eMedicine Specialties > Dermatology > Lymphoma and Related Processes

Angioimmunoblastic Lymphadenopathy With Dysproteinemia

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

Introduction

Background

In 1974, Frizzera et al1 described angioimmunoblastic lymphadenopathy with dysproteinemia (AILD). In some classifications, similar atypical lymphoproliferative disorders were later grouped as lymphogranulomatosis X or immunoblastic lymphadenopathy.

AILD is a type of peripheral T-cell lymphoma that is clinically characterized by high fever and generalized lymphadenopathy that sometimes has cutaneous involvement. As AILD progresses, hepatosplenomegaly, hemolytic anemia, and polyclonal hypergammaglobulinemia may develop. The skin is involved in approximately 40-50% of patients. Patients are usually aged 40-90 years. In one series, other symptoms included weight loss (58%), hepatomegaly (60%), polyclonal hyperglobulinemia (65%), and generalized adenopathy (87%).

AILD may represent a spectrum of disease ranging from a hyperplastic but still benign immune reaction to frank malignant lymphoma. Because clonal expansion of T cells has been demonstrated in most but not all cases of AILD, subclassification has been introduced and comprises 3 subsets of the disease: AILD with no evidence of clonal lymphoid proliferation; AILD-type dysplasia with inconsistent findings regarding the clonality of the proliferating cells; and AILD-type lymphoma with strong evidence of clonality by immunohistochemical tests, rearrangement analysis, and cytogenetic studies. However, AILD-type dysplasia with an oligoclonal T-cell pattern has frequently been shown to progress into AILD-type lymphoma. Thus, subclassification may reflect the existence of stages in the development of the disease rather than independent disease entities.

Krenacs et al2 have suggested that the phenotype of neoplastic cells in angioimmunoblastic T-cell lymphoma appears consistent with the phenotype of activated follicular B-helper T cells.

Pathophysiology

Evidence exists that AILD develops in a serial fashion. The initial reaction may be an unbalanced immune response to an unknown antigen. This stage is followed by an oligoclonal phase that is driven by persistence and ineffective handling of the primary and initial stimulus. Further events, assumed to take place on a molecular level, may then evolve into malignant monoclonal disease. In AILD, the factors that result in the serial evolution into malignant lymphoma have yet to be defined. Patients frequently pass through a phase of atypical immune reactions, such as an allergic drug reaction or an allergic reaction to an arthropod bite. Moreover, latent infections with Epstein-Barr virus (EBV) or human cytomegalovirus (CMV) as evidenced by data from in situ hybridization and polymerase chain reaction tests, may also be involved.

AILD, specifically angioimmunoblastic T-cell lymphoma, is mainly derived from CD2+ CD3+ CD4+ CD5+ CD7- mature T-helper cells with varying expression and partial loss of detectable CD4. A significant number of non-neoplastic T cells (resting CD4+ T cells and activated small- or medium-sized CD8+ lymphocytes) may coexist with a minor neoplastic T-cell population.

A deletion mutant of the LMP1 oncogene of EBV is associated with the evolution of angioimmunoblastic lymphadenopathy into B immunoblastic lymphoma.

Dunleavy et al3 noted that over expression of the chemokine CXCL13 and vascular endothelial growth factor-A in angioimmunoblastic T cell lymphoma suggests that it may be derived from follicular helper T cells.
 
Using immunohistochemistry, Grogg et al4 noted CD10 and CXCL13 staining in bone marrow samples in a subset of patients with AILD. The lymphomatous infiltrate in some bone marrow specimens from these AILD patients contained numerous small or scattered large B cells, and these cells resembled either benign lymphoid aggregates or T-cell – rich large B cell lymphoma, respectively. Trilineage hematopoietic hyperplasia and plasmacytosis were other changes noted by Grogg et al.

Murakami et al5 noted that, similarly to multiple myeloma, c-Maf expression occurs in persons with angioimmunoblastic T-cell lymphoma.

Frequency

United States

The exact incidence is not known. However, it is well reported. Approximately 1-2% of non-Hodgkin lymphomas are associated with AILD.

International

The exact incidence is not known. In one case series in Korea, 1 of 78 cases of lymphoma was diagnosed as AILD. In a series of 3194 cases of lymphoma in Japan, 2.35% were diagnosed as AILD.

Mortality/Morbidity

Treatment of AILD is suboptimal, with approximately 25% of patients achieving complete and sustained remission when combined chemotherapy agents are used. However, in most patients, the condition eventually evolves into AILD-type lymphoma.

