可逆性后脑病综合征和metamizole:一种新的药物沉淀剂?

André Aires Fernandes , Fátima Hierro , Frederico Garret , Andreia Costa , Carolina Soares
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引用次数: 0

摘要

可逆性后脑病综合征(PRES)与某些药物之间的联系已得到充分证明,特别是免疫抑制剂和/或细胞毒性药物。Metamizole是一种非阿片类镇痛药,其确切的作用机制尚不完全清楚,但似乎与抑制前列腺素合成有关。前列腺素是重要的血管活性分子,参与动脉血管收缩和血管舒张,因此可能促进血管循环自动调节的丧失。方法对1例服用安咪唑后出现PRES的病例进行描述。结果1例18岁女性,无明显病史,以新发全身性强直阵挛性癫痫和视力障碍就诊急诊。在审查了患者的医疗记录和脑MRI结果后,我们怀疑PRES的诊断,并排除了经典沉淀。然而,摄入甲硝唑被认为是唯一可能的诱发因素。患者给予尼莫地平60 mg / 4 h,开始给予左乙拉西坦500 mg / 2 d。出院时无症状,血压正常。出院后3个月随访的脑MRI无显著差异。结论本病例报告可能提示了一种新的与PRES相关的药物沉淀剂,我们的假设是前列腺素通路抑制导致的内皮功能障碍可能导致血脑屏障通透性破坏,导致血管循环自动调节功能丧失。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Reversible posterior encephalopathy syndrome and metamizole: A new pharmacological precipitant?

Introduction

The link between reversible posterior encephalopathy syndrome (PRES) and certain drugs is well documented, especially for immunosuppressive and/or cytotoxic drugs. Metamizole is a non-opioid analgesic whose exact mechanism of action is still not fully understood, but it seems to involve the inhibition of prostaglandin synthesis. Prostaglandins are important vasoactive molecules involved in either arterial vasoconstriction and vasodilation, thus may promote loss of autoregulation of vascular circulation.

Methods

Description of a case of PRES after metamizole intake.

Results

An 18-year-old female with no significant medical history presented to the emergency department with new-onset generalized tonic-clonic seizures and visual disturbances. After reviewing the patient's medical records and brain MRI findings, the diagnosis of PRES was suspected, and classical precipitants were ruled out. However, the ingestion of metamizole was found to be the only plausible precipitating factor. The patient was treated with nimodipine 60 mg every 4 h and started on levetiracetam 500 mg twice daily. She was discharged asymptomatic and normotensive. The follow-up brain MRI performed three months after discharge was unremarkable.

Conclusions

This case-report may suggest a new pharmacological precipitant associated with PRES. Our hypothesis is that endothelial dysfunction resulting from the inhibition of the prostaglandin pathway may lead to the disruption of blood-brain barrier permeability, resulting in the loss of autoregulation of vascular circulation.
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来源期刊
Brain disorders (Amsterdam, Netherlands)
Brain disorders (Amsterdam, Netherlands) Neurology, Clinical Neurology
CiteScore
1.90
自引率
0.00%
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审稿时长
51 days
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