伊克珠单抗诱发的间质性肺病:经支气管肺冷冻活组织切片证实的病例报告。

Shota Kaburaki, Naoko Okada, Toru Tanaka, Koichiro Kamio, Yosuke Tanaka, Yasuhiro Terasaki, Kazuo Kasahara, Masahiro Seike
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引用次数: 0

摘要

背景:伊克珠单抗是一种用于银屑病治疗的白细胞介素-17A(IL-17A)抑制剂,它与药物诱发的间质性肺病(DI-ILD)有关。关于这种不良反应的病理生理学机制和组织病理学特征仍鲜有记载:一名患有家族性银屑病的 69 岁男性患者在接受了 18 个月的 ixekizumab 治疗后出现了呼吸道症状。他的病史包括轻度吸烟相关性间质性肺炎和慢性阻塞性肺病。治疗一个月后,他出现咳嗽和呼吸困难。高分辨率胸部 CT 显示双侧磨玻璃不透光,伴有 Krebs von den Lungen-6 和表面活性蛋白-D 水平升高。经支气管肺冷冻活检(TBLC)显示,患者为纤维化非特异性间质性肺炎,伴有肉芽肿改变。免疫组化分析显示,CD4 阳性细胞和 IL-17A 阳性淋巴细胞占主导地位,这表明 Th17 细胞参与了发病机制。停用伊昔单抗后,患者病情有所好转:本病例确定了ixekizumab诱导的DI-ILD的独特组织病理学特征,尤其是肉芽肿病变的存在和Th17细胞的参与。研究结果表明,IL-17A抑制可能通过Th17细胞功能失调引发肺部炎症。这一观察结果支持了对接受银屑病生物疗法的患者,尤其是已有肺部疾病的患者进行仔细肺部监测的重要性。TBLC可能有助于了解这种药物诱发并发症的发病机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ixekizumab-induced interstitial lung disease: a case report confirmed by transbronchial lung cryobiopsy.

Background: Ixekizumab, an interleukin-17A (IL-17A) inhibitor used in psoriasis treatment, has been linked to drug-induced interstitial lung disease (DI-ILD). The pathophysiological mechanisms and histopathological features of this adverse effect remain poorly documented.

Case Presentation: A 69-year-old male with familial psoriasis developed respiratory symptoms after 18 months of ixekizumab therapy. His medical history included mild smoking-related interstitial pneumonia and chronic obstructive pulmonary disease. One month after treatment, he presented with cough and dyspnea. High-resolution chest CT showed bilateral ground-glass opacities, accompanied by elevated Krebs von den Lungen-6 and surfactant protein-D levels. Transbronchial lung cryobiopsy (TBLC) revealed a fibrotic non-specific interstitial pneumonia pattern with granulomatous changes. Immunohistochemical analysis demonstrated a predominance of CD4-positive cells and IL-17A-positive lymphocytes, suggesting Th17 cell involvement in the pathogenesis. The patient's condition improved following ixekizumab discontinuation.

Conclusions: This case identifies distinct histopathological features in ixekizumab-induced DI-ILD, particularly the presence of granulomatous changes and Th17 cell involvement. The findings suggest that IL-17A inhibition may trigger pulmonary inflammation through Th17 cell function dysregulation. This observation supports the importance of careful pulmonary monitoring in patients receiving biologic therapies for psoriasis, particularly those with pre-existing lung conditions. TBLC may contribute to understanding the pathogenesis of this drug-induced complication.

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