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抗インターロイキン-5受容体抗体投与中の喘息患者において、ムコイド圧迫による大量のアテレクトシスを発症した
Massive atelectasis by mucoid impaction in an asthma patient during treatment with anti-interleukin-5 receptor antibody.
PMID: 32566229 PMCID: PMC7300730. DOI: 10.1002/rcr2.599.
抄録
ベンラリズマブは、インターロイキン-5(IL-5)受容体α誘導性細胞溶解性モノクローナル抗体であり、抗体依存性細胞介在性細胞毒性を増強することにより、好酸球の急速かつほぼ完全な枯渇を抑制します。好酸球の枯渇は、粘液過多分泌やムコイドインパクションを減少させることが期待されています。75 歳の非喫煙女性が,制御不能な気管支喘息に対して複数の薬剤による治療を受けていた.喘息発作後にbenralizumabによる治療が開始されたが,4ヵ月後に左肺に大規模な無気管支炎を発症し,気管逸脱を引き起こし,鼻腔内高流量療法が必要となった.検査データは好中球数の上昇を示したが、血液中の好酸球はほぼ完全に枯渇していた。気管支ファイバースコピーで厚い粘液を除去し、無気管支炎は完全に消失した。ベンラリズマブ中止後,エリスロマイシンの投与開始後9カ月間,増悪は認められなかった.本症例は、抗IL-5受容体抗体投与中にムコイドインパクションによる無気力性無気力症を発症した初めての症例である。
Benralizumab is an interleukin-5 (IL-5) receptor α-directed cytolytic monoclonal antibody that reduces rapid and nearly complete depletion of eosinophils by enhancing antibody-dependent cell-mediated cytotoxicity. The depletion of eosinophilic inflammation is expected to reduce mucus hypersecretion and mucoid impaction. A 75-year-old non-smoking female had been treated for uncontrolled bronchial asthma with multiple drugs. Treatment with benralizumab was initiated after the asthma attack; however, four months later, she developed massive atelectasis in the left lung leading to the tracheal deviation, to the extent that nasal high-flow therapy was required. The laboratory data showed elevated neutrophil count, whereas blood eosinophils were almost completely depleted. The thick mucus was removed by bronchofiberscopy and the atelectasis was completely resolved. No exacerbation has been observed for nine months after discontinuation of benralizumab and initiation of erythromycin. This is the first documented case that developed atelectasis by mucoid impaction during treatment with anti-IL-5 receptor antibody.
© 2020 The Authors. Respirology Case Reports published by John Wiley & Sons Australia, Ltd on behalf of The Asian Pacific Society of Respirology.