AIDS-Related Lymphoma Treatment (PDQ®): Treatment - Health Professional Information [NCI]

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AIDS-Related Lymphoma Treatment

Purpose of This PDQ Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of AIDS-related lymphoma. This summary is reviewed regularly and updated as necessary by the PDQ Adult Treatment Editorial Board.

Information about the following is included in this summary:

  • Prognostic factors.
  • Cellular classification.
  • Staging.
  • Treatment options by cancer stage.

This summary is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

Some of the reference citations in the summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Adult Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations. Based on the strength of the available evidence, treatment options are described as either "standard" or "under clinical evaluation." These classifications should not be used as a basis for reimbursement determinations.

This summary is available in a patient version, written in less technical language, and in Spanish.

General Information

Note: Some citations in the text of this section are followed by a level of evidence. The PDQ editorial boards use a formal ranking system to help the reader judge the strength of evidence linked to the reported results of a therapeutic strategy. (Refer to the PDQ summary on Levels of Evidence for more information.)

The acquired immunodeficiency syndrome (AIDS) was first described in 1981, and the first definitions included certain opportunistic infections, Kaposi sarcoma, and central nervous system (CNS) lymphomas. (Refer to the PDQ summaries on Kaposi Sarcoma Treatment and Primary CNS Lymphoma Treatment for more information.) In 1984, a multicenter study described the clinical spectrum of non-Hodgkin lymphomas (NHLs) in the populations at risk for AIDS.[1] In 1985 and 1987, the Centers for Disease Control and Prevention (CDC) revised the definition of AIDS to include human immunodeficiency virus (HIV)-infected patients who had aggressive B-cell NHL. The incidence of NHL has increased in an almost parallel course with the AIDS epidemic and accounts for 2% to 3% of newly diagnosed AIDS cases.[2]

Pathologically, AIDS-related lymphomas are comprised of a narrow spectrum of histologic types consisting almost exclusively of B-cell tumors of aggressive type. These include:

  • Diffuse large B-cell lymphoma.
  • B-cell immunoblastic lymphoma.
  • Small noncleaved lymphoma, either Burkitt or Burkitt-like.

The HIV-associated lymphomas can be categorized into:

  • Aggressive B-cell lymphoma.
  • Primary central nervous system lymphoma (PCNSL), which represents 20% of all NHL cases in AIDS patients. (Refer to the PDQ summary on Primary CNS Lymphoma Treatment for more information.)
  • Primary effusion lymphoma.
  • Plasmablastic multicentric Castleman disease.
  • Hodgkin lymphoma.

Primary effusion lymphoma has been associated with Kaposi sarcoma-associated herpes-virus/human herpes virus type-8 (KSHV/HHV-8).[3,4] Primary effusion lymphoma presents as a liquid phase spreading along serous membranes in the absence of masses or adenopathy.[3] In addition to HHV-8, many cases are also associated with Epstein-Barr virus. Extension of lymphoma from the effusion to underlying tissue may occur. Plasmablastic multicentric Castleman disease is also associated with a coinfection of KSHV/HHV-8 and HIV.[5,6] Patients typically present with fever, night sweats, weight loss, lymphadenopathy, and hepatosplenomegaly. Patients may progress to primary effusion lymphoma or to plasmablastic or anaplastic large cell lymphoma. Anecdotal responses to rituximab, an anti-CD20 monoclonal antibody, have been reported.[5][Level of evidence: 3iiiDiv]

An international database of 48,000 HIV-seropositive individuals from the United States, Europe, and Australia found a 42% decline in the incidence of NHLs from 1997 to 1999 compared with 1992 to 1996, both for PCNSL and for systemic lymphoma.[7] The introduction of highly active antiretroviral therapy (HAART) is the proposed explanation for this decline.[8] The diagnosis of AIDS precedes the onset of NHL in approximately 57% of the patients, but in 30% of the patients the diagnosis of AIDS is made at the time of the diagnosis of NHL and HIV positivity.[9] The geographic distribution of these lymphomas is also similar to the geographic spread of AIDS. Unlike Kaposi sarcoma, which has a predilection for homosexual men and appears to be on the decline in incidence, all risk groups appear to have an excess number of NHLs; these risk groups include intravenous drug users and children of HIV-positive individuals.

