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Severe hepatopathy and neurological deterioration after start of valproate treatment in a 6-year-old child with mitochondrial tryptophanyl-tRNA synthetase deficiency.
Vantroys, E, Smet, J, Vanlander, AV, Vergult, S, De Bruyne, R, Roels, F, Stepman, H, Roeyers, H, Menten, B, Van Coster, R
Orphanet journal of rare diseases. 2018;(1):80
Abstract
BACKGROUND The first subjects with deficiency of mitochondrial tryptophanyl-tRNA synthetase (WARS2) were reported in 2017. Their clinical characteristics can be subdivided into three phenotypes (neonatal phenotype, severe infantile onset phenotype, Parkinson-like phenotype). RESULTS Here, we report on a subject who presented with early developmental delay, motor weakness and intellectual disability and who was considered during several years as having a non-progressive encephalopathy. At the age of six years, she had an epileptic seizure which was treated with sodium valproate. In the months after treatment was started, she developed acute liver failure and severe progressive encephalopathy. Although valproate was discontinued, she died six months later. Spectrophotometric analysis of the oxidative phosphorylation complexes in liver revealed a deficient activity of complex III and low normal activities of the complexes I and IV. Activity staining in the BN-PAGE gel confirmed the low activities of complex I, III and IV and, in addition, showed the presence of a subcomplex of complex V. Histochemically, a mosaic pattern was seen in hepatocytes after cytochrome c oxidase staining. Using Whole Exome Sequencing two known pathogenic variants were detected in WARS2 (c.797delC, p.Pro266ArgfsTer10/ c.938 A > T, p.Lys313Met). CONCLUSION This is the first report of severe hepatopathy in a subject with WARS2 deficiency. The hepatopathy occurred soon after start of sodium valproate treatment. In the literature, valproate-induced hepatotoxicity was reported in the subjects with pathogenic mutations in POLG and TWNK. This case report illustrates that the course of the disease in the subjects with a mitochondrial defect can be non-progressive during several years. The subject reported here was first diagnosed as having cerebral palsy. Only after a mitochondriotoxic medication was started, the disease became progressive, and the diagnosis of a mitochondrial defect was made.
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The critical interaction between valproate sodium and warfarin: case report and review.
Zhou, C, Sui, Y, Zhao, W, Dong, C, Ren, L, Song, P, Xu, B, Sun, X
BMC pharmacology & toxicology. 2018;(1):60
Abstract
BACKGROUND Valproic acid (VPA) and warfarin are commonly prescribed for patients with epilepsy and concomitant atrial fibrillation (AF). When VPA and warfarin are prescribed together, clinically important interactions may occur. VPA may replace warfarin from the protein binding sites and result in an abnormally increased anticoagulation effect. This is commonly underrecognized. CASE PRESENTATION In our case, we report a 78-year-old woman with a glioma who presented with status epilepticus. The patient was on warfarin to prevent cardiogenic embolism secondary to AF. Intravenous loading dose of VPA was administered, but international normalized ratio (INR) increased significantly to 8.26. Intravenous vitamin K1 was then given and the patient developed no overt bleeding during the hospitalization. CONCLUSION By reviewing the literature and discussing the critical interaction between valproate sodium and warfarin, we conclude that intravenous VPA and the co-administrated warfarin may develop critical but underrecognized complications due to effects on the function of hepatic enzymes and displacement of protein binding sites.
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Sudden valproate-induced hyperammonemia managed with L-carnitine in a medically healthy bipolar patient: Essential review of the literature and case report.
Cattaneo, CI, Ressico, F, Valsesia, R, D'Innella, P, Ballabio, M, Fornaro, M
Medicine. 2017;(39):e8117
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Abstract
RATIONALE Valproic Acid is a commonly used psychiatric drug primarily used as a mood stabilizer. Mild hyperammonemia is a Valproic Acid common adverse effect. This report presents an example of treated hyperammonemia on Valproic acid therapy managed with L-carnitine administration in BD patients characterized by sudden vulnerability. PATIENT CONCERNS We report the case of a 29-year-old man suffering from bipolar disorder (BD) and substance use disorder who exhibited sudden altered mental status upon admittance to the inpatient unit. The patient was started on Valproic acid with no improvement. DIAGNOSES The patient had remarkably high ammonia levels (594 μg/dL) without hepatic insufficiency, likely due to his valproate treatment. INTERVENTIONS The patient was administered lactulose, intravenous hydration, and i.v. levocarnitine supplementation 4.5 g/day. OUTCOMES The administration leads to reduction of ammonia levels to 99 μg/dL within 12 hours upon initiation of carnitine therapy and progressive restore of his mental status within 24 hours. LESSONS Resolution of hyperammonemia caused by Valproic acid therapy may be enhanced with the administration of L-carnitine. An interesting aspect of this case was how rapidly the patient responded to the carnitine therapy.
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Infiltration of sodium valproate with compartment syndrome and bullous reaction: case report and literature review.
Santivasi, WL, Kulkarni, S, Patton, ML, Haith, LR, Guilday, RE, Reigart, CL, Ackerman, BH
Burns : journal of the International Society for Burn Injuries. 2011;(7):e59-62
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Rowell's syndrome in the course of treatment with sodium valproate: a case report and review of the literature data.
