
Acute Myelocytic Leukemia
Mononucleosis and Epstein-Barr Virus Infection
Appendicitis
Neuroblastoma
Atypical Mycobacterial Infection
Rhabdomyosarcoma
Catscratch Disease
Sarcoidosis
Hodgkin Disease
Toxoplasmosis
Intussusception
Tuberculosis
Lymphadenitis
Wilms Tumor

Workup

Laboratory Studies

  • Obtain a CBC count with differential and a platelet count in patients with non-Hodgkin lymphoma (NHL) to assess for possible involvement of the bone marrow and to determine the patient's transfusion requirements.
  • Measure the prothrombin time, the activated partial thromboplastin time, fibrinogen, and the D-dimer level if the patient is febrile or if he or she has evidence of sepsis. The purpose is to assess for possible disseminated intravascular coagulation, which may require specific therapy.
  • Obtain blood and urine cultures if patient has a fever, especially if it is associated with neutropenia. If indicated, also obtain stool and throat cultures.
  • Analyze the measures listed below to assess the patient's renal and hepatic function and to monitor for possible tumor lysis syndrome. Of note, the level of lactate dehydrogenase at diagnosis had prognostic significance in many analyses of treatment outcomes.
    • Serum electrolytes
    • BUN
    • Creatinine
    • Uric acid
    • Lactate dehydrogenase
    • Bilirubin
    • Albumin
    • Total protein
    • Aspartate aminotransferase
    • Alanine aminotransferase
    • Calcium
    • Magnesium
    • Phosphorus
  • Perform HIV serologic tests in patients who have risk factors for HIV exposure or in those with primary CNS lymphoma to exclude these possible predisposing factors.

Imaging Studies

  • Chest radiography: Obtain posteroanterior and lateral views to assess for possible mediastinal masses, to evaluate the airway, and to exclude pulmonary parenchymal lesions and associated pneumonia.
  • Ultrasonography
    • Abdominal sonography helps in assessing the size of the kidneys and the patency of the urinary tract.
    • Abdominal sonography is useful particularly before chemotherapy in anticipation of prolonged excretion and excess toxicity, for example.
    • When symptoms are present, testicular ultrasonography aids in identifying additional sites of disease.
  • Computed tomography
    • CT scans of the chest, abdomen, and pelvis can be used to stage lesions (see Staging).
    • If the patient is stable, chest CT scan is indicated to assess for the degree of tracheal compression.
    • Head CT scans assist in excluding mass lesions and possible meningeal involvement among individuals with CNS disease.
  • Bone scanning and skeletal surveys: When additional symptoms are present, these tests help in identifying additional sites of disease.
  • Gallium-67 scanning
    • 67 Gal scanning is highly recommended.
    • Some tumors are gallium avid, and their response to treatment can be assessed by using this modality.
    • Occult sites of disease also may be identified on67 Gal scans.
  • Positron emission tomography: Positron emission tomography (PET) has recently been used for purposes similar to those for67 Gal scanning.24,25

Other Tests

  • Other tests may include serologic analyses for varicella, measles, herpes simplex virus, Epstein-Barr virus, cytomegalovirus (CMV), hepatitis A, hepatitis B, and hepatitis C.
    • Perform these tests to document susceptibility in patients who will be receiving immunosuppressive therapy.
    • These tests might provide evidence of the cause (eg, Epstein-Barr virus).
    • Serologic results can help in identifying patients who may benefit from transfusion with CMV-negative blood products, especially if bone marrow transplantation is eventually offered.
    • Order these tests to confirm previous exposure to a hepatitis virus before blood transfusions are administered.
  • Perform echocardiography to obtain baseline findings before patients are given chemotherapy with anthracyclines, which can cause cardiomyopathy.

Procedures

  • Bilateral (superior to unilateral) bone marrow aspiration and biopsy
    • Biopsy is necessary to assess for evidence of bone marrow involvement in patients with lymphomas.
    • A finding of more than 25% marrow blasts is generally regarded as diagnostic of acute leukemia. Levels of involvement lower than this with lymphoma indicate stage 4 disease.
    • Polymerase chain reaction assays are being used experimentally to detect and monitor minimal residual disease in the marrow.26,27 In the future, postinduction measurement of minimal residual disease may improve precision in determining treatment responses and/or treatment assignments.
  • Biopsy
    • A histologic diagnosis must be obtained.
    • For patients with an abdominal tumor, tissue is generally available from resection or intraoperative biopsy.
    • Patients with mediastinal disease frequently have enlarged supraclavicular or cervical nodes, which can enable diagnosis without thoracotomy.
    • As an alternative, a diagnosis may be made by using pleural fluid (see Media file 4) or by using involved bone marrow (especially if CBC counts are abnormal and/or if imaging studies demonstrate abnormal signal intensity of the marrow). In rare cases, cerebrospinal fluid (CSF) can be used.
  • Lumbar puncture with determination of the CSF cell count and differential: This test is done to assess CNS involvement, the presence of which alters therapy.
  • Acquisition of central venous access
    • For most patients, a central venous access device is necessary to manage chemotherapy.
    • If feasible, multiple procedures (eg, line placement, biopsy, lumbar puncture, bone marrow aspiration) can be performed during one session of anesthesia.
    • As noted previously, patients with mediastinal disease must be treated cautiously if the use of general anesthesia is being considered. Unrecognized airway compression can lead to obstruction, with disastrous consequences.

