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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  • AOTA Keiko
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • TAKANO Hideyuki
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • HOSOKAWA Hiroyoshi
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • KANI Kouichi
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • YAMAMURA Yoshiko
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry
  • AZUMA Masayuki
    Department of Oral Medicine, Institute of Health Biosciences, The University of Tokushima Graduate Faculty of Dentistry

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Other Title
  • 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
  • リツキシマブ ノ トウヨ ニ ヨッテ ショウジタ コウコウ ・ ジョウブ ショウカカン カイヨウ ノ 1レイ

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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.

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