Multiple extramedullary plasmacytomas responding to a reduced dose of carfilzomib following drug-induced thrombotic microangiopathy

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  • FUJIMORI Chika
    Department of Hematology, Tokyo Metropolitan Hospital Organization Tokyo Metropolitan Tama-Hokubu Medical Center
  • HAGINO Takeshi
    Department of Hematology, Tokyo Metropolitan Hospital Organization Tokyo Metropolitan Tama-Hokubu Medical Center
  • OSANAI Satoko
    Department of Hematology, Tokyo Women’s Medical University
  • SANO Shuhei
    Department of Hematology, Tokyo Metropolitan Hospital Organization Tokyo Metropolitan Tama-Hokubu Medical Center
  • SAGA Reina
    Department of Hematology, Tokyo Metropolitan Hospital Organization Tokyo Metropolitan Tama-Hokubu Medical Center
  • HIDAI Hiroko
    Department of Hematology, Tokyo Metropolitan Hospital Organization Tokyo Metropolitan Tama-Hokubu Medical Center
  • KURIMOTO Miwa
    Department of Hematology, Tokyo Metropolitan Hospital Organization Tokyo Metropolitan Tama-Hokubu Medical Center
  • MURAI Yoshiro
    Department of Hematology, Tokyo Metropolitan Hospital Organization Tokyo Metropolitan Tama-Hokubu Medical Center
  • AKIYAMA Hideki
    Department of Hematology, Tokyo Metropolitan Hospital Organization Tokyo Metropolitan Tama-Hokubu Medical Center
  • MOTOMURA Sayuri
    Department of Hematology, Tokyo Metropolitan Hospital Organization Tokyo Metropolitan Tama-Hokubu Medical Center

Bibliographic Information

Other Title
  • Carfilzomibによる薬剤性血栓性微小血管症発症後に減量再投与で奏効した多発髄外形質細胞腫
  • Carfilzomib ニ ヨル ヤクザイセイ ケッセンセイ ビショウ ケッカンショウ ハッショウ ゴ ニ ゲンリョウ サイトウヨ デ ソウコウ シタ タハツズイガイケイシツ サイボウ シュ

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Abstract

<p>Herein, we report the findings of a 79-year-old male patient who presented with multiple extramedullary plasmacytomas following a relapse of primary plasma cell leukemia. He developed thrombotic microangiopathy (TMA) while receiving carfilzomib, lenalidomide, and dexamethasone (KLd) therapy. He was diagnosed with plasma cell leukemia 3 years ago; he demonstrated a very good partial response (VGPR) after undergoing two regimens, including either bortezomib or lenalidomide, and he had been followed up without any other treatment due to complications of infection. Following relapse, KLd was initiated. On day 7 of KLd, TMA developed; therefore, the treatment was discontinued. The TMA improved only with the discontinuation of KLd. A reduced dose of KLd was readministered; the TMA did not relapse. He demonstrated VGPR after three courses of reduced-KLd; he has since remained in remission through ten courses. Therefore, carfilzomib therapy may be useful in relapsing and refractory cases. Drug-induced TMA has been reported to be caused by either immune-mediated or dose-dependent toxicity mechanisms. In patients who develop dose-dependent TMA with carfilzomib, dose reduction could be considered in cases showing an effective response to the treatment.</p>

Journal

  • Rinsho Ketsueki

    Rinsho Ketsueki 63 (12), 1626-1632, 2022

    The Japanese Society of Hematology

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