In general, the clinical setting and response to treatment of patients with AIDS-related lymphoma is very different from that of the non-HIV patients with lymphoma. The HIV-infected individual with aggressive lymphoma usually presents with advanced-stage disease that is frequently extranodal.[10] Common extranodal sites include bone marrow, liver, meninges, and gastrointestinal tract, while very unusual sites are also characteristic, including anus, heart, bile duct, gingiva, and muscles. The clinical course is more aggressive, and the disease is both more extensive and less responsive to chemotherapy. Immunodeficiency and cytopenias, common in these patients at the time of initial presentation, are exacerbated by the administration of chemotherapy. Treatment of the malignancy increases the risk of opportunistic infections that, in turn, further compromise the delivery of adequate treatment.

Prognoses of patients with AIDS-related lymphoma have been associated with stage (extent of disease, extranodal involvement, lactate dehydrogenase level, and bone marrow involvement), age, severity of the underlying immunodeficiency (measured by CD4 lymphocyte count in peripheral blood), performance status, and prior AIDS diagnosis (history of opportunistic infection or Kaposi sarcoma).[11] Patients with AIDS-related PCNSL appear to have more severe underlying HIV-related disease than do patients with systemic lymphoma. In one report, this severity was evidenced by patients with PCNSL having a higher incidence of a prior AIDS diagnoses (73% vs. 37%), lower median number of CD4 lymphocytes (30/dL vs. 189/dL), and a worse median survival time (2.5 months vs. 6.0 months).[12] This report also showed that patients with poor risk factors (defined as Karnofsky performance status <70%, history of prior AIDS diagnosis, and bone marrow involvement) had a median survival time of 4.0 months compared with a good prognosis group without any of these risk factors, who had a median survival time of 11.3 months.

In another report, prognostic factors were evaluated in a group of 192 patients with newly diagnosed AIDS-related lymphoma who were randomized to receive either low-dose methotrexate, bleomycin, doxorubicin, cyclophosphamide, vincristine, and dexamethasone (m-BACOD) or standard dose m-BACOD with granulocyte-macrophage colony-stimulating factor.[13] No differences existed between these two treatments in terms of efficacy for disease-free survival, median survival, or risk ratio for death.[13][Level of evidence: 1iiA] On multivariate analysis (NIAID-ACTG-142), factors associated with decreased survival included age older than 35, history of intravenous drug use, stage III or stage IV disease, and CD4 counts of less than 100 cells/mm3. The median survival rates were 46 weeks for patients with one or no risk factors, 44 weeks for patients with two risk factors, and 18 weeks for patients with three or more risk factors. The International Prognostic Index may also be predictive for survival.[14,15,16] In a multicenter cohort study of 203 patients, in a multivariable Cox model, response to HAART was independently associated with prolonged survival (relative hazard = 0.32; 95% confidence interval, 0.16–0.62).[17][Level of evidence: 3iiiDii]

HIV-ASSOCIATED HODGKIN LYMPHOMA

Since 1984, several series of cases of Hodgkin lymphoma occurring in patients at risk for AIDS have been reviewed;[18,19] however, Hodgkin lymphoma is still not part of the CDC definition of AIDS because of no clear demonstration of its increased incidence in conjunction with HIV, as is the case for aggressive NHL. The CDC, in conjunction with the San Francisco Department of Public Health, has reported a cohort study in which HIV-infected men had an excess risk that was attributable to the HIV infection of 19.3 cases of Hodgkin lymphoma per 100,000 person-years and 224.9 cases of NHL per 100,000 person-years. Although an excess incidence of Hodgkin lymphoma was found in HIV-infected homosexual men in this report, additional epidemiologic studies will be needed before the CDC will reconsider Hodgkin lymphoma as an HIV-associated malignancy.[20]

HIV-associated Hodgkin lymphoma presents in an aggressive fashion, often with extranodal or bone marrow involvement.[18,19,21] A distinctive feature of HIV-associated Hodgkin lymphoma is the lower frequency of mediastinal adenopathy compared with non-HIV-associated Hodgkin lymphoma. Most patients in these series had either mixed cellularity or lymphocyte-depleted Hodgkin lymphoma, expression of Epstein-Barr virus-associated proteins in Reed-Sternberg cells, B symptoms, and a median CD4 lymphocyte count of 300/dL or less.[22] In a retrospective multicenter review of 62 patients, those receiving HAART with chemotherapy had a 74% 2-year overall survival (OS) versus a 30% OS for those not receiving HAART (P < .001).[23][Level of evidence: 3iiiA]

References:

