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[Acute myeloid leukemia (M1) following chemotherapy for Ki-1 lymphoma complicated with rheumatoid arthritis].

作者信息

Yoshida K, Endoh K, Itoh Y, Kawai N, Matsuda A, Murohashi I, Jinnai I, Ino H, Bessho M, Takeuchi H

机构信息

First Department of Internal Medicine, Saitama Medical School.

出版信息

Rinsho Ketsueki. 1995 Dec;36(12):1365-71.

PMID:8587173
Abstract

A 58-year-old woman complicated with rheumatoid arthritis (RA) was admitted to our hospital with right axillar lymphadenopathy and splenomegaly in November 1992. She was diagnosed as an anaplastic large-cell lymphoma (Ki-1 +) (stage IIIB) on the histological findings of the right axillar lymph nodes. She was treated with 11 courses of CHOP regimen between February 1992 and May 1993, and with mitoxantrone, etoposide (VP-16) and predonisolone in April 1992 and May 1993. The right axillar lymph nodes and spleen were irradiated at a dose of 36Gy in October 1992 and May 1993 respectively. In May 1993, peripheral blood showed WBC 89,000/microliter with 96% myeloblasts, Hb 8.3 g/dl, and Plt 124,000/microliter. Bone marrow aspirate revealed hypercellularity with 90% myeloblasts, which were positive for CD13 and HLA-DR. She was diagnosed as AML (M1). The karyotype showed normal. Southern blot analysis did not reveal the rearrangement of the MLL gene. She received the BHAC-DMP regimen and obtained complete remission. However, she relapsed during consolidation therapy, and died of cerebral bleeding. An autopsy revealed absence of a residual tumor. The mean interval from exposure to alkylating agent to the onset of secondary leukemia has been reported to be about 5 years, in contrast to a shortened interval of about 2 years for VP-16-induced leukemia. In our patient, it took only 1 year to have AML following chemotherapy for Ki-1 lymphoma. This suggests that her AML might be induced not only by treatments for RA and Ki-1 lymphoma, but also by immunological background such as RA.

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