Acute hepatitis after parenteral amiodarone administration.

Pye, Maurice; Northcote, RJ; Cobbe, SM

doi:10.1136/hrt.59.6.690

Cited by 37 publications

(15 citation statements)

References 8 publications

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“…It is associated with extracardiac side effects, including asymptomatic hepatic dysfunction in 15-40% of patients [1], which resolves once the drug is either discontinued or the dose reduced and severe liver disease in the form of liver failure or death, which has been reported in 0-3% of cases [2]. One large series reported mild rise in liver enzymes in 23% (14-82%) of patients on orally administered amiodarone, of whom only 0.5% developed clinically overt disease [3].…”

Section: Discussionmentioning

confidence: 99%

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Amiodarone-induced acute hepatotoxicity

Rao

Agarwal

2011

Eur J Clin Pharmacol

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Dear Editor, We present the case of a 44-year-old man admitted with central chest pain associated with breathlessness that was not relieved by taking sublingual glyceryl nitrate. He presented with a background of old inferior infarct, dilated cardiomyopathy and poor left-ventricular (LV) function and hypertension. There was history of continued alcohol and cocaine abuse. Electrocardiogram on admission confirmed atrial flutter, ventricular rate of 160 bpm with evidence of heart failure, and systolic blood pressure 90 mmHg. All biochemical and hematological parameters were within normal limits. Intravenous (IV) amiodarone 300 mg was administered intravenous (i.v) over 30 min and a maintenance dose of 900 mg over 24 h to attempt pharmacological cardioversion. His heart rate slowed down and later reverted to sinus rhythm. However, over night, he became transiently hypotensive with reduced urine output that subsequently improved. Repeat blood tests the following day revealed an acute increase in alanine aminotransferase (ALT) to 4,428 (see Table 1) and bilirubin to 45. Amiodarone was discontinued. ALT peaked at 4,578 on day 3 but returned to normal at day10. Hepatic ultrasound revealed no abnormality. In particular, there was no evidence of hepatic congestion. The patient was started on digoxin, anti-heart-failure medication optimized his condition, and once he was stable. He was discharged with a further cardiology follow-up.

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Section: Discussionmentioning

confidence: 99%

“…It inhibits drugtransporter P-glycoprotein by impairing its adenosine triphosphatase (ATPase) activity and inhibiting CYP3A4, leading to higher concentrations of amiodarone. It has therefore been proposed that despite acute derangement of liver enzymes following intravenous (IV) amiodarone i.v., oral administration can still be safe [1].…”

Section: Discussionmentioning

confidence: 99%

Amiodarone-induced acute hepatotoxicity

Rao

Agarwal

2011

Eur J Clin Pharmacol

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“…its major metabolite, has not yet been clarified [9]. ' Early acute hepatitis due to parenteral amiodarone administration has been pre viously described in only 4 cases, as far as we know [1][2][3]. In all instances, the drug infu sion was immediately stopped.…”

Section: Discussionmentioning

confidence: 99%

Early Hepatitis during Intravenous Amiodarone Administration

et al. 1991

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“…1 Acute hepatotoxicity following intravenous (IV) amiodarone administration has been reported in several collections of adult case studies. [3][4][5] In 2005, Ra¨tz Bravo et al 6 reviewed 25 such adult cases reported between 1986 and 2002. Most cases occurred in patients aged 50 to 70 years with atrial tachyarrhythmia.…”

Section: Introductionmentioning

confidence: 99%

“…Several authors have noted that oral amiodarone therapy is well tolerated in patients even following acute hepatitis with parenteral therapy. 3,20 However, onset of action following oral administration is estimated to be 2 to 3 days, 21 which is not an acceptable time course for a patient with hemodynamic compromise in the critical care environment. Furthermore, given the potential for multiorgan dysfunction in patients with critical illness, poor gastrointestinal function may lead to unreliable absorption.…”

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Hepatotoxicity After Continuous Amiodarone Infusion in a Postoperative Cardiac Infant

Kicker

Haizlip

Buck

2012

The Journal of Pediatric Pharmacology and Therapeutics

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A former 34-week-old female infant with Down syndrome underwent surgical correction of a congenital heart defect at 5 months of age. Her postoperative course was complicated by severe pulmonary hypertension and junctional ectopic tachycardia. Following treatment with amiodarone infusion, she developed laboratory indices of acute liver injury. At their peak, liver transaminase levels were 19 to 35 times greater than the upper limit of normal. Transaminitis was accompanied by coagulopathy, hyperammonemia, and high serum lactate and lipid levels. Hepatic laboratory abnormalities began to resolve within 48 hr of stopping amiodarone infusion. Heart rate control was achieved concurrently with discovery of laboratory test result abnormalities, and no further antiarrhythmic therapy was required. The intravenous formulation of amiodarone contains the diluent polysorbate 80, which may have hepatotoxic effects. Specifically, animal studies suggest that polysorbate 80 may destabilize cell membranes and predispose to fatty change within liver architecture. Polysorbate was implicated in infant fatalities from Eferol use in the 1980s. This case illustrates a possible adverse event by the Naranjo probability scale. Given the extent of clinically apparent hepatic injury, this patient was not rechallenged with amiodarone during the remainder of her hospitalization. With amiodarone now used as first-line pharmacologic therapy for critical tachyarrhythmia in this population, the number of children exposed to this drug should be expected to increase. Laboratory indices of liver function should be evaluated at initiation of amiodarone therapy, as well as frequently throughout duration of therapy. Consideration should be given to polysorbate-free formulation of intravenous amiodarone for use in the cohort with congenital cardiac disease.INDEX TERMS amiodarone, congenital heart disease, hepatotoxicity, junctional ectopic tachycardia, polysorbate 80

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Acute hepatitis after parenteral amiodarone administration.

Abstract: Amiodarone is believed to have caused acute hepatitis 24 hours after intravenous administration in two patients in whom no other alternative cause of hepatitis was found.

Cited by 37 publications

References 8 publications

Amiodarone-induced acute hepatotoxicity

Amiodarone-induced acute hepatotoxicity

Early Hepatitis during Intravenous Amiodarone Administration

Hepatotoxicity After Continuous Amiodarone Infusion in a Postoperative Cardiac Infant

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