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<p><i>FGFR2</i> gene fusions are identified in approximately 10–16% of patients with intrahepatic cholangiocarcinoma and are targets of FGFR tyrosine kinase inhibitors (TKIs). While these agents are clinically effective, nail disorders are a documented class-effect toxicity, occurring in approximately 40%–50% of patients treated with various FGFR inhibitors, often impairing quality of life. We report a case of a 53-year-old man with locally advanced intrahepatic cholangiocarcinoma refractory to standard chemotherapy (cisplatin/gemcitabine, S-1) and proton beam therapy. Comprehensive genomic profiling revealed <i>FGFR2::WAC</i> and <i>KCNH8::FGFR2</i> fusion genes. Treatment was initiated with pemigatinib (13.5&#xa0;mg/day). One month later, painful nail deformities appeared, followed by thickening, black discoloration, and brittleness. Despite a dose reduction to 9&#xa0;mg/day, the nail toxicity remained. Consequently, high-potency topical corticosteroids were administered, and symptoms subsided. After disease progression, the treatment was switched to futibatinib (16&#xa0;mg daily), and during the three-month administration, the nail disorders did not worsen and tended to improve. In conclusion, we describe a case where severe nail toxicity induced by a reversible FGFR inhibitor was managed by switching to futibatinib and utilizing topical corticosteroids. Although effective treatments for nail-related events are limited, this case suggests the effectiveness of steroid ointments.</p>

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Severe nail toxicity induced by FGFR inhibitor in FGFR2-rearranged cholangiocarcinoma

  • 期刊论文

  • 发表日期：

    2026年3月14日

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  • Chiaki Kondo,
  • Ayako Mitsuma,
  • Yuichi Ando

摘要

FGFR2 gene fusions are identified in approximately 10–16% of patients with intrahepatic cholangiocarcinoma and are targets of FGFR tyrosine kinase inhibitors (TKIs). While these agents are clinically effective, nail disorders are a documented class-effect toxicity, occurring in approximately 40%–50% of patients treated with various FGFR inhibitors, often impairing quality of life. We report a case of a 53-year-old man with locally advanced intrahepatic cholangiocarcinoma refractory to standard chemotherapy (cisplatin/gemcitabine, S-1) and proton beam therapy. Comprehensive genomic profiling revealed FGFR2::WAC and KCNH8::FGFR2 fusion genes. Treatment was initiated with pemigatinib (13.5 mg/day). One month later, painful nail deformities appeared, followed by thickening, black discoloration, and brittleness. Despite a dose reduction to 9 mg/day, the nail toxicity remained. Consequently, high-potency topical corticosteroids were administered, and symptoms subsided. After disease progression, the treatment was switched to futibatinib (16 mg daily), and during the three-month administration, the nail disorders did not worsen and tended to improve. In conclusion, we describe a case where severe nail toxicity induced by a reversible FGFR inhibitor was managed by switching to futibatinib and utilizing topical corticosteroids. Although effective treatments for nail-related events are limited, this case suggests the effectiveness of steroid ointments.