Hepatocellular adenomas associated with antiepileptic drugs: A case report

Abstract

Hepatocellular adenoma (HCA) represents a rare benign liver tumor occurring predominantly in females of reproductive age and taking oral contraceptives. They are associated with various conditions. We report the case of a male patient with hepatic adenomas who has an association with long-term antiepileptic drugs in treatment for seizures of Rasmussen's encephalitis without a history of anabolic steroid use or any underlying hyperestrogenism. MRI findings show multiple hepatic nodules with mainly intermediate signal on T2, intratumoral fat content without diffusion restriction, and intense enhancement in the arterial phase with and without washout in portal and equilibrium phases. The imaging characteristics of these adenomas are indicative of the HNF1 alpha-inactivated subtype. No therapeutic interventions have been performed so far. This association is rare, and few cases have been reported in the literature. This case aims to reaffirm and remind people of the association of hepatic adenomas with antiepileptic drug use and make an additional analysis of the new molecular subtypes of hepatic adenoma, described recently in the literature. Exhaustive literature research reveals few case reports.

Keywords: Antiepileptic drugs; HNF1 alpha-inactivated; Hepatocellular adenoma; Male; Rasmussen encephalitis; Risk factor.

Fig. 1

CT Portal venous phase demonstrates peripheral hypodense liver nodules (circles).

Fig. 2

Axial FSET2 W images. There are 3 circumscribed slight hyperintense lesions (arrows).

Fig. 3

GRET1 W in- and out-phased images. The same lesions are mainly isointense in T1 W in-phase (arrows in A and C) and demonstrate marked diffuse chemical shift signal intensity loss (arrows in B and D).

Fig. 4

In dynamic evaluation after Gadolinium administration, the lesions of segments VII e posterior segment VI show intense enhancement in the arterial phase (A and B) with washout in the portal (C and D) and equilibrium (E and F) phases. The lesion anterior segment VI shows intense enhancement in the arterial phase (A and B) without washout in the portal (C and D) and equilibrium (E and F) phases.