Propafenone-induced liver injury: Report of a case and review of the literature

Mondardini, A.; Pasquino, Paola; Bernardi, Paolo; Aluffi, E; Tartaglino, Bruno; Mazzucco, Gianna; Bonino, Ferruccio; Verme, G; Negro, Francesco

doi:10.1016/0016-5085(93)90365-j

Cited by 25 publications

(6 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Non-cardiac adverse effects include cholestatic hepatitis, [29][30][31][32][33][34] reactive airway disease, 35,36 agranulocytosis, 37 hemolysis, 38 drug fever 39 and ataxia. 40 Cardiac adverse effects include hypotension, malignant ventricular dysrhythmias and sudden death.…”

Section: -28mentioning

confidence: 99%

Bicarbonate therapy for unstable propafenone-induced wide complex tachycardia

Brubacher

2004

CJEM

View full text Add to dashboard Cite

A previously healthy 73-year-old woman presented to hospital with acute atrial fibrillation. After intravenous procainamide failed to restore sinus rhythm, she was treated with 300 mg of oral propafenone and discharged with a prescription for propafenone and propranolol. Six hours later she took 150 mg of propafenone as prescribed. Within 1 hour she became dyspneic and collapsed. On arrival in hospital she was unconscious, with a wide complex tachycardia and no obtainable blood pressure. After defibrillation and lidocaine, she converted to a wide complex sinus rhythm, but remained profoundly hypotensive despite intravenous epinephrine and dopamine. Hypertonic sodium bicarbonate (HCO 3 ) was administered and, shortly thereafter, her blood pressure increased, her QRS duration normalized and her clinical status improved dramatically. In this case of severe refractory propafenone-related cardiac toxicity, intravenous HCO 3 led to a profound clinical improvement. Emergency physicians should be familiar with the syndrome of sodium-channel blocker poisoning and recognize the potentially important role of bicarbonate in its treatment. RÉSUMÉUne femme âgée de 73 ans auparavant en bonne santé s'est rendue à l'hôpital pour une fibrillation auriculaire aiguë. La procaïnamide intraveineuse n'ayant pas réussi à rétablir le rythme sinusal, la patiente reçut 300 mg de propafénone per os et fut renvoyée chez elle avec une ordonnance pour de la propafénone et du propranolol. Six heures plus tard, elle prit 150 mg de propafénone tel que prescrit. Dans l'heure qui suivit, elle devint dyspnéique et s'effondra. À son arrivée à l'hôpital, elle était inconsciente, en tachycardie à complexe large et il était impossible de prendre sa tension artérielle. Après la défibrillation et l'administration de lidocaïne, la tachycardie se changea en rythme sinusal à complexe large. Par contre, la patiente demeura profondément hypotendue malgré l'administration intraveineuse d'épinéphrine et de dopamine. On lui administra du bicarbonate de sodium hypertonique (HCO 3 ) et, peu de temps après, sa tension artérielle augmenta, la durée du complexe QRS redevint normale et son statut clinique s'améliora énormé-ment. Dans ce cas de toxicité cardiaque réfractaire grave liée à la propafénone, l'HCO 3 intraveineux conduisit à une amélioration clinique remarquable. Les médecins d'urgence devraient se familiariser avec le syndrome de l'empoisonnement par un bloqueur des canaux sodiques et reconnaître le rôle potentiellement important du bicarbonate dans le cadre de son traitement.

show abstract

Section: -28mentioning

confidence: 99%

Bicarbonate therapy for unstable propafenone-induced wide complex tachycardia

Brubacher

2004

CJEM

View full text Add to dashboard Cite

show abstract

“…Despite these limitations, antiarrhythmics are still widely prescribed for the management of symptomatic AF. Several case reports and reviews have addressed the potential adverse effects associated with these agents, including liver toxicity [ 3 – 6 ], hepatic dysfunction [ 7 , 8 ], steatohepatitis [ 9 ], liver injury [ 10 ], and intrahepatic cholestatic jaundice [ 11 ]. However, few systemic analyses have been conducted in this setting, and little evidence of an association between the use of antiarrhythmic agents and the risk of developing malignant neoplasm of liver and intrahepatic bile ducts (MNLIHD) has been reported.…”