Kacalak-Rzepka, A, Kiedrowicz, M, Bielecka-Grzela, S, Ratajczak-Stefanska, V, Maleszka, R, Mikulska, D
Clinical and experimental dermatology. 2009;(6):702-4
Abstract
Rowell's syndrome (RS) is a rare type of coexistence of one of the lupus erythematosus (LE) types (systemic, subacute cutaneous or discoid) and erythema multiforme (EM) (including toxic epidermal necrolysis). We present the case of a 51-year-old patient with a diagnosis of RS, most probably caused by drugs given as psychiatric treatment. After cessation of sodium valproate and initiation of treatment with prednisolone, a spectacular clinical remission was achieved. The likely role of psychiatric drugs, namely sodium valproate and sertraline, as triggering factors, is discussed.
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[Successful treatment with cyclosporine of sodium valproate-induced pure red cell aplasia].
Kanda, J, Chonabayashi, K, Watanabe, M, Arima, N, Tsudo, M
[Rinsho ketsueki] The Japanese journal of clinical hematology. 2005;(10):1114-7
Abstract
We report a 67-year-old man who developed pure red cell aplasia (PRCA) during therapy for epilepsy with sodium valproate since April 2004. He was admitted to our hospital because of severe anemia (Hb 5.0g/dl, reticulocyte 0.1%) in August 2004. A bone marrow examination showed marked erythroid hypoplasia and a diagnosis of drug-induced PRCA was made. Because the discontinuation of valproate for one month failed to increase the number of reticulocytes and frequent blood transfusions were necessary, cyclosporine therapy was initiated. Within a week, substantial recovery of the numbers of reticulocytes was obtained, the cyclosporine had, however, to be changed to prednisolone due to the refusal of the patient to continue with it, resulting in the exacerbation of his anemia. After three weeks, cyclosporine therapy was resumed, which achieved rapid and remarkable recovery of red blood cells (Hb 8.9g/dl, reticulocyte 4.9%) within one month. Sixteen cases of valproate-induced PRCA have been reported in the literature and all cases except one recovered only by discontinuing or reducing the administration of valproate. However, our case required cyclosporine therapy in addition to the discontinuation of valproate. These results suggest that not only the direct toxic effect on erythropoiesis but also T lymphocyte-mediated immunological mechanism was involved in the pathogenesis of valproate-induced PRCA.
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Tubulo-interstitial nephritis caused by sodium valproate.
Yoshikawa, H, Watanabe, T, Abe, T
Brain & development. 2002;(2):102-5
Abstract
A severely handicapped 14-year-old Japanese girl had epilepsy and was treated with sodium valproate (SV) from the age of 7 years. Although the epileptic seizures were well controlled, she sometimes had a fever and hypokalemia from the age of 13 years. Laboratory examinations revealed metabolic acidosis, hypouricemia, hypophosphatemia, glycosuria, proteinuria and aminoaciduria, thus suggesting Fanconi syndrome. Gallium scanning showed marked renal uptake. A renal biopsy revealed interstitial nephritis without immuno-deposition. SV was replaced since it was considered to be the most probable cause of the renal involvement. Thereafter, she showed marked improvement of the clinical symptoms and the laboratory data gradually, and she never had a fever. Although SV is an effective anti-epileptic drug, we have to pay attention to adverse renal effects such as Fanconi syndrome and interstitial nephritis.
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Divalproex sodium in substance abusers with mood disorder.
Albanese, MJ, Clodfelter, RC, Khantzian, EJ
The Journal of clinical psychiatry. 2000;(12):916-21
Abstract
BACKGROUND Substance abuse is a common comorbid illness in patients with mood disorders. Little has been written about the pharmacologic treatment of patients with affective lability and co-occurring substance abuse, however. The following report will describe clinical experience using divalproex sodium in substance-abusing patients with mood disorder. METHOD Twenty patients admitted to an intermediate-care inpatient substance abuse program were diagnosed with comorbid mood disorder (according to DSM-IV criteria) and treated with divalproex sodium in an open-label, naturalistic trial with no blind. All patients were followed clinically and were assessed using the Clinical Global Impressions scale (CGI) and laboratory studies. RESULTS Seven patients referred while on divalproex treatment continued to exhibit improved mood. Eleven others had at least 1 week of follow-up, and 10 of these also showed improvement. In 13 cases, divalproex was used safely with other psychiatric medications. Two patients complained of slight tremor, 1 of whom was also taking fluoxetine. Fifteen of 17 patients in whom biochemistry and hematology laboratory studies were completed had unremarkable results; 2 other patients had pretreatment abnormalities, which worsened over the course of treatment. Mean plasma valproate level was 58.53 microg/mL. Mean length of follow-up was 38 days. Mean period of abstinence prior to starting medication was 48 days. Some patients reported decreased cravings, and, by self-report, all patients remained abstinent. CONCLUSION This report suggests that divalproex sodium is efficacious and safe, both alone and in combination with other psychiatric medications, in treating substance-abusing patients with mood disorder.