1. Ziegler JL, Beckstead JA, Volberding PA, et al.: Non-Hodgkin's lymphoma in 90 homosexual men. Relation to generalized lymphadenopathy and the acquired immunodeficiency syndrome. N Engl J Med 311 (9): 565-70, 1984.
2. Rabkin CS, Yellin F: Cancer incidence in a population with a high prevalence of infection with human immunodeficiency virus type 1. J Natl Cancer Inst 86 (22): 1711-6, 1994.
3. Simonelli C, Spina M, Cinelli R, et al.: Clinical features and outcome of primary effusion lymphoma in HIV-infected patients: a single-institution study. J Clin Oncol 21 (21): 3948-54, 2003.
4. Nador RG, Cesarman E, Chadburn A, et al.: Primary effusion lymphoma: a distinct clinicopathologic entity associated with the Kaposi's sarcoma-associated herpes virus. Blood 88 (2): 645-56, 1996.
5. Goedert JJ: Multicentric Castleman disease: viral and cellular targets for intervention. Blood 102 (8): 2710-11, 2003.
6. Marcelin AG, Aaron L, Mateus C, et al.: Rituximab therapy for HIV-associated Castleman disease. Blood 102 (8): 2786-8, 2003.
7. International Collaboration on HIV and Cancer.: Highly active antiretroviral therapy and incidence of cancer in human immunodeficiency virus-infected adults. J Natl Cancer Inst 92 (22): 1823-30, 2000.
8. Stebbing J, Gazzard B, Mandalia S, et al.: Antiretroviral treatment regimens and immune parameters in the prevention of systemic AIDS-related non-Hodgkin's lymphoma. J Clin Oncol 22 (11): 2177-83, 2004.
9. Knowles DM, Chamulak GA, Subar M, et al.: Lymphoid neoplasia associated with the acquired immunodeficiency syndrome (AIDS). The New York University Medical Center experience with 105 patients (1981-1986). Ann Intern Med 108 (5): 744-53, 1988.
10. Sparano JA: Clinical aspects and management of AIDS-related lymphoma. Eur J Cancer 37 (10): 1296-305, 2001.
11. Bower M, Gazzard B, Mandalia S, et al.: A prognostic index for systemic AIDS-related non-Hodgkin lymphoma treated in the era of highly active antiretroviral therapy. Ann Intern Med 143 (4): 265-73, 2005.
12. Levine AM, Sullivan-Halley J, Pike MC, et al.: Human immunodeficiency virus-related lymphoma. Prognostic factors predictive of survival. Cancer 68 (11): 2466-72, 1991.
13. Kaplan LD, Straus DJ, Testa MA, et al.: Low-dose compared with standard-dose m-BACOD chemotherapy for non-Hodgkin's lymphoma associated with human immunodeficiency virus infection. National Institute of Allergy and Infectious Diseases AIDS Clinical Trials Group. N Engl J Med 336 (23): 1641-8, 1997.
14. Navarro JT, Ribera JM, Oriol A, et al.: International prognostic index is the best prognostic factor for survival in patients with AIDS-related non-Hodgkin's lymphoma treated with CHOP. A multivariate study of 46 patients. Haematologica 83 (6): 508-13, 1998.
15. Rossi G, Donisi A, Casari S, et al.: The International Prognostic Index can be used as a guide to treatment decisions regarding patients with human immunodeficiency virus-related systemic non-Hodgkin lymphoma. Cancer 86 (11): 2391-7, 1999.
16. Straus DJ, Huang J, Testa MA, et al.: Prognostic factors in the treatment of human immunodeficiency virus-associated non-Hodgkin's lymphoma: analysis of AIDS Clinical Trials Group protocol 142--low-dose versus standard-dose m-BACOD plus granulocyte-macrophage colony-stimulating factor. National Institute of Allergy and Infectious Diseases. J Clin Oncol 16 (11): 3601-6, 1998.
17. Hoffmann C, Wolf E, Fätkenheuer G, et al.: Response to highly active antiretroviral therapy strongly predicts outcome in patients with AIDS-related lymphoma. AIDS 17 (10): 1521-9, 2003.
18. Spina M, Vaccher E, Nasti G, et al.: Human immunodeficiency virus-associated Hodgkin's disease. Semin Oncol 27 (4): 480-8, 2000.
19. Thompson LD, Fisher SI, Chu WS, et al.: HIV-associated Hodgkin lymphoma: a clinicopathologic and immunophenotypic study of 45 cases. Am J Clin Pathol 121 (5): 727-38, 2004.
20. Hessol NA, Katz MH, Liu JY, et al.: Increased incidence of Hodgkin disease in homosexual men with HIV infection. Ann Intern Med 117 (4): 309-11, 1992.
21. Re A, Casari S, Cattaneo C, et al.: Hodgkin disease developing in patients infected by human immunodeficiency virus results in clinical features and a prognosis similar to those in patients with human immunodeficiency virus-related non-Hodgkin lymphoma. Cancer 92 (11): 2739-45, 2001.
22. Dolcetti R, Boiocchi M, Gloghini A, et al.: Pathogenetic and histogenetic features of HIV-associated Hodgkin's disease. Eur J Cancer 37 (10): 1276-87, 2001.
23. Hentrich M, Maretta L, Chow KU, et al.: Highly active antiretroviral therapy (HAART) improves survival in HIV-associated Hodgkin's disease: results of a multicenter study. Ann Oncol 17 (6): 914-9, 2006.

