eMedicine Specialties > Dermatology > Lymphoma and Related Processes

Angioimmunoblastic Lymphadenopathy With Dysproteinemia: Differential Diagnoses & Workup

Author: Noah S Scheinfeld, MD, JD, FAAD, Assistant Clinical Professor, Department of Dermatology, Columbia University; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Private Practice
Contributor Information and Disclosures

Updated: Feb 11, 2008

Differential Diagnoses

Other Problems to Be Considered

  • Multicentric giant lymph node hyperplasia
  • Acute viral lymphadenitis
  • Lymphoma
  • Leukemia
  • Viral exanthem
  • Crohn disease: Kang et al16 described angioimmunoblastic T-cell lymphoma mimicking Crohn disease.

Workup

Laboratory Studies

  • Almost any laboratory value can be abnormal in AILD. As is true with its clinical symptoms, incongruous laboratory values, especially pancytopenia, should prompt a consideration of AILD as a diagnosis. Patients also exhibit autoimmune laboratory findings, such as circulating immune complexes, a positive Coombs test result, smooth muscle antibodies, rheumatoid factors, autoimmune hemolysis, cold agglutinins, paraproteinemia, antinuclear antibodies, and cryoglobulins.
  • In AILD, a variety of hematologic anomalies are present; anticardiolipin antibodies and anemia with hemoglobin with values below 10 g/dL can be present, and a direct Coombs test result can be positive. Often, thrombocytopenia with platelet counts below 100 X 109/L is present. Platelet-associated immunoglobulin G can be present. In many patients, whole complement activity (CH50) is reduced. Pancytopenia can also be present. These changes are related to compromised bone marrow function.
  • In some cases, trisomies 3, 5, and X in AILD can be detected with fluorescence in situ hybridization. Cells with +5, +15, +19, +21, +22 trisomies have been seen as well.
  • Blood chemistry values that can be abnormal include erythrocyte sedimentation rate (almost all cases), lactate dehydrogenase (LDH) level (commonly increased), polyclonal gammaglobulins (common), autoantibodies, antinuclear antibodies, antismooth muscle antibodies, anticardiolipin antibodies, rheumatoid factor (less common), and cryoglobulins (less common).
  • AILD shows a high proportion of tumor necrosis factor-alpha–positive T lymphocytes, and, in addition, the percentages of interleukin (IL)–2, IL-4, IL-5, IL-6, IL-13, and interferon-gamma–positive T lymphocytes were relatively higher than in other diseases. These data underlie the state of multiple hypercytokinemia typically observed in AILD.
  • The role of EBV infection in skin lesions is not clear.
  • Tumor cells in AILD express T-cell–associated antigens and are usually CD4 positive. The clonality of cells can be detected, with T-cell clonality eventually detected in 75% of cases. After treatment, residual disease can be detected by polymerase chain reaction (PCR) by analyzing the rearrangement of TCR genes. PCR amplification and sequencing of immunoglobulin H (IgH) genes is advisable because a gene rearrangement is detected in 10% of cases.
  • Yamane et al17 reported angioimmunoblastic T-cell lymphoma with polyclonal proliferation of plasma cells in peripheral blood and marrow.

Imaging Studies

  • Radiography and CT scanning can demonstrate lymphadenopathy. They can also demonstrate pulmonary abnormalities, such as pleural effusions and multiple opacities, predominantly basal, of variable size.
    • Radiographic findings include bilateral mediastinal and hilar lymphadenopathy, pleural effusion, interstitial shadow, alveolar shadow, and atelectasis.
    • Diffuse CT contrast enhancement of cervical lymph nodes can aid in diagnosing angioimmunoblastic lymphadenopathy.
  • Magnetic resonance imaging of bone marrow can demonstrate angioimmunoblastic lymphadenopathy. They show lymphadenopathy, ie, enlargement of the lymph nodes; this finding is not diagnostic.
  • Gallium scans and radiographic appearances may assist in diagnosing AILD, but lymph node biopsy is necessary to distinguish AILD from lymphoma.

Procedures

  • Biopsies of the bone marrow, lymph node, and skin are key in diagnosing AILD.
    • AILD is diagnosed by a positive biopsy result obtained from an affected lymph node, although sometimes biopsy results are only suggestive of AILD, not diagnostic.
    • A tap of ascites fluid is useful as well. Ascites is present in 25% of cases and requires cytologic examination.

Histologic Findings

On examination of the skin biopsy sample, a perivascular dermal infiltrate with eosinophils, histiocytes, plasma cells, and lymphoid cells is observed. The infiltrate can be patchy. The number of blood vessels can be increased. The endothelial cells, which are often cuboidal, are prominent.

