由反复使用非类固醇抗炎药物 (NSAIDs) 诱导的间歇性炎 用于持续发烧:一个病例报告
Norihito Yoshida1, Yusuke Suzuki1, Mai Hitaka1
1Nephrology, Toho University Sakura Medical Center, Sakura, JPN.
Cureus
|August 5, 2025
概括
非类固醇抗炎药物诱导的急性间歇性炎 (DI-AIN) 可以导致损伤. 尿管标志物升高,不仅仅是蛋白尿,信号DI-AIN,早期的类固醇治疗可能有助于恢复.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 药理学 药理学是指药理学的学科.
- 内部医学 内部医学
背景情况:
- 非类固醇抗炎药物 (NSAIDs) 广泛用于疼痛和炎症,但可能导致脏损伤,特别是药物诱导的急性间歇性炎 (DI-AIN).
- 早期诊断和管理DI-AIN对于预防永久性损伤至关重要.
研究的目的:
- 在一个46岁的男性中呈现NSAID诱导的DI-AIN病例.
- 要突出尿管生物标志物的诊断价值在疑似DI-AIN.
- 在基因病理学确认之前讨论实证类固醇治疗的合理性和有效性.
主要方法:
- 在每天使用布洛芬后,对患有急性损伤 (AKI) 的患者进行了监测.
- 评估了尿路生物标志物,包括N-乙-β-D-葡萄糖胺酶 (NAG),β2-微型球蛋白 (β2MG) 和L型脂肪酸结合蛋白 (L-FABP).
- 经验性口服普雷迪尼索隆 (PSL) 治疗是在脏活检结果之前基于临床怀疑开始的.
主要成果:
- 患者在暴露于ibuprofen后呈现AKI和血清肌氨酸升高.
- 尿液分析显示轻度蛋白尿,但明显增加了尿管损伤标志物.
- 开始PSL导致功能改善,活检后证实了AIN.
结论:
- 在患有AKI和NSAID病史的患者中怀疑DI-AIN至关重要.
- 尿管样标记的升高与最小的蛋白尿可能表明DI-AIN.
- 经验性类固醇治疗,以强烈的临床怀疑为指导,可以成为DI-AIN的有效早期干预.
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