S3662 From Androgen to Adenoma: A Ruptured Affair

Introduction: Hepatic adenomas develop in the setting of anabolic-androgenic steroid (AAS) use. Cessation of AAS often leads to adenoma regression. We present a case of hepatic adenoma rupture and extensive adenomatosis in a patient with remote AAS use. Case Description/Methods: A 32 year-old man with no medical history presented with abdominal pain. History included AAS use, discontinued 3 years ago. Upon arrival, he was hemodynamically stable. Laboratory values were notable for AST 2,817 IU/L and ALT 3,398 IU/L but intact synthetic function. Triphasic computed tomography (CT) demonstrated a 27 cm peri-hepatic hematoma and numerous heterogeneous, hypodense lesions in liver segments III/IVb. Hemoglobin decreased from 8.1 g/dL to 6.7 g/dL, requiring blood transfusion. Due to concern for hemorrhage, the patient underwent hepatic angiography with embolization of the distal right lobe branches. Biopsy of a right hepatic lobe lesion confirmed the diagnosis of beta-catenin mutated hepatic adenoma. Given extent of disease, the patient underwent surgical resection of segments IVb, VI, and VII with plans for ablation of 4 smaller lesions. Intraoperative findings revealed diffuse hepatic adenomatosis involving all segments, deemed too numerous for ablation. The patient is undergoing surveillance imaging and the most recent MRI revealed significant interval decrease in size and number of multiple hepatic lesions. Discussion: Hepatic adenomas are benign, solid, and usually solitary lesions of the liver that primarily occur in women on oral contraception with a female/male ratio of 8:1. Overall incidence is estimated to be 5 per 1,000,000. Exogenous hormone exposure and obesity are the most common risk factors. While generally asymptomatic, adenomas may lead to complications including malignant transformation (∼5%) and rupture with hemorrhage (∼15%), particularly if lesions exceed 5cm. Management includes discontinuation of the offending agent and resection of large lesions. Our patient did not have active AAS use or large lesions. Despite this, he presented with hemorrhage, dense adenomatosis years after AAS cessation, and a high-risk mutation, prompting aggressive management. There is increasing use of both medically administered testosterone and AAS. It is crucial to recognize a patient who is at risk for hepatic adenomas, even years after exposure, and understand the life-threatening risks that can occur with rupture, hemorrhage, and malignant transformation (Figure 1).Figure 1.: (a-c) Histologic and gross findings of a liver mass: (a) Hematoxylin and eosin (H&E) stain (100x) shows hepatocytes with mild cytologic atypia, pseudoglandular architecture (white arrow), prominent unpaired arterioles (black arrows), and absence of inter-lobular bile ducts; (b) Immunohistochemical (IHC) stain (200x) for beta catenin shows focal nuclear positivity; (c) Representative gross specimen of hepatic segment IVb lesion showing well-circumscribed tan lobulated mass with irregular borders and central hemorrhagic infarction.