Race

This disease has been reported in Asia, the United States, and Europe. Few reports in the literature describe this disease in African American and Hispanic persons.

Sex

In 2000, in a series of 10 patients, Martel et al6 reported 7 women and 3 men. In 1995, Siegert et al7 reported a female-to-male ratio of 1:1.4 in a series of 62 patients.

Age

Most patients are middle aged or elderly. AILD has been reported in children. In 1995, Siegert et al7 reported a median patient age of 64 years (range, 21-87 y) in a series of 62 patients.

Clinical

History

  • AILD usually starts in a nonspecific fashion with maculopapular rashes (that can resemble a viral rash), seropositive polyarthritis, fever, pruritus, lymphadenopathy, night sweats, and weight loss. Bone pain can occur in AILD. Such symptoms are also generally the presenting signs of lymphoma. Initially, AILD has a waxing and waning course; however, as it progresses, symptoms persist. Patients can also have edema, ascites, and hepatosplenomegaly.
  • Patients can manifest with odd infections. For example, immunoblastic lymphadenopathy presented as an acute abdomen and mixed bacteremia with Eikenella corrodens and group C streptococci infection. Some patients have had disseminated infections with herpesvirus type 6 and other viral infections.
  • Incongruous clinical symptoms raise the possibility of AILD. For example, a case of AILD manifested with sick sinus syndrome, and others have the appearance of collagen vascular diseases. Some patients have a history of collagen-vascular diseases, such as rheumatoid arthritis and dermatomyositis.
  • In 2004, Singh et al8 reported a case of AILD with pulmonary involvement that was initially mistaken for tuberculosis based on fine-needle aspiration cytology and was treated with antituberculous therapy for 3 months. The case was subsequently diagnosed as AILD based on lymph node biopsy results.
  • Also in 2004, De Samblanx et al9 described a 67-year-old man with a nephrotic syndrome secondary to a proliferative glomerulonephritis, which was coincident with angioimmunoblastic T-cell lymphoma.
  • Batinac et al10 reported a case of AILD that resulted in death following the administration of doxycycline.
  • In 2007, Hosoki et al11 described angioimmunoblastic T-cell lymphoma developing with lymphocytic pleural effusion.
  • Renner et al12 described eosinophilic cellulitis (Wells' syndrome) in association with angioimmunoblastic lymphadenopathy.
  • Karube et al13   reported on 11 cases of adult T-cell lymphoma/leukemia with angioimmunoblastic T-cell lymphomalike features.

Physical

All organ systems can be affected by AILD. At diagnosis, patients present with a skin rash (50%), pruritus (30%), edema (40%), pleural effusion (40%), arthritis (20%), and ascites (25%).

  • Skin findings often include a morbilliform rash. It is a vascular reaction pattern rash that can resemble a viral exanthem, a toxic-mediated erythema, or a drug reaction. It can manifest as erythroderma or with pruritus that is intense and dermatitis herpetiformis – like lesions. Ferran et al14 suggested the “deck-chair sign” is specific for cutaneous involvement by angioimmunoblastic T cell lymphoma. AILD with scleromyxedemalike lesions and serum monoclonal protein has been reported.15
  • Gastrointestinal findings include ascites, gastrointestinal lymphomatous polyposis, and sclerosing cholangitis.
  • Lymph node and glandular findings include adenopathy and lacrimal and salivary gland and systemic lymphadenopathy.
  • Hepatic and splenic findings include hepatosplenomegaly.
  • Renal findings include renal amyloidosis, proliferative glomerulonephritis, and acute interstitial nephritis.
  • Pulmonary findings are varied and include hypoxemia. Some patients have interstitial pneumonia or bronchopneumonia. Patients with bronchopneumonia can have opportunistic infections, such as Pneumocystis carinii, and 1 patient had CMV.
  • Neurologic, rheumatologic, and related findings include retrobulbar neuritis, neuropathy, polyneuropathy, arthritis, papilledema, myelofibrosis, and inflammatory myopathy.

Causes

  • AILD has been linked to a variety of viral infections, such as EBV, CMV, and herpesvirus type 6. It has also been linked with a variety of genetic mutations. The body's immune system is also thought to misapprehend some antigens, resulting in the cascade of cytokines and gene expression that underlies AILD. The actual proximate cause is not known.
  • Medications linked to the induction of AILD include salazosulfapyridine, azithromycin, and doxycycline.

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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