Histologic Findings

Several classification systems for non-Hodgkin lymphoma are available. Examples are the Kiel classification and the NCI Working Formulation. At present, the Revised European-American Lymphoma (REAL) classification is gaining acceptance as the criterion standard for classifying adult non-Hodgkin lymphoma. For classifying childhood non-Hodgkin lymphoma, this system is overly complicated because it includes numerous diagnoses that are rarely or never observed in children.

Adult non-Hodgkin lymphomas are characterized as low, intermediate, or high grade, and they can have a diffuse or nodular appearance. In contrast, childhood non-Hodgkin lymphomas are almost always high grade and diffuse. In general, they can be divided into 3 major classes, or even 4 classes if one differentiates the 2 most common types of large cell lymphomas (LCLs), B-cell or T-cell LCLs. The 3 major classes are described below.

For a particular tumor, achieving agreement among pathologists is sometimes difficult. However, synthesis of the histologic, immunohistochemical, cytogenetic, and clinical and/or anatomic data almost always results in a clear diagnosis.

Lymphoblastic lymphomas

Lymphoblastic lymphoma cells are indistinguishable from the lymphoblasts of acute lymphoblastic leukemia (ALL). The cells are monotonous and associated with a high nuclear-to-cytoplasmic ratio. Their nuclei are often convoluted and contain finely stippled chromatin. Nucleoli are usually visible but are not prominent.

Immunohistochemical analysis usually reveals T-cell markers, including CD5 and CD7. Common ALL antigen (CALLA) is occasionally observed.

A minor subset of lymphoblastic lymphomas expresses the precursor B-cell phenotype typical of childhood ALL. This phenotype includes the surface antigens CALLA and B4 and the human leukocyte antigen (HLA)-DR.

Small noncleaved cell lymphomas

Small noncleaved cell lymphoma (SNCCLs) can be classified Burkitt or non-Burkitt (Burkittlike) lymphomas. The distinction may be subtle, and its clinical significance is unclear.

Burkitt lymphoma cells are notably uniform in size and shape, and they usually contain multiple prominent nucleoli. In contrast, extensive cellular pleomorphism, or occasionally the presence of a single nucleolus in most cells, suggests a diagnosis of Burkittlike lymphoma. SNCCL cells have slightly more cytoplasm than do lymphoblastic lymphoma cells. The cytoplasm is basophilic and usually contains lipid-filled vacuoles.

Macrophages often infiltrate the tumors, lending the classic starry-sky appearance. However, this observation is not pathognomic of Burkitt lymphoma.

The tumor cells are mature B cells, as evidenced by the surface expression of immunoglobulin (usually immunoglobulin M), CD19, CD20, and HLA-DR. CALLA is usually present.

Immunophenotyping results suggest that Burkittlike lymphoma cells are more likely than Burkitt lymphoma cells to express the BCL-6 oncogene, and they exhibit relatively low levels of apoptosis.28

Because of the features described, Burkittlike lymphoma appears to be biologically distinct from Burkitt lymphoma, and it is perhaps most closely related to the B-cell LCLs.

Large cell lymphomas

LCLs are a heterogeneous group. Most cases can be classified as B-cell or T-cell LCLs.

The B-cell—derived LCLs histologically merge with the SNCCLs. In terms of the expression of cell-surface proteins, these tumors are currently indistinguishable. If infiltrating macrophages are present, these cells can serve as a reference by which the tumor cells are measured. In B-cell LCLs, many or most of the tumoral nuclei are larger than those of the macrophages.

Anaplastic LCLs are more common than B-cell LCLs and are derived from T cells, as evidenced by their TCR gene rearrangements. However, anaplastic LCLs may express few T-cell surface markers. Their hallmark is the expression of CD30, or Ki-1+, an antigen first recognized on Hodgkin lymphoma cells. Aberrant expression of myeloid markers CD13 and CD33 has more recently been reported as a sensitive (but not specific) marker of ALK+ anaplastic LCL.29

Other cell surface markers that may be observed are HLA-DR and the interleukin-2 receptor.

