Mirabegron向前迈进:创伤性脊髓损伤中神经源性逼尿肌过度活动的新治疗选择

Muhamad Faizal Zainudin, Pong Mei Yin, Nadzurah Mohamed Zainuddin
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引用次数: 0

摘要

背景和目的:抗胆碱能药物如托特罗定因其耐受性而臭名昭著。除了常见的副作用,如口干和便秘,该药物已被证明会引发老年人的认知障碍。近年来,mirabegron,更广为人知的商业名称Betmiga,因其更好的耐受性和相当的疗效,作为抗胆碱能药物治疗膀胱过度活动症(OAB)的替代品而引起了人们的关注。然而,其用于治疗神经源性逼尿肌过度活动(NDO)几乎是前所未闻的康复。我们提出了一个年轻的创伤性截瘫的情况下,已成功地治疗与米拉比龙。方法:1例21岁男性于2019年8月转入康复病房。他的T8椎体遭受创伤性爆裂骨折,导致T8完全截瘫。他有多种损伤,包括神经源性膀胱、神经源性肠和下肢痉挛。入院时行单通道膀胱术,发现高压膀胱,依从性差。他很快开始服用托特罗定,随后便秘恶化,导致自主神经反射障碍。我们改用丙酸,这是我们的下一种可用的抗胆碱能药物。不幸的是,它使便秘和自主神经反射障碍长期存在。撤掉导尿管的计划被放弃了。他于2020年2月第二次入院接受自我导尿培训。结果:我们开始给他服用每日25毫克的米瑞比龙,并训练他进行自我导尿。失禁发作逐渐减少,尽管不是完全减少。因此,我们决定在一个月后将剂量优化到50毫克,此后他不再有尿漏事件。他对药物的耐受性很好,没有肠道常规的干扰,并且自米拉贝隆以来没有自主神经反射障碍。结论:Mirabegron是一种治疗神经源性膀胱的有效方法。展望未来,我们应该考虑这种新的途径,特别是对抗胆碱能药物敏感的患者。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Marching Forward with Mirabegron: A Novel Treatment Option for Neurogenic Detrusor Overactivity in Traumatic Spinal Cord Injury
Background and aim: Anticholinergics such as tolterodine are notorious for their intolerability. Besides the commonly encountered side effects such as dry mouth and constipation, the medication has been shown to instigate cognitive impairment in the elderly population. In recent years, mirabegron, more commercially known as Betmiga, has garnered attention as an alternative to anticholinergics in treating Overactive Bladder (OAB) for its better tolerability and comparable efficacy. However, its usage in treating Neurogenic Detrusor Overactivity (NDO) is almost unheard of in rehabilitation. We present a case of young traumatic paraplegia who has been successfully treated with mirabegron. Methods: A 21-year-old man was transferred to the rehabilitation ward in August 2019. He had sustained a traumatic burst fracture of the T8 vertebra resulting in T8 complete paraplegia. He had multiple impairments, including neurogenic bladder, neurogenic bowel, and lower limb spasm. Single-channel cystometry was performed during the admission revealed a high-pressure bladder with poor compliance. He soon was started on tolterodine which subsequently worsened constipation, leading to autonomic dysreflexia. We switched to propiverine, the next available anticholinergic in our setting. Unfortunately, it perpetuated constipation and autonomic dysreflexia. The plan to remove the urinary catheter was abandoned. He was admitted for the second time in February 2020 for self-catheterisation training. Results: We started him on mirabegron 25 mg daily and trained him in self-catheterisation. The incontinence episodes reduced gradually, albeit not entirely. Therefore, we decided to optimise the dosage to 50 mg one month later, following which he no longer suffers leaking urine episodes. He tolerated the medication well without disturbance in the bowel routine and was free of autonomic dysreflexia ever since on mirabegron. Conclusion: Mirabegron is a promising treatment option in neurogenic bladder management. Marching forward, we should consider this novel avenue, especially in patients with sensitivity to anticholinergics.
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