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Epstein-Barr virus-associated Hodgkin's lymphoma in a rheumatoid arthritis patient treated with methotrexate and cyclosporin A.

Methotrexate (MTX) and cyclosporin A (CSA) are increasingly employed to treat progressive rheumatoid arthritis (RA), even in combination (1). We describe here the development of an Epstein-Barr virus (EBVtassociated Hodgkin’s disease after a period of combined therapy in a patient with RA that was refractory to MTX alone. The patient, a 61-year-old man, developed symmetric RA in November 1990. At another institution, he was given sulfasalazine (SSZ) up to 2 gmlday. Because of lack of efficacy after 6 months, the SSZ was stopped and azathioprine (AZA), 100 mg/day, was started, along with 5 mg/day of prednisone. The arthritis went into partial remission until April 1993, when a sudden relapse occurred. The patient was seen at our institution, and his treatment was stopped. At that time, he was found to have small, mobile, nontender lymph nodes in both axillae. His medical records showed no mention of extraarticular features. He was given MTX (10 mg/week) and leukovorin (7.5 mg, 24 hours later) plus prednisone (5 mg each morning). In September 1993, because of chronic active disease, CSA 3.5 mg/kg/day was added to the regimen. By November, the RA was in full clinical remission (no pain, no rigor, no stiffness), and the prednisone was stopped. However, a firm mass of lymph nodes was present in the right axilla. During the followup at our institution, there had been no changes in the lymphocyte count or in the CD4 and CD8 T cell subsets (Table 1). His HLA type was A3,26;B35,38; Cw4,X;DR3,1 I ;Dw52;DQ2,3. A biopsy of the right axillary lymph nodes was performed in December 1993. The clinicopathologic examination showed a stage IA Hodgkin’s lymphoma, mixed cellularity subtype (Figure 114). The Reed-Sternberg cells harbored an EBV genome (tylpe A by the polymerase chain reaction) and were latent membrane protein 1 (LMP-I) positive (Figure lB), Epstein-Barr nuclear antigen-2 negative (the antigenic characteristics of EBV-associated Hodgkin’s lymphoma). The MTX and CSA regimen was stopped; no prednisone was given. Unlike the cases reported by Kame1 et a1 (2) and Shiroky et a1 (3), only a partial spontaneous regression was observed in this patient after 2 months. This clinical behavior is unusual for Hodgkin’s lymphoma. The persistence of Hodgkin’s lymphoma was confirmed by a second lymph node biopsy, which revealed focal involvement, and surgical and echographic assessments showed only 50% regression. The patient had refused laparotomy, and bipedal lymphography was unsuccessful. Because the patient had some negative prognostic factors (i.e., male sex, age >60 years, histotype, and mass size >2.5 cm) and because of the likelihood that the Hodgkin’s lymphoma had developed (and had persisted) during immunosuppression (poor prognosis for lymphomas during immunosuppression after transplantation [4]), he was treated with MOPP (mechlorethamine, vincristine, procarbazine, prednisone) and local radiotherapy. B cell lymphomas, but few Hodgkin’s lymphomas, are increasingly recognized during long-term treatment of RA with immunosuppressantis. However, Hodgkin’s lymphoma is not a neoplasm associated with immunosuppression. During long-term treatment with immunosuppressants and with CSA (5,6), EBV-,associated, LMP-I-positive, EBNA-Zpositive B cell lymplhomas are increasingly recognized, yet few Hodgkin’s lymphomas have been described in this setting. However, we know that EBV-associated Hodgkin’s lymphoma arises only in moderately immunosuppressed, human immunodeficiency virus-infected intravenous drug abusers (7).