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一名肺腺癌患者出现异常延长的培美曲塞细胞毒性:病例报告

Unusually prolonged pemetrexed cytotoxicity in a patient with a lung adenocarcinoma: a case report.

作者信息

Sakhri Linda, Pinsolle Julian, Moro-Sibilot Denis, Pluchart Hélène

机构信息

Institut de Cancérologie Daniel Hollard, Groupe Hospitalier Mutualiste, 124 rue d'Alembert, 38000, Grenoble, France.

UM Oncologie Thoracique, Clinique de pneumologie, Pôle Thorax et vaisseaux, Centre Hospitalier Universitaire Michallon, BP217, 38043, Grenoble cedex 9, France.

出版信息

J Med Case Rep. 2017 Sep 16;11(1):262. doi: 10.1186/s13256-017-1436-7.

Abstract

BACKGROUND

We describe a case of pemetrexed toxicities related to reabsorption by an ileal neobladder, which caused prolonged hematotoxicity and nephrotoxicity.

CASE PRESENTATION

A 59-year-old white man was diagnosed with metastatic wild-type adenocarcinoma of the upper lobe of his right lung. After a first cycle of cisplatin and pemetrexed, he had unusually prolonged aplasia and acute kidney injury. The prolonged aplasia was caused by pemetrexed reabsorption by the ileal mucosa of the neobladder as pemetrexed was eliminated renally in an active form and is partly lipophilic.

CONCLUSIONS

Pemetrexed may be reabsorbed by the ileal mucosa of the neobladder because of its hydrophobic structure and renal excretion in its active form. Acute urinary retention may maintain this phenomenon. Published data excluded a potential role for cisplatin in this toxicity; furthermore, we could not assess pemetrexed concentrations in the blood or urine as these assay techniques are not validated. Thus, care is needed when giving chemotherapy to patients with a neobladder.

摘要

背景

我们描述了一例培美曲塞毒性反应,该反应与回肠新膀胱的重吸收有关,导致了长期的血液毒性和肾毒性。

病例介绍

一名59岁白人男性被诊断为右肺上叶转移性野生型腺癌。在接受顺铂和培美曲塞的第一个周期治疗后,他出现了异常延长的再生障碍和急性肾损伤。延长的再生障碍是由于培美曲塞被新膀胱的回肠黏膜重吸收所致,因为培美曲塞以活性形式经肾脏排泄且部分具有亲脂性。

结论

由于培美曲塞的疏水结构及其以活性形式经肾脏排泄,它可能被新膀胱的回肠黏膜重吸收。急性尿潴留可能会维持这种现象。已发表的数据排除了顺铂在这种毒性反应中的潜在作用;此外,由于这些检测技术未经验证,我们无法评估血液或尿液中的培美曲塞浓度。因此,对有新膀胱的患者进行化疗时需要谨慎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/72dc/5603063/6216843476b6/13256_2017_1436_Fig1_HTML.jpg

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