Enflurane Hepatotoxicity

Lewis, James H.

doi:10.7326/0003-4819-98-6-984

Cited by 114 publications

(4 citation statements)

References 74 publications

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“…Hypersensitivity from aromatic anticonvulsants might share common mechanisms and some patients could have cross-sensitivity to these drugs—cross-sensitivity frequently is observed between phenytoin and carbamazepine. 37 Cross-sensitivity has been reported from erythromycin derivatives, 38 phenothiazines, 39 haloalkane anesthetics, 40 and anti-androgens. 41 There is a case report of DILI that arose from cross-sensitivity between the propionic acid derivatives naproxen and fenoprofen.…”

Section: Nongenetic Risk Factorsmentioning

confidence: 99%

Risk Factors for Idiosyncratic Drug-Induced Liver Injury

2010

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Idiosyncratic drug-induced liver injury (DILI) is a rare disorder that is not related directly to dosage and little is known about individuals who are at increased risk. There are no suitable preclinical models for the study of idiosyncratic DILI and its pathogenesis is poorly understood. It is likely to arise from complex interactions among genetic, nongenetic host susceptibility, and environmental factors. Nongenetic risk factors include age, sex, and other diseases (eg, chronic liver disease or human immunodeficiency virus infection). Compound-specific risk factors include daily dose, metabolism characteristics, and propensity for drug interactions. Alcohol consumption has been proposed as a risk factor for DILI from medications, but there is insufficient evidence to support this. Many studies have explored genetic defects that might be involved in pathogenesis and focused on genes involved in drug metabolism and the immune response. Multicenter databases of patients with DILI (the United States Drug Induced Liver Injury Network, DILIGEN, and the Spanish DILI registry) are important tools for clinical and genetic research. A genome-wide association study of flucloxacillin hepatotoxicity has yielded groundbreaking results and many similar studies are underway. Nonetheless, DILI is challenging to investigate because of its rarity, the lack of experimental models, the number of medications that might cause it, and challenges to diagnosis.

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Section: Nongenetic Risk Factorsmentioning

confidence: 99%

Risk Factors for Idiosyncratic Drug-Induced Liver Injury

2010

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“…However, the incidence of enflurane-induced hepatotoxicity appears to be less compared to halothane. As with halothane hepatotoxicity, this injury is marked by acute elevations in serum ALT (5- to 50-fold) and appearance of jaundice 2 to 21 days after the operation and anesthesia ( 25 - 27 ).…”

Section: Resultsmentioning

confidence: 99%

Hepatotoxicity of Halogenated Inhalational Anesthetics

Safari¹,

Motavaf²,

Siamdoust³

et al. 2014

Iran Red Crescent Med J

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Context:Halogenated inhalational anesthetics are currently the most common drugs used for the induction and maintenance of general anesthesia. Postoperative hepatic injury has been reported after exposure to these agents. Based on much evidence, mechanism of liver toxicity is more likely to be immunoallergic. The objective of this review study was to assess available studies on hepatotoxicity of these anesthetics.Evidence Acquisition:We searched PubMed, Google Scholar, Scopus, Index Copernicus, EBSCO and the Cochrane Database using the following keywords: “inhalational Anesthetics” and “liver injury”; “inhalational anesthetics” and “hepatotoxicity”; “volatile anesthetics” and “liver injury”; “volatile anesthetics” and hepatotoxicity for the period of 1966 to 2013. Fifty two studies were included in this work.Results:All halogenated inhalational anesthetics are associated with liver injury. Halothane, enflurane, isoflurane and desflurane are metabolized through the metabolic pathway involving cytochrome P-450 2E1 (CYP2E1) and produce trifluoroacetylated components; some of which may be immunogenic. The severity of hepatotoxicity is associated with the degree by which they undergo hepatic metabolism by this cytochrome. However, liver toxicity is highly unlikely from sevoflurane as is not metabolized to trifluoroacetyl compounds.Conclusions:Hepatotoxicity of halogenated inhalational anesthetics has been well documented in available literature. Halothane-induced liver injury was extensively acknowledged; however, the next generation halogenated anesthetics have different molecular structures and associated with less hepatotoxicity. Although anesthesia-induced hepatitis is not a common occurrence, we must consider the association between this disorder and the use of halogenated anesthetics.

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“…Unexplained postoperative jaundice was then definitely associated with halothane itself, and not with the nature or duration of the surgical procedure. Although liver problems have been reported with enflurane (16), none has been definitely linked to isoflurane . Our patient # 1 did show a flare of serum transaminases after an isoflurane exposure; possibly, crosssensitivity to this agent was present, or the anesthetic circuitry may have contained traces of halothane.…”

Section: Discussionmentioning

confidence: 99%

Halothane Hepatitis in Children

Hassall,

Israel,

Gunasekaran

et al. 1990

J. pediatr. gastroenterol. nutr.

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Halothane hepatitis is now a well‐recognized distinct entity in adults, but there prevails an often‐taught “axiom” that halothane hepatitis “does not occur” in children. We describe 2 children who developed cholestatic hepatitis following halothane anesthesia. The first patient had no antecedent liver disease, and presented with anorexia, abdominal pain and delayed onset of jaundice after multiple halothane exposures. Halothane‐specific antibodies were positive, and liver tests resolved completely. The second patient had antecedent liver disease and presented with delayed onset of unexplained high fevers for 10 days following a single halothane exposure. Gradually increasing cholestasis ensued in the absence of other causes of liver disease. Halothane antibodies were negative. These cases illustrate different clinical presentations of halothane hepatitis, such as delayed onset of jaundice or fever following halothane exposure. The difficulties in making a definitive diagnosis and the need to exclude other causes of liver disease are detailed. Risk factors and other presentations are discussed. While halothane hepatitis appears to be an uncommon entity in children, it does occur, and may present with manifestations less than fulminant hepatic failure. A high index of suspicion and a detailed history of the time sequence of events are necessary as the diagnosis is primarily clinical. Halothane‐specific antibodies are helpful if positive. In any child developing unexplained jaundice or high fevers following halothane anesthesia, further exposures should be avoided and halothane‐specific antibodies obtained.

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Enflurane Hepatotoxicity

Cited by 114 publications

References 74 publications

Risk Factors for Idiosyncratic Drug-Induced Liver Injury

Risk Factors for Idiosyncratic Drug-Induced Liver Injury

Hepatotoxicity of Halogenated Inhalational Anesthetics

Halothane Hepatitis in Children

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