Section: Introductionmentioning

confidence: 99%

Antiarrhythmic Agents and the Risk of Malignant Neoplasm of Liver and Intrahepatic Bile Ducts

Lim

Lin

et al. 2015

PLoS ONE

View full text Add to dashboard Cite

BackgroundThe objective of this study was to determine the association between the use of antiarrhythmic agents and the risk of malignant neoplasm of liver and intrahepatic bile ducts (MNLIHD).MethodsWe used the research database of the Taiwan National Health Insurance Program to conduct a population-based, case-control study. We identified 9944 patients with antiarrhythmic history who were first diagnosed as having MNLIHD between 2005 and 2010. We identified an additional 19,497 patients with antiarrhythmic history in the same period who did not develop MNLIHD and were frequency-matched using age, sex, and index year to form a control group. Five commercially available antiarrhythmic agents, amiodarone, mexiletine, propafenone, quinidine, and procainamide, were analyzed.ResultsThe adjusted odds ratio (OR) of MNLIHD was 1.60 (95% confidence interval [CI], 1.45–1.77) for amiodarone users versus nonamiodarone users. In subgroup analysis, amiodarone use was significantly associated with an increased risk of MNLIHD with an adjusted OR of 18.0 (95% CI, 15.7–20.5) for patients with comorbidities compared to an OR of 2.43 (95% CI, 1.92–3.06) for those without comorbidities. After adjustment for age, sex, statins, anti-diabetes medications, non-steroidal antiinflammatory drugs, propafenone use, quinidine use, and comorbidities, the ORs were 1.49, 1.66, and 1.79 for MNLIHD associated with annual mean defined daily doses of ≤30, 31–145, and >145, respectively.ConclusionsThe results of the present study indicated that amiodarone might be associated with the development of MNLIHD in a dose-dependent manner, particularly among patients with comorbidities.

show abstract

“…The clinical presentation of propafenone hepatotoxicity can be cholestatic and/or hepatocellular. [67] It presents with jaundice as reported in all cases. The latency period varied between two and six weeks.…”

Section: Discussionmentioning

confidence: 95%

“…A temporal relationship between the intake of the drug and the development of symptoms[56]Clinical and biochemical recovery occurred following the withdrawal of the drug[6]Exclusion of other causes of liver dysfunction[7] andThe histologic changes were consistent with drug toxicity. [8]…”

Section: Discussionmentioning

confidence: 99%

Propafenone hepatotoxicity: Report of a new case and review of the literature

Younan

Barada

Faraj

et al. 2013

Saudi J Gastroenterol

View full text Add to dashboard Cite

Propafenone is a class Ic antiarrhythmic drug. It is a beta-adrenergic blocker that causes bradycardia and bronchospasm. It is metabolized primarily in the liver. Its bioavailability and plasma concentration differ among patients under long-term therapy. They are genetically determined by the hepatic cytochrome P-450 2D6. Hepatic toxicity is highly uncommon. To date, only eight patients were reported in the reviewed world literature. In this article, one new case will be reported emphasizing the importance of medication history taking in patients presenting with new-onset liver enzymes abnormalities.

show abstract

Propafenone-induced liver injury: Report of a case and review of the literature

Cited by 25 publications

References 5 publications

Bicarbonate therapy for unstable propafenone-induced wide complex tachycardia

Bicarbonate therapy for unstable propafenone-induced wide complex tachycardia

Antiarrhythmic Agents and the Risk of Malignant Neoplasm of Liver and Intrahepatic Bile Ducts

Propafenone hepatotoxicity: Report of a new case and review of the literature

Contact Info

Product

Resources

About