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Case Reports
. 2018 Apr 14;12(1):95.
doi: 10.1186/s13256-018-1629-8.

Amiodarone-induced reversible and irreversible hepatotoxicity: two case reports

Affiliations
Case Reports

Amiodarone-induced reversible and irreversible hepatotoxicity: two case reports

Toyonobu Tsuda et al. J Med Case Rep. .

Abstract

Background: Amiodarone is a highly effective treatment for supraventricular and ventricular tachyarrhythmia; however, it could be associated with several serious adverse effects, including liver injury.

Case presentation: We report the clinical and histological features of two contrasting Japanese patients with amiodarone-induced reversible and irreversible hepatotoxicity. One patient with amiodarone-induced irreversible hepatotoxicity showed liver cirrhosis during treatment with amiodarone and died of hepatic failure; the other patient, who had reversible hepatotoxicity, showed a reversible course of liver function and imaging after discontinuation of amiodarone.

Conclusions: We emphasize the importance of close monitoring of liver enzymes and evaluation of liver computed tomographic imaging as well as liver biopsy during treatment with amiodarone, and discontinuation should be considered when amiodarone-induced hepatotoxicity is suspected.

Keywords: Amiodarone; Hepatotoxicity.

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Conflict of interest statement

Ethics approval and consent to participate

The publication of this case report was approved by the clinical research ethics committees of Kanazawa University Hospital.

Consent for publication

Written informed consent was obtained from the patients or their relatives for publication of this case report and any accompanying images. A copy of the written consents is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
a Computed tomographic scan shows diffuse high attenuation of the liver parenchyma (96 Hounsfield units). b Massive ascites and splenomegaly were found, in addition to diffuse high attenuation of the liver parenchyma. c Regenerative nodules and well-developed bridging fibrosis were observed (hematoxylin and eosin stain, magnification × 20), as were marked neutrophilic infiltration, a remarkable amount of Mallory bodies (arrowheads), and ballooned hepatocytes (arrow) (hematoxylin and eosin stain, magnification × 200). d Numerous whorled or lamellar inclusions in lysosomes were detected by electron microscopy
Fig. 2
Fig. 2
a Computed tomogram shows diffuse high attenuation of the liver parenchyma (120 Hounsfield units). b Distinct collagen deposition is seen in the periportal, perivenular, and pericellular locations, which formed bridging fibrosis (Azan stain, magnification × 100). There were numerous Mallory bodies (arrowheads) as well as hepatocellular ballooning (arrows) and mild macrovesicular and microvesicular fatty changes. Mild lymphocytic and neutrophilic infiltration was also observed (hematoxylin and eosin stain, magnification × 400). c After discontinuation of amiodarone, the patient’s liver density dramatically improved to a normal level (45 Hounsfield units) during the course of 9 months

References

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