Valproate-induced hyperammonemic encephalopathy with normal liver function (original) (raw)
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Valproate-Induced Hyperammonemic Encephalopathy
Cureus, 2017
Valproate is the best choice drug for a variety of medical conditions. As with any other drug, it has adverse effects, and it is important to emphasize the possibility of those adverse effects to prevent complications. We present the case history of a 44-year-old male with valproateinduced hyperammonemic encephalopathy, despite having normal liver function tests. This case includes a detailed literature review of this rare adverse event. In the light of this case report, we illustrate the importance of checking ammonia levels in all psychiatric patients receiving valproate as a treatment who present with new onset neurological symptoms or altered mental status.
Cureus
Patients presenting with hyperammonemic encephalopathy are likely to have hepatic encephalopathy. However, valproate (an anticonvulsant and mood stabilizer) can also cause hyperammonemic encephalopathy and belongs on the differential for patients taking it, especially if there are recent contributory medication changes. We present a case report of a 61-year-old woman with valproate-induced hyperammonemic encephalopathy but with an initial valproate level within the therapeutic range (50-100 mcg/dL). After withholding valproate and before additional treatment could be initiated, she became fully alert and oriented. We present a literature review exploring valproate toxicity and treatment. Our case shows that clinical suspicion for valproate-induced hyperammonemic encephalopathy is warranted even if the valproate level is within the therapeutic range.
Valproate-Induced Hyperammonemic Encephalopathy: A Case Report and Brief Review of the Literature
American Journal of Therapeutics, 2013
Almost 50 years after its discovery, valproic acid remains a mainstay in the treatment of epilepsy, both alone and in combination with other anticonvulsants. It is also associated with a hyperammonemic encephalopathy, when used in combination with other drugs. We present a case of valproate-induced hyperammonemic encephalopathy in a patient on multiple anticonvulsant and psychotropic medications. The patient presented with altered mental status and became progressively more obtunded and finally began to experience seizures. Her symptoms resolved with the discontinuation of valproic acid and with supportive care.
Psychiatry and Clinical Psychopharmacology
Divalproex sodium/valproic acid (VPA) is an antiepileptic drug which is frequently prescribed in neurology and psychiatric clinics. Common side effects of VPA are side effects of the digestive system, weight gain, tremor, sedation, hematologic side effects and hair loss. Valproate-induced hyperammonemia is almost seen in 50% of patients treated with VPA, some of which may develop encephalopathy. Valproate-induced hyperammonemic encephalopathy (NE) is a well-known subject and there are numerous publications in the current literature. Although there is substantial evidence for this side effect in patients with neurological disorders, the data in the psychiatric area are limited. When we look at publications, it seems that VHE is seen more often because it starts earlier in psychiatric patients, but we think that it is often missed. Here, we presented five cases in which we followed up and treated with VHE diagnosis in our clinic within one year and other reports published previously in a table.
Valproate-associated Hyperammonemic Encephalopathy
The Journal of the American Board of Family Medicine, 2007
The use of valproic acid (VPA) (also known as Depakote, Depakene, and others) frequently results in elevated plasma ammonia. In some people, hyperammonemia may be clinically significant, resulting in hyperammonemic encephalopathy, which may be severe. Valproic acid-induced hyperammonemic encephalopathy may occur in people with normal liver function, despite normal doses and serum levels of VPA. We describe 2 cases of valproic acid-induced hyperammonemic encephalopathy in patients with supratherapeutic VPA levels, although the condition has been described in people with normal VPA levels. With the increasing indications and off-label uses of VPA, family physicians should be aware of this potential complication of VPA and check ammonia levels in patients taking VPA who present with alterations in mental status. Treatment with L-carnitine may be beneficial in reducing ammonia levels. (J Am Board Fam Med 2007;20:499-502.) This article was externally peer reviewed.
