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Journal of Clinical Oncology, Vol 25, No 21 (July 20), 2007: pp. 3176-3178 © 2007 American Society of Clinical Oncology. DOI: 10.1200/JCO.2007.12.0154
AIDS-Associated Plasmablastic Lymphoma Presenting at the Insertion Site of a Peritoneal Dialysis CatheterDana Farber Cancer Institute, Boston, MA
Brigham & Women's Hospital, Boston, MA
Glens Falls Hospital Cancer Center, Glens Falls, NY
Dana Farber Cancer Institute, Boston, MA A 37-year-old man with known HIV disease and end-stage renal disease (ESRD) sought medical attention because of a persistent mass at the site of his peritoneal dialysis catheter. Six years earlier, he had been diagnosed with HIV when he presented with P. jirovecii pneumonia and a CD4 count of 154/µL. He was started on highly active antiretroviral therapy (HAART) without significant toxicity, and his most recent viral load was undetectable and CD4 T-cell count had risen to 333/µL. Shortly after his diagnosis of HIV, he developed end-stage renal disease which was attributed to immunoglobulin A nephropathy. After initial attempts with hemodialysis resulted in profound hemodynamic instability, peritoneal dialysis was instituted, which he had been successfully undergoing for the last 3 years. The patient had no other significant HIV-related complications. One month before presentation, the patient had noted a 1-cm mass at the site of his peritoneal dialysis catheter insertion site with some associated purulent discharge. The mass subsequently grew to 4 to 5 cm in size over the next 3 to 4 weeks. A computed axial tomography scan image of the mass (arrow) is shown in Figure 1. He was taken to the operating room for excision of the mass and removal of his catheter. Pathology of the excised mass showed a malignant neoplasm comprised of large atypical cells with round to oval nuclei, vesicular chromatin, large nucleoli, and an abundant amount of cytoplasm without any evidence of infection (Figs 2A and 2B; original magnification x400 and x1,000, respectively). The large atypical cells displayed anaplastic and plasmacytic features with numerous apoptotic bodies and mitotic figures present. Immunohistochemical studies (Figs 2C to 2E; original magnification x400) showed that the atypical cells were positive for CD138 (Fig 2D), MUM-1 (Fig 2E), CD56, and CD10 and negative for CD5, CD20 (Fig 2C), CD22, CD23, CD30, Bcl-2, Bcl-6, and surface immunoglobulin. Staining for Epstein-Barr virus encoded RNA was positive (Fig 2F) while human herpesvirus 8 (HHV-8) staining was negative (data not shown). Further staging studies included a full body positron emission tomography scan, bone marrow biopsy, and lumbar puncture, all of which showed no evidence of disease involvement. He was therefore diagnosed as a stage IAE plasmablastic AIDS-associated non-Hodgkin's lymphoma localized to the insertion site of his peritoneal dialysis catheter. Surgical margins did show evidence of disease involvement and the patient completed 45 Gy of local external-beam radiation therapy. Positron emission tomography scan after radiation showed no evidence of residual or distant disease. He was subsequently treated with four cycles of standard cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy. HAART was continued throughout. As of April 2007 (10 months after finishing chemotherapy), the patient was alive and well without evidence of disease.
Patients with HIV/AIDS are at a significantly increased risk of developing NHL, which is classified as an AIDS-defining illness. The most common types of AIDS-related NHL (ARL) are Burkitt's lymphoma and diffuse large B-cell lymphoma, which includes immunoblastic lymphoma; rare types include primary effusion lymphoma (PEL), primary CNS lymphoma (PCNSL), and plasmablastic lymphoma (PBL). Viral activation is thought to play a significant role in the development of NHL in HIV patients as evidence of Epstein-Barr virus infection is found in approximately 30% of Burkitt's lymphoma, 40% to 90% of diffuse large B-cell lymphoma, approximately 90% of PEL, almost all cases of PCNSL, and the majority of cases of PBL.1 In addition, infection with HHV-8 is essential to the pathogenesis of PEL as well as multicentric Castleman's disease-associated PBL. Based on recent series of ARL, PBL accounts for approximately 2% to 4% of all AIDS-related lymphomas.1-3 PBL can arise independently or in the background of HHV-8–driven multicentric Castleman's disease. Initially described as tumors which developed primarily in the oral cavity,4 HIV-associated PBL can frequently present with disseminated disease, most commonly involving other extranodal sites such as the bones, soft tissue, and gastrointestinal tract.5 Diagnostically, cases of PBL will have a distinctive morphology showing plasmacytoid differentiation as seen in Figure 2. The characteristic immunophenotype includes lack of expression of the pan B-cell antigen CD20, but expression of both MUM-1 and CD138, two markers of plasma cell differentiation. Rearrangement of the immunoglobulin