Neurogenic dysphagia: current pharmacogenomic perspectives

J. Guerra, V. Naidoo, R. Cacabelos
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Abstract

Neurogenic dysphagia (ND) is characterized by a swallowing disorder where nervous system, muscle, and neuromuscular diseases are involved. DRD1, COMT, BDNF, and APOE are genes that may have a predictive role in the occurrence and evolution of ND. Many drugs that improve swallowing or can induce or exacerbate swallowing difficulties are related to dopamine metabolism and substance P. These pharmacological treatments for ND include dopamine precursors (levodopa), dopamine agonists (amantadine, apomorphine, cabergoline, and rotigotine), and TRP channel activators (capsaicin, piperine, and menthol). Since treatment outcomes are highly dependent on the genomic profiles of ND patients, personalized treatments should rely on pharmacogenetic procedures to optimize therapeutic interventions. Knowledge of the pharmacogenetic profiles of these drugs would minimize the occurrence of adverse drug reactions (especially to antidopaminergic medications) that may induce dysphagia and optimize pharmacological treatment that can ameliorate it. This knowledge should also be applied to the use of medications that control symptoms associated with dysphagia, such as sialorrhea, xerostomia, reflux, or hiccups.
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神经源性吞咽困难:当前的药物基因组学观点
神经性吞咽困难(ND)是一种伴有神经系统、肌肉和神经肌肉疾病的吞咽障碍。DRD1、COMT、BDNF和APOE等基因可能在ND的发生和进化中具有预测作用。许多改善吞咽或可诱发或加重吞咽困难的药物都与多巴胺代谢和p物质有关。ND的药物治疗包括多巴胺前体(左旋多巴)、多巴胺激动剂(金刚烷胺、阿波啡、卡麦角林和罗替戈汀)和TRP通道激活剂(辣椒素、胡椒碱和薄荷醇)。由于治疗结果高度依赖ND患者的基因组图谱,个性化治疗应依靠药物遗传学程序来优化治疗干预措施。了解这些药物的药理学特征可以最大限度地减少可能导致吞咽困难的药物不良反应(特别是抗多巴胺能药物)的发生,并优化可以改善吞咽困难的药物治疗。这一知识也应应用于控制吞咽困难相关症状的药物的使用,如唾液、口干、反流或打嗝。
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