Rituximab treatment may cause or exacerbate Kaposi's sarcoma (KS) in patients with human immunodeficiency virus (HIV)-associated multicentric Castleman's disease. Despite the widespread use of rituximab, rituximab-induced KS has not yet been reported in HIV-negative patients with diffuse large B cell lymphoma (DLBCL). We herein report a case of KS that developed after undergoing rituximab-containing chemotherapy in an HIV-negative patient with DLBCL. An 84-year-old man who received rituximab-containing chemotherapy for the treatment of DLBCL developed severe infection, and subsequently KS. Our observations indicate that serious infections under rituximab treatment may trigger KS. KS should therefore be considered when skin tumors appear in lymphoma patients receiving rituximab-containing chemotherapy.
Spontaneous regression of methotrexate-related lymphoproliferative disorders (MTX-LPDs) occurs in some patients after withdrawal of MTX. However, the mechanisms by which MTX withdrawal contributes to the spontaneous regression of MTX-LPDs have not been fully elucidated. We herein show that spontaneous regression of MTX-LPDs is associated with the development of significant and transient T-cell large granular lymphocyte (T-LGL) lymphocytosis induced by MTX withdrawal. Since T-LGLs show strong cytotoxicity, their expansion may contribute to the spontaneous regression of lymphoma. Therefore, the development of T-LGL lymphocytosis maybe associated with a favorable prognosis in MTX-LPD patients.
Ataxia telangiectasia mutated (ATM) is a tumor suppressor gene, and its somatic inactivation plays a role in the pathogenesis of lymphoid malignancies. However, the role of ATM in patients with myeloid malignancies is still unknown. We herein report a case of acute megakaryoblastic leukemia (AMKL) with ATM gene deletion. An 84-year-old Japanese woman presenting with a pale face and pancytopenia was admitted to our institution and diagnosed to have AMKL with ATM gene deletion. She was treated with intravenous azacitidine. The azacitidine treatment was effective for approximately 1 year. Somatic inactivation of the ATM gene may therefore be involved in the pathogenesis of AMKL.
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