Cellular Classification

Pathologically, AIDS-related lymphomas are comprised of a narrow spectrum of histologic types consisting almost exclusively of B-cell tumors of aggressive type. These include:

  • Diffuse large B-cell lymphoma.
  • B-cell immunoblastic lymphoma.
  • Small noncleaved lymphoma, either Burkitt or Burkitt-like.

All three pathologic types are equally distributed and represent aggressive disease.

AIDS-related lymphomas, though usually of B-cell origin as demonstrated by immunoglobulin heavy-chain gene rearrangement studies, have also been shown to be oligoclonal and polyclonal as well as monoclonal in origin. Although HIV does not appear to have a direct etiologic role, HIV infection does lead to an altered immunologic milieu. HIV generally infects T lymphocytes whose loss of regulation function leads to hypergammaglobulinemia and polyclonal B-cell hyperplasia. B cells are not the targets of HIV infection. Instead, Epstein-Barr virus (EBV) is thought to be at least a cofactor in the etiology of some of these lymphomas. The EBV genome has been detected in varying numbers of patients with AIDS-related lymphomas; molecular analysis suggests that the cells were infected before clonal proliferation began.[1] EBV is detected in 30% of patients with small, noncleaved lymphomas and in 80% of patients with diffuse, large cell lymphomas. The rare, primary effusion lymphoma consistently harbors human herpes virus type-8 and frequently contains EBV.[2] HIV-related T-cell lymphomas have also been identified and appear to be associated with EBV infection.[3]

References:

1. Thorley-Lawson DA, Gross A: Persistence of the Epstein-Barr virus and the origins of associated lymphomas. N Engl J Med 350 (13): 1328-37, 2004.
2. Simonelli C, Spina M, Cinelli R, et al.: Clinical features and outcome of primary effusion lymphoma in HIV-infected patients: a single-institution study. J Clin Oncol 21 (21): 3948-54, 2003.
3. Thomas JA, Cotter F, Hanby AM, et al.: Epstein-Barr virus-related oral T-cell lymphoma associated with human immunodeficiency virus immunosuppression. Blood 81 (12): 3350-6, 1993.

Stage Information

Although stage is important in selecting the treatment of patients with non-Hodgkin lymphoma (NHL) who do not have acquired immunodeficiency syndrome (AIDS), the majority of patients with AIDS-related lymphomas have far-advanced disease. In general, the staging system used is the Ann Arbor system, which is identical to that used for non-AIDS-related NHLs.

Staging Subclassification System

Stages I, II, III, and IV NHL can be subclassified into A and B categories: B for those with well-defined generalized symptoms and A for those without. The B designation is given to patients with any of the following symptoms:

  • Unexplained loss of more than 10% of body weight in the 6 months before diagnosis.
  • Unexplained fever with temperatures higher than 38° C.
  • Drenching night sweats. (Refer to the PDQ summary on Fever, Sweats, and Hot Flashes for more information.)

The designation "E" is used when extranodal lymphoid malignancies arise in tissues away from the major lymphatic aggregates. If pathologic proof of involvement of one or more extralymphatic sites has been documented, the symbol for the site of involvement, followed by a plus sign (+), is listed. Sites are identified by the following notation:

Notation for identification of sites

N = nodes H = liver L = lung M = marrow
S = spleen P = pleura O = bone D = skin

STAGE I

Stage I NHL means involvement of a single lymph node region (I), or localized involvement of a single extralymphatic organ or site (IE).[1,2]

STAGE II

Stage II NHL means involvement of two or more lymph node regions on the same side of the diaphragm (II) or localized involvement of a single associated extralymphatic organ or site and its regional lymph nodes with or without other lymph node regions on the same side of the diaphragm (IIE).[1,2]

STAGE III

Stage III NHL means involvement of lymph node regions on both sides of the diaphragm (III) that may also be accompanied by localized involvement of an extralymphatic organ or site (IIIE), involvement of the spleen (IIIS), or both (IIIS+E).[1,2]

