鉄イソマルトシド治療による医原性鉄過剰症:症例報告
Yao Hu1, Min Sun1, Lihui Zhong2
1Department of Nephrology, Affiliated Hospital & Clinical Medical College of Chengdu University, Chengdu, Sichuan Province, China.
Medicine
|January 10, 2026
まとめ
過剰な静脈内鉄イソマルトシドは、フェリチン高値と臓器沈着によって確認される鉄過剰症を引き起こす可能性があります。デフェラシロクスによる迅速な鉄キレート療法は、鉄レベルを低下させ、患者の症状を改善しました。
科学分野:
- 腎臓病学
- 血液学
- 薬理学
背景:
- 静脈内(IV)鉄補充療法は、鉄欠乏性貧血の標準治療です。
- 過剰な鉄投与は、鉄過剰症や臓器障害を引き起こす可能性があります。
- より新しいIV鉄製剤である鉄イソマルトシドも、鉄過剰症のリスクをもたらす可能性があります。
研究 の 目的:
- 鉄イソマルトシド療法による医原性鉄過剰症の最初の症例を報告すること。
- 静脈内鉄療法中の鉄レベルモニタリングの重要性を強調すること。
主な方法:
- 全身性エリテマトーデス患者が5週間で7500 mgの鉄イソマルトシドを受けました。
- 鉄過剰症の診断は、血清フェリチン値の上昇と肝臓および脾臓の鉄沈着を示すMRIによって確認されました。
- 治療には、デフェラシロクスによる鉄キレート療法が含まれていました。
主要な成果:
- デフェラシロクス治療8ヶ月後、血清フェリチン値は4336.47 ng/mLから1236.2 ng/mLに低下しました。
- 色素沈着過剰と疲労の改善が見られました。
- デフェラシロクスは忍容性が高く、腎機能は安定していました。
結論:
- この症例は、過剰でモニタリングされていない静脈内鉄イソマルトシドによる鉄過剰症のリスクを強調しています。
- 合併症を防ぐためには、鉄代謝の注意深いモニタリングが不可欠です。
- 早期発見と鉄キレート療法は、鉄過剰症を効果的に管理できます。
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