A case of severe digital vasculopathy during imatinib therapy in a hemodialysis patient with chronic myeloid leukemia

DOI Web Site Web Site 13 References
  • Yamatani Kotoko
    Department of Nephrology, Tokyo Rosai Hospital Department of Medicine, Kidney Center, Tokyo Women’s Medical University
  • Mikami Hayato
    Department of Nephrology, Tokyo Rosai Hospital Department of Medicine, Kidney Center, Tokyo Women’s Medical University
  • Yoshikura Tetsuya
    Department of Nephrology, Tokyo Rosai Hospital
  • Osawa Sachiyo
    Department of Plastic Surgery, Tokyo Rosai Hospital
  • Takami Yoshihiro
    Department of Plastic Surgery, Tokyo Rosai Hospital
  • Honda Kazuho
    Department of Anatomy, Showa University School of Medicine
  • Nitta Kosaku
    Department of Medicine, Kidney Center, Tokyo Women’s Medical University
  • Naito Takashi
    Department of Nephrology, Tokyo Rosai Hospital

Bibliographic Information

Other Title
  • イマチニブを長期内服していた維持透析患者に生じた多発末梢血管障害の1例
  • 症例報告 イマチニブを長期内服していた維持透析患者に生じた多発末梢血管障害の1例
  • ショウレイ ホウコク イマチニブ オ チョウキ ナイフク シテ イタ イジ トウセキ カンジャ ニ ショウジタ タハツ マッショウ ケッカン ショウガイ ノ 1レイ

Search this article

Abstract

<p>A 49-year-old male presented with rapidly progressive necrotic ulcers on his fingers. At the age of 44, hemodialysis therapy was commenced to treat end-stage renal failure caused by diabetic nephropathy. At the age of 46, he was diagnosed with chronic myeloid leukemia and was started on imatinib, a first-generation tyrosine kinase inhibitor (TKI, 400 mg daily). Three years later, pain and necrotic ulcers appeared on the fingers of both hands and progressed rapidly within several months. We initially suspected calciphylaxis. The ulcers and necrosis did not respond to medical treatment, and the affected fingers were eventually amputated. A histopathological examination of the amputated finger specimens revealed intimal fibrosis and thickening of the subcutaneous vessels, luminal stenosis, and mildly calcified vessels, which were inconsistent with calciphylaxis. We concluded that imatinib had caused these symptoms because the necrosis stopped progressing when the imatinib treatment was ceased. Recent studies have reported that nilotinib, a second-generation TKI, is associated with progressive peripheral arterial occlusive disease (PAOD). However, imatinib-associated PAOD is rare. We speculate that hemodialysis patients that exhibit hypometabolism are at higher risk of vasculopathy than healthy individuals, and blood vessels exhibiting high-grade arteriosclerosis related to end-stage renal disease might be vulnerable to the effects of TKI.</p>

Journal

References(13)*help

See more

Keywords

Details 詳細情報について

Report a problem

Back to top