heavy chain is variable. This case is unique in presenting in a localized extranodal fashion at the insertion site of a peritoneal dialysis catheter. Tropism to sites of catheter implantation is a rarely described phenomenon in hematological malignancies and, to our knowledge, this is the first description of involvement by an ARL. Previous cases have been reported in patients with diffuse large cell lymphoma,6 Burkitt's lymphoma,7 multiple myeloma,7-9 and acute myelogenous leukemia.10,11 In addition, a case of one individual who developed subcutaneous plasmacytomas at sites of previous trauma from indwelling catheters, cellulitis, and injection sites has been reported.12 The mechanism by which this unique tropism occurs is unclear. An older study had previously shown that increased numbers of tumor cells localize to sites of trauma in a mouse model,13 suggesting that the local inflammatory response was responsible for the apparent tropism. As immunologic cell localization is thought to be controlled by a series of specific receptor-ligand interactions, this tropism may be due to the expression of trafficking molecules by the tumor cells (eg, chemokine or cytokine receptors).12 Historically, the prognosis for patients with AIDS-associated PBL has been poor with very few long-term survivors; however, the introduction of modern HAART appears to be associated with better prognoses in large series of ARLs.3,14 Much like other NHLs, combination chemotherapy forms the backbone of therapy for PBL, and CHOP-like regimens are considered first-line therapy. Rituximab, an anti-CD20 monoclonal antibody that has been incorporated into the standard therapy for many B-cell NHLs, does not play a role in PBL therapy as CD20 is not usually expressed by PBL cells. In addition, there is one case report of a patient with PBL achieving a prolonged remission with antiretroviral therapy alone,15 suggesting a role for immune reconstitution in control of this aggressive lymphoma. Thus, initiating or continuing HAART as part of supportive therapy is recommended when commencing treatment for HIV-positive patients with PBL. Lastly, the routine use of growth factors to avoid prolonged periods of neutropenia is standard practice for all ARL patients as well. AUTHORS’ DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST The author(s) indicated no potential conflicts of interest.
REFERENCES 1. Carbone A, Gloghini A: AIDS-related lymphomas: From pathogenesis to pathology. Br J Haematol 130:662-670, 2005[CrossRef][Medline] 2. Carbone A, Gaidano G, Gloghini A, et al: AIDS-related plasmablastic lymphomas of the oral cavity and jaws: A diagnostic dilemma. Ann Otol Rhinol Laryngol 108:95-99, 1999[Medline] 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 21:3948-3954, 2003 4. Delecluse HJ, Anagnostopoulos I, Dallenbach F, et al: Plasmablastic lymphomas of the oral cavity: A new entity associated with the human immunodeficiency virus infection. Blood 89:1413-1420, 1997 5. Dong HY, Scadden DT, de Leval L, et al: Plasmablastic lymphoma in HIV-positive patients: An aggressive Epstein-Barr virus-associated extramedullary plasmacytic neoplasm. Am J Surg Pathol 29:1633-1641, 2005[CrossRef][Medline] 6. Andrada JMLC, DlPC, Zamudio JLG: Non-Hodgkin's lymphoma in a totally implantable subcutaneous venous access port system. Haematologica 86:560, 2001 7. Stellato TA, Gauderer MW, Kazura J: Tumor metastasis from multiple myeloma and Burkitt's lymphoma in Broviac catheter tracts. Cancer 55:2715-2717, 1985[CrossRef][Medline] 8. Davidson NG: Tumour metastasis from multiple myeloma in Hickman catheter tract. Eur J Surg Oncol 16:170-171, 1990[Medline] 9. Kerob D, Vantelon JM, Ribrag V, et al: Cutaneous localization of multiple myeloma on the tract of a central venous catheter. Ann Dermatol Venereol 129:311-314, 2002[Medline] 10. Amiraian R, Penn TE, Hamann S, et al: Leukemic dermal infiltrates as a complication of central venous catheter placement. Cancer 62:2223-2225, 1988[CrossRef][Medline] 11. Martino R, Sureda A, Sitjas D, et al: Leukemic dermal infiltrate at the exit site of a central venous catheter. Haematologica 78:132-134, 1993[Medline] 12. Rosenblum MD, et al: Subcutaneous plasmacytomas with tropism to sites of previous trauma in a multiple myeloma patient treated with an autologous bone marrow transplant. Am J Hematol 72:274-277, 2003[CrossRef][Medline] 13. Fisher B, Fisher ER, Feduska N: Trauma and the localization of tumor cells. Cancer 20:23-30, 1967[CrossRef][Medline] 14. Lim ST, Karim R, Tulpule A, et al: Prognostic factors in HIV-related diffuse large-cell lymphoma: Before versus after highly active antiretroviral therapy. J Clin Oncol 23:8477-8482, 2005 15. Nasta SD, Carrum GM, Shahab I, et al: Regression of a plasmablastic lymphoma in a patient with HIV on highly active antiretroviral therapy. Leuk Lymphoma 43:423-426, 2002[CrossRef][Medline]
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Copyright © 2007 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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