Abstract
Objective:
To report a case of acute hepatitis related to atenolol administration in a liver transplant (LT) recipient.
Case Summary:
A 57-year-old woman was evaluated for LT because of liver failure due to cirrhosis of unknown origin. LT was performed in November 2006. In March 2007, results of liver function tests (LFTs) were within the reference ranges. She had received atenolol for hypertension for 3 years prior to surgery and it was reintroduced at a dose of 100 mg/day because of recurrence of hypertension. One month later, she presented with acute hepatitis. The first post-LT liver biopsy was performed. Histologic examination disclosed a combination of portal and centrilobular inflammatory lesions. The diagnosis of acute rejection was accepted and 3 bolus doses of prednisone 500 mg/day were administered. Evolution was not favorable and a second liver biopsy was obtained. Histologic examination showed the complete disappearance of portal inflammatory lesions but an increase of centrilobular lesions. Toxic hepatitis was suspected and atenolol was stopped. No other therapeutic modification was done and resolution of the toxicity was good. An objective causality assessment revealed that the adverse drug event was probable.
Discussion:
This case report represents a very rare severe hepatotoxicity due to atenolol and illustrates the diagnostic difficulties raised by such clinical situations in the context of LT. It is noteworthy that the initial diagnosis considered in this patient was acute rejection. This diagnosis had to be reconsidered because of the unfavorable outcome, despite specific treatment of rejection. Moreover, the patient had been treated with atenolol for 3 years before LT: in the absence of any other etiology, the possibility that she had drug-induced cirrhosis may therefore be considered. The mechanism of β-blocker–related hepatotoxicity is debatable. In our case, the composition of the inflammatory infiltrates observed in the liver biopsy specimens suggests an immune-mediated mechanism.
Conclusions:
Despite the fact that β-blocker–induced hepatotoxicity is probably extremely rare, it must be suspected and the drug therefore discontinued.
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