In some cases, skin histologic analysis shows extensive perivascular and periadnexal mixed lymphoid infiltrates, including centroblasts and immunoblasts, with a high proliferative index and with focal erythrocyte extravasation.

In skin lesions, T- and B-cell blasts predominate together with endothelial cell proliferation. T-cell receptor gene rearrangement analysis reveals a monoclonality T cell; however, B-cell proliferations are usually polyclonal.

Histologic examination of the lymph nodes can show nearly complete effacement of the follicular architecture, a mixed lymphoid infiltrate, and numerous high endothelial venules in an expanded T-cell zone. In some cases, the lymph nodes show diffuse obliteration of their architecture by lymphoid infiltrates consisting of lymphocytes, immunoblasts, plasma cells, and histiocytes together with numerous high endothelial venules surrounded by an expanded network of follicular dendritic cells.

Immunohistochemical analysis can demonstrate preservation of at least some follicular structures.

Attygalle et al18 reported in 2007 that clear cells and EBV infection (when present) are useful distinguishing features and that CD10 is a sensitive and specific marker of AILD. Hyperplastic follicles are present in a significant minority of AILD patients.

Sakai et al19 described an angioimmunoblastic T-cell lymphoma patient initially presenting with replacement of bone marrow and peripheral plasmacytosis.

Staging

The standard staging system used for angioimmunoblastic T-cell lymphoma is the same as that proposed for Hodgkin disease at the Ann Arbor Conference in 1971. Its use is not certain because its staging does not seem to match the prognosis, but it is the only system available and is used nevertheless.

The Ann Arbor staging system uses both the number of sites of involvement and the presence of disease above or below the diaphragm. The Ann Arbor staging system defines 4 stages of disease:

  • Stage I - Involvement of a single lymph node region (I) or a single extranodal site (IE)
  • Stage II - Involvement of 2 or more lymph node regions on the same side of the diaphragm (II) or localized involvement of an extralymphatic site (IIE)
  • Stage III - Involvement of lymph node regions on both sides of the diaphragm (III) and localized involvement of an extralymphatic site (IIIE) or spleen (IIIs) or both (IIIEs)
  • Stage IV - Diffuse or disseminated involvement of 1 or more extralymphatic organs with or without associated lymph node involvement; localized involvement of liver or bone marrow is also considered stage IV

Patients are divided into 2 subsets according to the presence (A) or absence (B) of systemic symptoms. Fever of no evident cause, night sweats, and weight loss of more than 10% of the patient's body weight are considered systemic symptoms. Even though it is a frequently accompanying symptom, itching should not be considered a systemic symptom. The presence of a bulky mass, such as a lesion of 10 cm or more in the longest diameter, is signaled as "X," whereas the extranodal involvement should be identified by a symbol such as the following: O for bone, L for lung, and D for skin.

Miura et al20 reported acute renal failure resulting from immunoglobulin M – lambda glomerular thrombi and membranoproliferative glomerulonephritis – like lesions in a patient with angioimmunoblastic T-cell lymphoma.

More on Angioimmunoblastic Lymphadenopathy With Dysproteinemia

Overview: Angioimmunoblastic Lymphadenopathy With Dysproteinemia
Differential Diagnoses & Workup: Angioimmunoblastic Lymphadenopathy With Dysproteinemia
Treatment & Medication: Angioimmunoblastic Lymphadenopathy With Dysproteinemia
Follow-up: Angioimmunoblastic Lymphadenopathy With Dysproteinemia
References
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Further Reading

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Keywords

AILD, angioimmunoblastic T-cell lymphoma, diffuse plasmacytic sarcomatosis, immunoblastic lymphadenopathy, lymphogranulomatosis X, immunologic aberrations in idiopathic reticulosis, angioimmunoblastic lymphadenopathy, AIL

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Contributor Information and Disclosures

Author

Noah S Scheinfeld, MD, JD, FAAD, Assistant Clinical Professor, Department of Dermatology, Columbia University; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Private Practice
Noah S Scheinfeld, MD, JD, FAAD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Optigenex Consulting fee Independent contractor

Medical Editor

Evan R Farmer, MD, Professor of Dermatology, Johns Hopkins University School of Medicine, Clinical Professor of Pathology, Virginia Commonwealth University School of Medicine; Consulting Staff, Department of Dermatology, Johns Hopkins Hospital, VCU Health Services
Evan R Farmer, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, American Medical Association, American Society of Dermatopathology, and International Society of Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Daniel S Loo, MD, Associate Professor, Residency Program Director, Department of Dermatology, Boston University School of Medicine
Daniel S Loo, MD is a member of the following medical societies: American Academy of Dermatology and Association of Professors of Dermatology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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