The hepatobiliary effects of direct oral anticoagulants (DOACs) have been under close surveillance since hepatotoxicity was demonstrated with ximelagatran during the post marketing phase, necessitating its withdrawal in 2006 [1]. All currently available DOACs are associated with a small risk of idiosyncratic hepatotoxicity [2]. The 2013 European guidance for the use of DOACs recommends yearly monitoring of liver function. With the exception of dabigatran, all DOACs are metabolized in the liver, and therefore associated with liver function alteration.
