Decreased serum carnitine in valproate induced Reye syndrome

Böhles, H.; Richter, K; Wagner-Thiessen, E; Schäfer, Hermann

doi:10.1007/bf01377353

Cited by 82 publications

(23 citation statements)

References 13 publications

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“…In addition, homocysteineuria due to methylenetetrahydrofolate reductase defi ciency, 3-hydroxy-3-methylglutaryl-CoA defi ciency, and cytochome C oxidase defi ciency are associated with low carnitine levels. Acquired disorders, such as alcoholic cirrhosis, renal failure as a result of chronic hemodialysis, and epilepsy treated with valproic acid, also have been associated with secondary carnitine defi ciency (192)(193)(194). However, the exact mechanism for carnitine defi ciency and the possible benefi ts of carnitine replacement under these conditions need further study ( 183,189,190,195 ).…”

Section: Dunnigan-type Familial Partial Lipodystrophymentioning

confidence: 99%

Delineating the role of alterations in lipid metabolism to the pathogenesis of inherited skeletal and cardiac muscle disorders

Saini-Chohan

Mitchell

Vaz

et al. 2012

Journal of Lipid Research

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Section: Dunnigan-type Familial Partial Lipodystrophymentioning

confidence: 99%

Delineating the role of alterations in lipid metabolism to the pathogenesis of inherited skeletal and cardiac muscle disorders

Saini-Chohan

Mitchell

Vaz

et al. 2012

Journal of Lipid Research

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“…VPA-induced secondary carnitine deficiency has been reported in several studies [23][24][25][26][27]. Chronic VPA treatment has been shown to den crease total and free carnitine in serum and urine in both humans and rats [16 28-30].…”

Section: Carnitine Deficiencymentioning

confidence: 99%

Valproate hepatotoxicity syndrome: Hypotheses of pathogenesis

Stephens

1992

Pharmaceutisch Weekblad Scientific Edition

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Therapeutic use of the anticonvulsant valproate (VPA) has been associated with a rare, but severe and often fatal hepatotoxicity. Cases usually present with lethargy, anorexia, and vomiting with rapid progression to coma. Liver histopathology is characterized by steatosis with and without necrosis. In some instances only necrosis was present. Several hypotheses of pathogenesis have been postulated. These deal mainly with biochemical systems that are known to be affected by VPA, or with the possible idiosyncratic production of toxic VPA metabolites, especially delta 4-VPA. At present, no hypothesis entirely explains the diverse characteristics of the disorder.

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“…This hypocarnitinemia by itself would not produce an acute illness, but it could render these children susceptible to a critical, even fatal, disease when it is accompanied by a metabolic load mainly on the fatty acid metabolism [3,31] .…”

Section: Discussionmentioning

confidence: 99%

Carnitine and Liver Functions Assessment in ChildrenTreated with Anticonvulsant Drugs

Abdel-Ghany¹,

Saleem²,

Ghazaly³

et al. 2000

med

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ABSTRACT. This study was conducted to evaluate the impact of antiepileptic drugs on the liver function and L-carnitine levels in children suffering from epilepsy. Sixty epileptic children aged from 1 to 15 years, together with 20 healthy controls were studied. Among them twenty-five children were treated with phenytoin (group I), 25 were treated with carbamazepine (group II) and 10 patients were treated with phenobarbital (group III). In each of the three groups, serum free carnitine levels were significantly decreased after one month of therapy compared with pretherapy levels (p<0.01, p<0.01, p<0.01 respectively). Meanwhile, the levels of L-carnitine in treated children collectively were significantly decreased in comparison with healthy children (p<0.01). Hypocarnitinemia was detected in 28% of group I, 56% of group II , and 30% of group III. Serum SGOT was significantly increased in patients treated with phenytoin and phenobarbital (p<0.01, p<0.05 respectively) compared with pretherapy levels. Whereas serum lactate and total bilirubin were significantly increased after therapy in patients treated with carbamazepine in comparison to that before significantly increased (p<0.05 for each) in comparison with controls. Moreover, a significant negative correlation was found between values of carnitine and both lactate (p<0.01) and lactate/pyruvate ratio (p<0.05) after therapy in carbamazepine treated group. It should be taken into account that carnitine rich food in the form of milk and milk products must be taken as a supplement to the antiepileptic drugs especially carbamazepine.

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Decreased serum carnitine in valproate induced Reye syndrome

Cited by 82 publications

References 13 publications

Delineating the role of alterations in lipid metabolism to the pathogenesis of inherited skeletal and cardiac muscle disorders

Delineating the role of alterations in lipid metabolism to the pathogenesis of inherited skeletal and cardiac muscle disorders

Valproate hepatotoxicity syndrome: Hypotheses of pathogenesis

Carnitine and Liver Functions Assessment in ChildrenTreated with Anticonvulsant Drugs

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