Case reportPrimidone-induced hyperammonemic encephalopathy in a patient with cerebral astrocytoma
References (7)
- et al.
Secondary hyperammonemia: a possible mechanism for valproate encephalopathy
Lancet
(1980) - et al.
Primidone-induced “uremic flap”
Lancet
(1979) - et al.
Valproate induced encephalopathy treated with carnitine in an adult
J Neurol Neurosurg Psychiatry
(1996)
Cited by (12)
Hyperammonemia induced by prophylactic administration of antiepileptic drugs during the perioperative period of craniotomy
2016, Clinica Chimica ActaCitation Excerpt :The liver synthetic function decreased after AED administration, and the degree of decrease was greater in patients with postoperative hyperammonemia. Previous studies have reported a few cases of AHE during the perioperative period of craniotomies (Table 4) [8,11,12,15,16]. Different AEDs were given to the five reported patients, and they all developed AHE, which presented as a depressed mental state or seizures along with hyperammonemia during the postoperative period.
Valproate (VPA)-associated hyperammonemic encephalopathy independent of elevated serum VPA levels: 21 cases in China from May 2000 to May 2012
2013, Comprehensive PsychiatryCitation Excerpt :Although the precise pathophysiological mechanism underlying VHE with VPA treatment is unclear, excessive activation of NMDA receptors [26] in CNS toxicity due to hyperammonemia, might account for some of these findings. VPA-induced hyperammonemia may be due to the inhibition of the activity of carbamoyl-phosphate synthetase I (CPS-I) [27]. Another possible mechanism for VPA-induced hyperammonemia is the direct inhibition of N-acetylglutamate synthase (NAGS) activity by valproyl-CoA (VP-CoA), which has been reported in rats treated with VPA [28].
Valproate-induced hyperammonemic encephalopathy: An update on risk factors, clinical correlates and management
2012, General Hospital PsychiatryCitation Excerpt :As a branched chain carboxylic acid, VPA is extensively metabolized by the liver via glucuronic acid conjugation, mitochondrial beta- and cytosolic omega-oxidation to produce metabolites such as propionate and 4-en-VPA which are involved in the genesis of VPA-induced hyperammonemia [31,32]. Propionate is remarkable for decreasing hepatic NAG levels, thus leading to an increase in blood ammonia levels due to inhibition of CPS-I [33–35]. 4-en-VPA causes a decrease in the availability of acetyl-CoA due to the formation of valproyl-CoA (VP-CoA), thereby leading to decreased production of NAG.
Barbiturates
2007, Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose, Fourth EditionMeyler’s Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions, Sixteenth Edition
2015, Meyler's Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions
- f1
Correspondence to: Hiroyuki Katano, MD Department of Neurosurgery, Nagoya City Higashi General Hospital, 1-2-23 Wakamizu, Chikusa-ku, Nagoya 464-8547, Japan. Tel.: +81-52-721-7171; Fax: +81-52-721-1308; E-mail: [email protected]