STAGE IV

Stage IV NHL means disseminated (multifocal) involvement of one or more extralymphatic organs with or without associated lymph node involvement or isolated extralymphatic organ involvement with distant (nonregional) nodal involvement.[1,2]

A number of factors that are important for determining prognosis are not included in the staging system for NHLs. All of these factors should be considered when selecting treatment. Prognosis is related to the severity of the underlying immune deficiency (CD4 lymphocyte count), the presence or history of opportunistic infections (prior AIDS-defining illness), bone marrow involvement, performance status, and presence of extranodal disease.[3] Typically, AIDS-related lymphomas are widespread with extranodal disease at the time of presentation. The most common extranodal sites are the gastrointestinal (GI) tract, central nervous system, bone marrow, and liver. In one series, the largest group of patients had both extranodal and nodal disease (43%), but 33% of the patients presented with extranodal disease only.[4] In a second series, 87% of the patients had extranodal disease at presentation.[5]

At diagnosis, 66% of the patients have stage IV disease. In addition, unusual presentations include involvement of the rectum, heart, pericardium, pulmonary parenchyma, bile ducts, mouth, and subcutaneous and soft tissues. The clinical features of AIDS-related lymphomas correlate with histopathology. The majority of patients with small noncleaved cell (Burkitt) lymphomas present with stage IV disease, mostly because of bone marrow involvement. This compares with an approximately 40% stage IV presentation by those with immunoblastic and large cell lymphomas. A particular prevalence for GI involvement has been noted in patients who have immunoblastic and large noncleaved cell lymphoma types.[6] While high-risk behavior should be looked for in every patient, HIV testing should probably be done for any patient who has Burkitt lymphoma or the atypical presentation of extranodal lymphoma that involves rare sites, i.e., rectum, GI tract, bone, or orbit. Similarly, malignant lymphoma should be considered in any HIV-infected patient who has progressive lymphadenopathy, tumors at any site, central nervous system symptoms, or unexplained wasting, fever, or abdominal pain.

References:

1. Lymphoid neoplasms. In: American Joint Committee on Cancer.: AJCC Cancer Staging Manual. 6th ed. New York, NY: Springer, 2002, pp 393-406.
2. National Cancer Institute sponsored study of classifications of non-Hodgkin's lymphomas: summary and description of a working formulation for clinical usage. The Non-Hodgkin's Lymphoma Pathologic Classification Project. Cancer 49 (10): 2112-35, 1982.
3. Levine AM: Acquired immunodeficiency syndrome-related lymphoma: clinical aspects. Semin Oncol 27 (4): 442-53, 2000.
4. Kaplan LD, Abrams DI, Feigal E, et al.: AIDS-associated non-Hodgkin's lymphoma in San Francisco. JAMA 261 (5): 719-24, 1989.
5. Knowles DM, Chamulak GA, Subar M, et al.: Lymphoid neoplasia associated with the acquired immunodeficiency syndrome (AIDS). The New York University Medical Center experience with 105 patients (1981-1986). Ann Intern Med 108 (5): 744-53, 1988.
6. Raphael BG, Knowles DM: Acquired immunodeficiency syndrome-associated non-Hodgkin's lymphoma. Semin Oncol 17 (3): 361-6, 1990.

Treatment Option Overview

The treatment of patients with acquired immunodeficiency syndrome (AIDS)-related lymphomas presents the challenge of integrating therapy appropriate for the stage and histologic subset of malignant lymphoma with the limitations imposed by HIV infection, which to date is a chronic incurable illness.[1] In addition to antitumor therapy, essential components of an optimal non-Hodgkin lymphoma treatment strategy include highly active antiretroviral therapy, prophylaxis for opportunistic infections, and rapid recognition and treatment of intercurrent infections.[2] Patients with HIV positivity and underlying immunodeficiency have poor bone marrow reserve, which compromises the potential for drug dose intensity. Intercurrent opportunistic infection is a risk that may also lead to a decrease in drug delivery. Furthermore, chemotherapy itself compromises the immune system and increases the likelihood of opportunistic infection.

References:

1. Levine AM: Acquired immunodeficiency syndrome-related lymphoma: clinical aspects. Semin Oncol 27 (4): 442-53, 2000.
2. Tirelli U, Bernardi D: Impact of HAART on the clinical management of AIDS-related cancers. Eur J Cancer 37 (10): 1320-4, 2001.

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Changes to This Summary (09 / 25 / 2008)

The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.

STAGE INFORMATION

Editorial changes were made to this section.

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Date Last Modified: 2008-09-25

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