Non-Hyperammonemic valproate encephalopathy
Annals of Neurosciences
A 21-year-old male known case of primary hypothyroidism, Seizure disorder sequelae of an old trauma receiving sodium valproate, clobazam and phenobarbitone for control of Generalized tonic clonic seizures reported to neurology OPD with history of altered sensorium and gait unsteadiness for 1 week with history of hike in valproate dose 2 weeks before. On examination he was drowsy. Neurological examination was unremarkable except for gait unsteadiness and ataxia. Patient was admitted and evaluated for acute worsening. All (the) biochemical parameters including complete blood count, liver function tests, kidney function tests, routine urine examination, arterial blood gas analysis, blood and urine culture tests were normal. CSF analysis was also normal. Repeat MRI brain was also done which depicted all old changes with no fresh changes which will account for worsening of his sensorium. EEG was suggestive of diffuse encephalopathy. Thyroid function tests were also normal. Valproate ence...
Hyperammonemia and hepatic status during valproate therapy
Indian Journal of Clinical Biochemistry, 2009
The present study was conducted to assess correlation of ammonia levels with valproate levels in epileptic patients presenting with valproate toxicity and also whether liver enzymes and ammonia levels could serve as biochemical marker of valproate toxicity. 100 patients with epilepsy who had received valproate therapy for more than 12 months and had presented with valproate toxicity and 100 controls were included in the study. The serum valproate, ammonia and liver enzymes were measured in these subjects. In patients with valproate toxicity, the mean level of serum valproate was 110.91 ± 28.68 mg/dL (therapeutic range 50–100 mg/dL). Serum ammonia was higher (86.37 ± 39.90 µg/dL) in patients with valproate toxicity compared to controls (68.73 ± 30.07 µg/dL). Out of 100 patients, only 37 patients had serum valproate level > 120 mg/dL and 22 patients had raised levels of valproate as well as ammonia. Age < 30 years and serum ammonia > 69 μg/dL is risk factors for valproate toxicity. Serum ammonia, liver enzymes should be regularly investigated in patients on valproate therapy for early diagnosis of valproate toxicity.
Valproic Acid-Induced Hyperammonemia with Encephalopathy (VIHE): A Case Report
Journal of Medical Research and Innovation, 2018
Valproic acid (VPA) is a wide spectrum antiepileptic medication indicated for seizure prophylaxis across the spectrum of epilepsy. Since coming into clinical use, VPA has also been recommended for the management of a variety of other pathologies, including, most notably, mood stabilization in the manic patient. VPA’s common adverse effects include gastrointestinal, influenza-like symptoms, headache, and difficulties with sleep; nonetheless, in rare instances, VPA has been noted to cause the severe and potentially lethal condition of hyperammonemia with encephalopathy (VIHE). VIHE is the result of a dose-independent increase in ammonia levels. Often the patient is asymptomatic; if symptoms reach clinical threshold, lethargy is most common, though seizures, focal neurologic deficits and even coma are possible. VIHE can occur in patients despite normal hepatic function, normal loading doses, chronic stable doses and normal free serum drug levels. Once the diagnosis is confirmed, the fi...
The Menacing Side of Valproate: A Case Series of Valproate-induced Hyperammonemia
Indian journal of psychological medicine
Valproate (VPA) is a well-tolerated and commonly used drug to treat variety of psychiatric and neurological disorders. VPA-induced hyperammonemic encephalopathy is a rare adverse effect which can commonly occur in the background of normal liver function and therapeutic serum levels. Any delay in treatment of VPA-induced hyperammonemic encephalopathy can lead to life-threatening coma thus a strong clinical suspicion, fair understanding of the pathophysiology, and management of this drug-related complication can prevent fatal outcome. We hereby report a series of cases admitted to a tertiary care center that developed hyperammonemia and all patients recovered on stopping VPA. This case series cautions the clinicians about hyperammonemia as an uncommon but highly plausible life-threatening side effect, emphasizing astute observation, and high degree of clinical suspicion to prevent mortality and limit morbidity. Early recognition of subtle gastrointestinal, cognitive, and behavioral si...