Carbamazepine-Induced Liver Injury

Ee, Soffer; Rj, Taylor; Pd, Bertram; Rc, Haggitt; Mj, Levinson

doi:10.1097/00007611-198305000-00043

Cited by 25 publications

(5 citation statements)

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“…Being primary metabolic site, it is prone to damage mediated by exogenously administered or endogenous intoxicants released during metabolism of various substances in human body. These agents cause severe damage to liver thereby resulting in hepatitis, cholestatic, fibrosis, granulomas and vascular lesions [1], [2], [3], [4], [5]. Various hepato-toxins act by initiating secondary and tertiary changes in the gene expression, eliciting immune mediated allergic responses and modulating activities of xenobiotic and anti-oxidative enzymes [6].…”

Section: Introductionmentioning

confidence: 99%

Diminution of Hepatic Response to 7, 12-dimethylbenz(α)anthracene by Ethyl Acetate Fraction of Acacia catechu Willd. through Modulation of Xenobiotic and Anti-Oxidative Enzymes in Rats

et al. 2014

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BackgroundLiver is the primary metabolizing site of body and is prone to damage by exogenous as well as endogenous intoxicants. Polycyclic aromatic hydrocarbons such as 7, 12- dimethylbenz(α)anthracene (DMBA) is an exogenous hepatotoxin, which is well known for modulating phase I, II and anti-oxidative enzymes of liver. Plants contain plethora of polyphenolic compounds which can reverse the damaging effect of various xenobiotics. The present study investigated protective role of the ethyl acetate fraction of Acacia catechu Willd. (EAF) against DMBA induced alteration in hepatic metabolizing and anti-oxidative enzymes in rats.Methodology and Principal FindingsThe rats were subjected to hepatic damage by treating with DMBA for 7 weeks on alternative days and treatment schedule was terminated at the end of 14 weeks. The rats were euthanized at the end of protocol and livers were homogenized. The liver homogenates were used to analyse phase I (NADPH-cytochrome P450 reducatse, NADH-cytochrome b5 reductase, cytochrome P420, cytochrome b5), phase II (glutathione-S-transferase, DT diaphorase and γ-Glutamyl transpeptidase) and antioxidative enzymes (catalase, superoxide dismutase, ascorbate peroxidase, glutathione reductase, guiacol peroxidase and lactate dehydrogenase). Furthermore, other oxidative stress parameters (thiobarbituric acid reactive substances, lipid hydroperoxides and conjugated dienes and reduced glutathione) and liver marker enzymes (serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase and alkaline phosphatase) were also studied. The DMBA induced significant changes in activity of hepatic enzymes that was reversed by treatment with three dose levels of EAF.ConclusionIt is concluded that EAF affords hepato-protection against DMBA in rats through modulation of phase I, II and anti-oxidative enzymes.

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Section: Introductionmentioning

confidence: 99%

Diminution of Hepatic Response to 7, 12-dimethylbenz(α)anthracene by Ethyl Acetate Fraction of Acacia catechu Willd. through Modulation of Xenobiotic and Anti-Oxidative Enzymes in Rats

et al. 2014

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“…Carbamazepine-induced hepatitis is well documented in the literature. [9][10][11][12] Suspicion of a drug-related etiology in this patient grew only after many days, probably because it is not commonly seen in children. This delay in establishing the presumptive diagnosis led to late withdrawal of the drug and contributed to the severity of the ADR.…”

Section: Discussionmentioning

confidence: 99%

Suspected Carbamazepine‐Induced Hepatotoxicity

1999

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Carbamazepine is a potent anticonvulsant agent with proven efficacy in the treatment of partial and tonic-clonic seizures. An epileptic child treated with therapeutic dosages of carbamazepine developed severe hepatitis and hepatic insufficiency. She had a positive response to withdrawal of the drug and administration of corticosteroids. The Roussel UCLAF method for estimating causality of the adverse event was applied for an acute hepatocellular problem, with a final score of 8. This method has advantages over other tools because it involves many clinical factors that give additional guides to clinicians in patients with liver injury, but it must be adapted for adverse events in the pediatric population.

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“…14, 15 The reaction appears within the first month of therapy and improves with drug withdrawal. Soffer et al 14 suggest two types of mechanisms: an idiosyncratic hypersensitivity type 16 and a toxin-induced reaction secondary to accumulation of toxic metabolites, 17 particularly when enzyme-inducing agents are given concurrently. Carbamazepine is structurally related to the tricyclic antidepressant imipramine, which has been an occasional cause of cholestatic liver injury.…”

Section: Case Reportsmentioning

confidence: 99%