Abstract：
OBJECTIVE: Phenibut (4-amino-3-phenyl-butyric acid) is a structural analog of GABA with central nervous system depressant and anxiolytic properties, developed in the former Soviet Union for anxiety, insomnia, and alcohol withdrawal. Its primary mechanism of action is believed to be a GABA-B receptor agonist-with high affinity at the α 2 δ subunit-containing voltage-dependent calcium channels and therefore gabapentinoid activity-as well as, to a lesser extent, GABA-A agonist activity. While not approved or regulated by the FDA, phenibut is easily obtainable online, where it is marketed as a nootropic, or cognitive enhancer. However, phenibut can lead to problems related to intoxication, dependency, and withdrawal, similar to other sedatives.
METHODS: We present a case of phenibut intoxication and withdrawal delirium that provided diagnostic and management challenges because of a patient that was initially not forthcoming about his phenibut use which resulted in five presentations to the hospital including two admissions.
RESULTS: Initial differential including adrenergic, serotonergic or anticholinergic toxidrome based on clinical picture and history reported at that time, however phenibut use of 50 g daily was eventually revealed, an amount exceeding the highest reported cases in our review of the English literature.
CONCLUSIONS: High-dose phenibut intoxication and withdrawal can appear as dramatic and dangerous as high-dose sedative withdrawal, however given its specified receptor affinity and binding profile we found that a pharmacotherapeutic approach targeting GABA-B, GABA-A, and gabapentenoid receptors were effective in stabilizing this patient, eventually leading to the patient\'s full and sustained recovery.
METHODS: We present a case of phenibut intoxication and withdrawal delirium that provided diagnostic and management challenges because of a patient that was initially not forthcoming about his phenibut use which resulted in five presentations to the hospital including two admissions.
RESULTS: Initial differential including adrenergic, serotonergic or anticholinergic toxidrome based on clinical picture and history reported at that time, however phenibut use of 50 g daily was eventually revealed, an amount exceeding the highest reported cases in our review of the English literature.
CONCLUSIONS: High-dose phenibut intoxication and withdrawal can appear as dramatic and dangerous as high-dose sedative withdrawal, however given its specified receptor affinity and binding profile we found that a pharmacotherapeutic approach targeting GABA-B, GABA-A, and gabapentenoid receptors were effective in stabilizing this patient, eventually leading to the patient\'s full and sustained recovery.
摘要：
目的：Phenibut（4-氨基-3-苯基-丁酸）是GABA的结构类似物，具有中枢神经系统抑制和抗焦虑特性，在前苏联因焦虑而发展起来，失眠,酒精戒断。其主要作用机制被认为是GABA-B受体激动剂-对含α2δ亚基的电压依赖性钙通道具有高亲和力，因此具有类加巴喷丁活性-以及，在较小程度上，GABA-A激动剂活性。虽然未经FDA批准或监管，Phenibut很容易在网上获得，它作为一种促智药销售，或者认知增强剂.然而,会导致与中毒有关的问题，依赖性，和退出，类似于其他镇静剂。
方法：我们介绍了一例苯尼布中毒和戒断性谵妄的病例，该病例的诊断和管理方面存在挑战，因为一名患者最初不了解他的苯尼布使用情况，导致五次医院就诊，包括两次入院。
结果：初始差异，包括肾上腺素，根据当时报道的临床表现和病史，血清素能或抗胆碱能毒物，然而，最终发现每天使用50克，超过我们对英语文献的评论中报告的最高病例。
结论：大剂量镇静剂戒断与大剂量镇静剂戒断一样严重和危险，然而，鉴于其特定的受体亲和力和结合谱，我们发现靶向GABA-B的药物治疗方法，GABA-A,加巴酚丁素受体有效地稳定了这个病人，最终导致患者的全面和持续的康复。
方法：我们介绍了一例苯尼布中毒和戒断性谵妄的病例，该病例的诊断和管理方面存在挑战，因为一名患者最初不了解他的苯尼布使用情况，导致五次医院就诊，包括两次入院。
结果：初始差异，包括肾上腺素，根据当时报道的临床表现和病史，血清素能或抗胆碱能毒物，然而，最终发现每天使用50克，超过我们对英语文献的评论中报告的最高病例。
结论：大剂量镇静剂戒断与大剂量镇静剂戒断一样严重和危险，然而，鉴于其特定的受体亲和力和结合谱，我们发现靶向GABA-B的药物治疗方法，GABA-A,加巴酚丁素受体有效地稳定了这个病人，最终导致患者的全面和持续的康复。
