Valproic Acid-Induced Hyperammonemia in the Elderly: A Review of the Literature

Mittal, Vikrant; Muralee, Sunanda; Tampi, Rajesh R.

doi:10.1155/2009/802121

Cited by 22 publications

(21 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the liver, it inhibits carbamoylphosphate synthetase I (CPS I), thereby preventing the incorporation of ammonia into the urea cycle; this inhibition is through the inhibition of N-acetylglutamate; an activator of CPS I. It also increases pyruvate, which is a potent inhibitor of CPS I (34).…”

Section: Discussionmentioning

confidence: 99%

Disorders associated with abnormal acylcarnitine profile among high risk Egyptian children

El-Mesellamy¹,

Gouda²,

Fateen³

et al. 2014

BLL

View full text Add to dashboard Cite

Acylcarnitine profi le (ACP) is a useful tool in the biochemical diagnosis and monitoring of many acquired and inherited metabolic disorders. In the present study, acylcarnitines (ACs) were quantifi ed in dried blood spot samples collected from 150 high risk Egyptian newborns and children using LC/MS/MS technique. They were referred to the Biochemical Genetics department in the National Research Center. Their age ranged from 1 to 36 months. Thirty seven patients had abnormal ACP diagnostic of some inherited metabolic disorders and other acquired conditions. The study revealed 5 (13.5 %) with medium chain acyl CoA dehydrogenase defi ciency (MCADD), 1 (2.7 %) with long chain hydroxyacyl CoA dehydrogenase defi ciency (LCHADD), 1 (2.7 %) with multiple acyl CoA dehydrogenase defi ciency (MADD), 28 (75.7 %) with secondary carnitine defi ciency (SCD), 1 (2.7 %) with glutaric aciduria type I (GA I), and 1 (2.7 %) with methylmalonic aciduria (MMA) (Tab. 8, Ref. 39). Text in PDF www.elis.sk. Key words: inborn errors of metabolism, fatty acid oxidation disorders, acylcarnitine profi le, LC/MS/MS.

show abstract

Section: Discussionmentioning

confidence: 99%

Disorders associated with abnormal acylcarnitine profile among high risk Egyptian children

El-Mesellamy¹,

Gouda²,

Fateen³

et al. 2014

BLL

View full text Add to dashboard Cite

show abstract

“…Although there were no reports about valproate-induced intraoperative hypocapnia, we found few reports about valproate-induced hyperventilation [19,20]. Valproate-induced hyperventilation is thought to arise from valproate-induced hyperammonemia, decreasing the PaCO 2 level [20,21]. Nonetheless, a causal relationship between valproate and intraoperative hypocapnia could not be conclusively proved because we did not check the level of ammonia corresponding to the PaCO 2 level in our patients.…”

Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 94%

Risk Factors for Intraoperative Hypocapnia in Pediatric Neurosurgical Patients: A Retrospective Cohort Study

et al. 2018

View full text Add to dashboard Cite

Background: Hypocapnia has been associated with an increased risk and adverse outcomes in the injured brain. This study aimed to identify risk factors of intraoperative hypocapnia in pediatric neurosurgical patients when tidal volumes and respiratory rates were determined based on their weight and age, respectively. Methods: Electronic medical records of pediatric patients (≤18 years) who underwent neurosurgery from December 2014 to January 2016 were retrospectively reviewed. Minute ventilation was fixed according to each patient's weight and age. Hypocapnia was defined as arterial partial pressure of carbon dioxide <35 mm Hg from intraoperative arterial blood gas analysis. Patients were divided into hypocapnia and nonhypocapnia groups. Risk factors for intraoperative hypocapnia were found using univariable and multivariable logistic regression analyses. Results: Of the 333 pediatric patients analyzed, 101 (30%) and 232 (70%) were included in the hypocapnia and nonhypocapnia groups, respectively. There was no difference in the minute ventilation between the two groups. The hypocapnia group had more patients taking valproate (8.9 vs. 2.2%; p = 0.008; OR, 4.441; 95% CI, 1.449-13.61) and carbonic anhydrase inhibitors (7.9 vs. 2.2%; p = 0.018; OR, 3.905; 95% CI, 1.245-12.25). An operation for hydrocephalus was more commonly performed in the hypocapnia group (26.7 vs. 15.9%; p = 0.017; OR, 1.923; 95% CI, 1.094-3.379). In the multivariable regression analysis, valproate (OR, 3.939; 95% CI, 1.250-12.41; p = 0.019), carbonic anhydrase inhibitor (OR, 3.345; 95% CI, 1.029-10.88; p = 0.045), and operation for hydrocephalus (OR, 1.838; 95% CI, 1.032-3.272; p = 0.039) were independent risk factors for intraoperative hypocapnia. Conclusions: Pediatric patients taking valproate and carbonic anhydrase inhibitors and who were scheduled for surgery of hydrocephalus were at risk of developing intraoperative hypocapnia during neurosurgery, a finding warning the surgeon that a conventional ventilatory strategy would endanger these patients.

