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AZD-9291诱导的中毒性表皮坏死松解症在一名非小细胞肺癌患者中的成功治疗:病例报告

Successful treatment after toxic epidermal necrolysis induced by AZD-9291 in a patient with non-small cell lung cancer: A case report.

作者信息

Li Wen, He Xiang, Liu Hui, Zhu Jiong, Zhang Hui-Min

机构信息

Department of Dermatology, Shuguang Hospital Affiliated to Shanghai University of TCM, Shanghai 201203, China.

Department of Oncology, Shuguang Hospital Affiliated to Shanghai University of TCM, Shanghai 201203, China.

出版信息

World J Clin Cases. 2021 Oct 16;9(29):8846-8851. doi: 10.12998/wjcc.v9.i29.8846.

DOI:10.12998/wjcc.v9.i29.8846
PMID:34734065
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8546833/
Abstract

BACKGROUND

Toxic epidermal necrolysis and Stevens-Johnson syndrome are acute life-threatening skin reactions. AZD9291 has been developed as a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) with activity against T790M mutation.

CASE SUMMARY

Herein we report a 68-year-old woman who developed a large area of skin necrosis and was diagnosed with toxic epidermal necrolysis after AZD-9291 ingestion. To the best of our knowledge, this is the first case reported in patients with EGFR T790M mutation in non-small cell lung cancer (NSCLC). Cabozantinib combined with erlotinib had clinically meaningful effectiveness, with additional toxicity that was generally manageable.

CONCLUSION

Treatment with AZD-9261 is effective in regressing the growth of the NSCLC and can bring some hope to despairing patients. We hope that more research will be carried out on the association between severe rashes and EGFR-TKIs, and more safe and effective drugs can be developed.

摘要

背景

中毒性表皮坏死松解症和史蒂文斯-约翰逊综合征是危及生命的急性皮肤反应。AZD9291已被开发为第三代表皮生长因子受体(EGFR)-酪氨酸激酶抑制剂(TKI),对T790M突变具有活性。

病例摘要

在此,我们报告一名68岁女性,在服用AZD-9291后出现大面积皮肤坏死,被诊断为中毒性表皮坏死松解症。据我们所知,这是首例在非小细胞肺癌(NSCLC)EGFR T790M突变患者中报告的病例。卡博替尼联合厄洛替尼具有临床意义上的疗效,且额外毒性通常可控。

结论

AZD-9261治疗对使NSCLC肿瘤缩小有效,可为绝望的患者带来一些希望。我们希望对严重皮疹与EGFR-TKIs之间的关联开展更多研究,并开发出更安全有效的药物。

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Drug Des Devel Ther. 2018 Jul 11;12:2163-2167. doi: 10.2147/DDDT.S168248. eCollection 2018.
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