Finally, a small number of LCLs do not exhibit a clear T-cell or B-cell phenotype. At least some of these tumors are of histiocytic origin.

Staging

Several systems for classifying non-Hodgkin lymphomas have been proposed. The St Jude system (ie, the Murphy system) has gained the widest acceptance.30 This system is as follows:

  • Stage I - Single extranodal tumor or single anatomic area (nodal), excluding the mediastinum or abdomen
  • Stage II - Single extranodal tumor with regional node involvement; primary GI tumor with or without associated involvement of mesenteric nodes, with gross total resection; or, on same side of diaphragm, 2 or more nodal areas, or 2 single (extranodal) tumors with or without regional node involvement
  • Stage III - Any primary mediastinal, pleural, or thymic intrathoracic tumor; any extensive and unresectable abdominal tumor; any primary paraspinous or epidural tumor regardless of other sites; or, on both sides of the diaphragm, 2 or more nodal areas, or 2 single (extranodal) tumors with or without regional node involvement
  • Stage IV - Any of the above with initial CNS or marrow (<25%) involvement

More on Non-Hodgkin Lymphoma

Overview: Non-Hodgkin Lymphoma
Differential Diagnoses & Workup: Non-Hodgkin Lymphoma
Treatment & Medication: Non-Hodgkin Lymphoma
Follow-up: Non-Hodgkin Lymphoma
Multimedia: Non-Hodgkin Lymphoma
References
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Further Reading

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Keywords

non-Hodgkin lymphoma, NHL, non-Hodgkin's lymphoma, lymphoblastic lymphoma, LL, T-lymphoblastic lymphoma, T-LL, BL, Burkitt lymphoma, Burkitt's lymphoma, non-Burkitt lymphoma, non-Burkitt's lymphoma, non Burkitt lymphoma, Burkitt-like lymphoma, BLL, malignant small noncleaved lymphoma, small noncleaved cell lymphoma, SNCCL, SNCC lymphoma, undifferentiated lymphoma, large cell lymphomas, large-cell lymphomas, LCLs, B-cell LCLs, B-cell lymphoma, B-cell large cell lymphomas, BLCLs

ALCLs, anaplastic LCLs, anaplastic large cell lymphomas, Ki-1+ lymphoma, Ki 1+ lymphoma, malignant anaplastic lymphoma, histiocytic lymphoma, immunoblastic lymphoma, myeloid lymphoma, lymphosarcoma, reticulum cell sarcoma, acute lymphoblastic lymphoma, ALL, common ALL antigen, CALLA, diffuse large cell lymphoma

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Contributor Information and Disclosures

Author

J Martin Johnston, MD, Associate Professor of Pediatrics, Mercer University School of Medicine; Director of Pediatric Hematology/Oncology, Backus Children's Hospital; Consulting Oncologist/Hematologist, St Damien's Pediatric Hospital
J Martin Johnston, MD is a member of the following medical societies: American Society of Pediatric Hematology/Oncology
Disclosure: Nothing to disclose.

Medical Editor

Kathleen M Sakamoto, MD, PhD, Professor and Chief, Division of Hematology-Oncology, Vice-Chair of Research, Mattel Children's Hospital at UCLA; Department of Pathology and Laboratory Medicine, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA and California Nanosystems Institute and Molecular Biology, UCLA
Kathleen M Sakamoto, MD, PhD is a member of the following medical societies: American Society of Hematology, American Society of Pediatric Hematology/Oncology, New York Academy of Sciences, Society for Pediatric Research, and Western Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Timothy P Cripe, MD, PhD, Professor of Pediatric Hematology/Oncology, University of Cincinnati; Director, Translational Research Trials Office, Department of Pediatrics, Cincinnati Children's Hospital Medical Center
Timothy P Cripe, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American Pediatric Society, American Society of Hematology, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Samuel Gross, MD, Professor Emeritus, Department of Pediatrics, University of Florida, Clinical Professor, Department of Pediatrics, UNC, Adjunct Professor, Department of Pediatrics, Duke University
Samuel Gross, MD is a member of the following medical societies: American Association for Cancer Research, American Society for Blood and Marrow Transplantation, American Society of Clinical Oncology, American Society of Hematology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Max J Coppes, MD, PhD, MBA, Executive Director, Center for Cancer and Blood Disorders, Children's National Medical Center; Professor of Medicine, Oncology, and Pediatrics, Georgetown University
Max J Coppes, MD, PhD, MBA is a member of the following medical societies: American Association for Cancer Research, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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