show abstract

“…Secondly valproate induced hyperammonemia developed while on monotherapy with valproate and there was neither polypharmacy [8] nor known medical comorbidity [8,9]. Lastly stoppage of divalproex sodium for few days lead to prompt recovery and no other treatment measure like carnitine, lactulose, heamodylysis [12,13] were required.…”

Section: Discussionmentioning

confidence: 99%

Valproate Induced Delirium due to Hyperammonemia in a Case of Acute Mania: A Diagnostic Dilemma

Dixit¹

2015

JCDR

View full text Add to dashboard Cite

A 31-year-old male with no past history of any significant medical illness manifested with acute onset of behavioural problems of seven-eight days duration in form of increased psychomotor activity, elated mood, verbosity, distractibility, enhanced self esteem, hyper-religiosity, delusion of grandiosity, impaired biodrives (sleep, appetite and libido) in absence of any perceptual disturbance and with intact sensorium. There was no history of fever, altered sensorium, neurological deficit and significant weight loss prior to onset of behavioural abnormalities. There were no developmental issues. Physical examination revealed pulse 82/min, BP 130/82 mm of Hg, afebrile, respiratory rate was 16/min, no digital tremors or hyperhydrosis. Lab investigations including heamogram, LFT, urea, creatinine, blood sugar, lipid profile, serum electrolyte, X-ray chest, CT Scan Brain, T3, T4, and TSH was within normal limits and HIV status was negative. He was diagnosed as a case of mania with psychotic symptoms as per International Classification of Diseases 10 (ICD10) [1] and started on mood-stabilizer tab divalproex sodium 500 mg BD and olanzapine 5 mg BD. Patient started showing improvement. By 10 th day his symptoms remitted to about 40% however his hyper-religiosity, self esteem and grandiose manners though less severe persisted, however on 13 th day patient complained of headache right hemi-cranium lasting for half hour to one hour accompanied by nausea and vomiting. His pulse, BP and temp were normal. MRI brain and fundoscopy revealed no abnormality. A neurophysician referral resulted in prescription of tab topiamate 25 mg BD in view of vascular headache and the same evening (15 th day of admission) after receiving tab topiramate patient developed disorientation, confusion, unsteadiness of gait, irrelevant talks and agitation which continued for next three-five days. His topiramate was stopped immediately. His MMSE score was 13/30. Subsequently divalproex sodium was increased to 1500 mg along with 15 mg of olanzapine by 22 nd day. EEG revealed normal bilateral symmetrical 9-12 Hz posteriorly dominant alfa rhythms. Patient did not show any improvement and continued to remain puzzled, dazed, confused and disoriented during day time with irrelevant talk and exhibited more hyperactivity towards evening with altered sleep-Wake schedule. His physical examination revealed pulse 88/min, BP 136/88 mm of Hg, respiratory rate 18/ min. There were no menningeal, cerebellar or extra pyramidal signs. keywords: Bipolar disorder, Encephalopathy, Non hepatic hyperammonemia, Valproic acidHis neurological examination was non contributory. His repeat liver function, electrolyte, urea, creatinine and CPK levels were within normal range. A pre-anesthetic check up was done and after taking appropriate consent of patient and relatives, he was taken up for electroconvulsive therapy (ECT) on 29 th day suspecting it to be a case of Delirious mania. ECT was planned twice a week. Before starting ECT dose of divalproex sodium was reduced to 250 mg BD t...

show abstract

Valproic Acid-Induced Hyperammonemia in the Elderly: A Review of the Literature

Cited by 22 publications

References 51 publications

Disorders associated with abnormal acylcarnitine profile among high risk Egyptian children

Disorders associated with abnormal acylcarnitine profile among high risk Egyptian children

Risk Factors for Intraoperative Hypocapnia in Pediatric Neurosurgical Patients: A Retrospective Cohort Study

Valproate Induced Delirium due to Hyperammonemia in a Case of Acute Mania: A Diagnostic Dilemma

Contact Info

Product

Resources

About