TWO CASES OF GASTROINTESTINAL ULCERATION FOLLOWING SORAFENIB ADMINISTRATION FOR HEPATOCELLULAR CARCINOMA

DOI
  • SAITO Daisuke
    The Third Department of Internal Medicine, Kyorin University School of Medicine.
  • HAYASHIDA Mari
    The Third Department of Internal Medicine, Kyorin University School of Medicine.
  • MIURA Miki
    The Third Department of Internal Medicine, Kyorin University School of Medicine.
  • SAKURABA Akihito
    The Third Department of Internal Medicine, Kyorin University School of Medicine.
  • OKUYAMA Syuhei
    The Third Department of Internal Medicine, Kyorin University School of Medicine.
  • YAMADA Yuji
    The Third Department of Internal Medicine, Kyorin University School of Medicine.
  • TOKUNAGA Kengo
    The Third Department of Internal Medicine, Kyorin University School of Medicine.
  • KOYAMA Genichi
    The Third Department of Internal Medicine, Kyorin University School of Medicine.
  • KAWAMURA Naohiro
    The Third Department of Internal Medicine, Kyorin University School of Medicine.
  • TAKAHASHI Shin'ichi
    The Third Department of Internal Medicine, Kyorin University School of Medicine.

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Other Title
  • ソラフェニブ投与開始後に消化管潰瘍を認めた進行肝細胞癌の2例

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Abstract

Two patients who had gastrointestinal ulceration due to sorafenib presented at our department. Case 1 : A 69-year-old male was admitted to our hospital for the treatment of anemia, which occurred 50 days after he started sorafenib treatment. Upper gastrointestinal endoscopic findings revealed ulcerative lesions in the posterior wall of the upper body of the stomach. Case 2 : A 62-year-old male was admitted for bloody stool that occurred 60 days after the start of sorafenib administration. Colonoscopic findings revealed ulcerative lesions in the sigmoid colon. Both of the ulcerative lesions were shallow, and a colonic ulcer was located along the longitudinal axis of the intestine. After stopping sorafenib administration, the symptoms disappeared rapidly in both cases. It was suggested that sorafenib might induce thrombosis via the inhibition of vascular endothelial growth factor and provoke ischemic gastrointestinal ulceration.

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