Alhagamhmad Moftah, Elarwah Aisha, Alhassony Alia, Alougly Shirin, Milad Hamza, Dehoam Aziza, Elbrgathy Suliman, Shembesh Nuri, Mousa Emhemed, ElShiky Abdulhamid
J Pediatr Pharmacol Ther. 2021;26(2):210-212. doi: 10.5863/1551-6776-26.2.210. Epub 2021 Feb 15.
Clinical manifestations of valproic acid (VPA) toxicity can range from just mild confusion and drowsiness to serious encephalopathy, leading to depressed sensorium and even coma and death. The exact cause(s) of how VPA influences the integrity of brain function remains unknown. Nevertheless, several mechanisms have been postulated including a surge in the blood ammonia concentration. Valproic acid-induced hyperammonemic encephalopathy is a rare yet serious sequalae and that can lead to grave outcomes. We report a case of hyperammonemic encephalopathy with preserved liver function following a moderate VPA intoxication in a toddler, who was successfully managed conservatively. Additionally, we briefly discuss mechanistic basis of VPA toxicity and highlight some of the available potential therapies.
丙戊酸(VPA)中毒的临床表现范围广泛,从轻微的意识模糊和嗜睡到严重的脑病,可导致感觉迟钝,甚至昏迷和死亡。VPA如何影响脑功能的完整性的确切原因尚不清楚。然而,已经提出了几种机制,包括血氨浓度的激增。丙戊酸诱导的高氨血症性脑病是一种罕见但严重的后遗症,可导致严重后果。我们报告了一例幼儿中度VPA中毒后肝功能正常的高氨血症性脑病病例,该病例通过保守治疗成功治愈。此外,我们简要讨论了VPA毒性的机制基础,并强调了一些现有的潜在治疗方法。