リツキシマブの投与によって生じた口腔・上部消化管潰瘍の1例 A case of oral, pharyngeal, esophageal, and gastric ulcer in a patient with primary macroglobulinemia showing remission by treatment with rituximab

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著者

    • 青田 桂子 AOTA Keiko
    • 徳島大学大学院ヘルスバイオサイエンス研究部口腔内科学分野 Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
    • 高野 栄之 TAKANO Hideyuki
    • 徳島大学大学院ヘルスバイオサイエンス研究部口腔内科学分野 Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
    • 細川 浩良 HOSOKAWA Hiroyoshi
    • 徳島大学大学院ヘルスバイオサイエンス研究部口腔内科学分野 Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
    • 可児 耕一 KANI Kouichi
    • 徳島大学大学院ヘルスバイオサイエンス研究部口腔内科学分野 Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
    • 山村 佳子 YAMAMURA Yoshiko
    • 徳島大学大学院ヘルスバイオサイエンス研究部口腔内科学分野 Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
    • 東 雅之 AZUMA Masayuki
    • 徳島大学大学院ヘルスバイオサイエンス研究部口腔内科学分野 Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry

抄録

We report a case of oral, pharyngeal, esophageal, and gastric ulcer in patient with Waldenström macroglobulinemia( WM) in a 64-year-old woman in whom remission was induced by the administration of rituximab 6 months previously. She consulted our hospital because of ulcer formation in the right side of the floor of the mouth. A biopsy specimen showed inflammation. Five days later, the patient had a fever of 39℃, and the ulcer extended to the tongue and the left side of the floor of the mouth. Blood examination demonstrated delayed-onset neutropenia after treatment with rituximab. Although the symptoms were improved by antibacterial therapy, the ulcer with fever recurred 4 months later. The ulcer was observed not only in the mouth, but also in the pharynx, esophagus, and stomach. Since neutropenia continued and CD19, a monoclonal B cell antibody, was 0% , the patient received both G-CSF and an antibacterial drug. In addition, a proton pump inhibitor was given. These treatments led to improvement of the ulcer. <BR>The fact that severe delayed-onset neutropenia was induced by rituximab in the patient suggested that infection with endogenous microbial flora caused the ulcer in the mouth, pharynx, esophagus, and stomach. On the other hand, in the stomach with few endogenous microbial flora, the lack of the regulatory B cells apparently inhibited IL-10 production. Consequently, the activation of macrophages and neutrophils may have caused the ulcer formation.

We report a case of oral, pharyngeal, esophageal, and gastric ulcer in patient with Waldenström macroglobulinemia( WM) in a 64-year-old woman in whom remission was induced by the administration of rituximab 6 months previously. She consulted our hospital because of ulcer formation in the right side of the floor of the mouth. A biopsy specimen showed inflammation. Five days later, the patient had a fever of 39℃, and the ulcer extended to the tongue and the left side of the floor of the mouth. Blood examination demonstrated delayed-onset neutropenia after treatment with rituximab. Although the symptoms were improved by antibacterial therapy, the ulcer with fever recurred 4 months later. The ulcer was observed not only in the mouth, but also in the pharynx, esophagus, and stomach. Since neutropenia continued and CD19, a monoclonal B cell antibody, was 0% , the patient received both G-CSF and an antibacterial drug. In addition, a proton pump inhibitor was given. These treatments led to improvement of the ulcer. <BR>The fact that severe delayed-onset neutropenia was induced by rituximab in the patient suggested that infection with endogenous microbial flora caused the ulcer in the mouth, pharynx, esophagus, and stomach. On the other hand, in the stomach with few endogenous microbial flora, the lack of the regulatory B cells apparently inhibited IL-10 production. Consequently, the activation of macrophages and neutrophils may have caused the ulcer formation.

収録刊行物

  • 日本口腔外科学会雑誌

    日本口腔外科学会雑誌 59(7), 478-482, 2013

    社団法人 日本口腔外科学会

各種コード

  • NII論文ID(NAID)
    130004707973
  • 本文言語コード
    JPN
  • ISSN
    0021-5163
  • データ提供元
    J-STAGE 
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