LAUSR

Case 1 A previously healthy 16-year-old man was initially evaluated in the emergency department for traumatic injuries following a high-impact motor vehicle accident. He was a bodybuilder who used anabolic steroids. He denied abdominal or back pain. His physical examination was significant for a palpable liver edge. Routine laboratory tests including liver function tests were unremarkable. A computed tomographic (CT) scan showed an unsuspected mass in the right lobe of the liver. A subsequent triple-phase magnetic resonance imaging (MRI) scan of the abdomen showed a 15.1 × 15.0 × 10.8 cm mass in the right hepatic lobe that exhibited heterogeneous arterial and thin capsular enhancement, concerning for a hepatic neoplasm (Fig. 1). He underwent partial hepatectomy; the resected surgical specimen showed a well-differentiated hepatocellular carcinoma that on immunohistochemical staining (Fig. 2a) showed β-catenin activation via aberrant nuclear expression. The tumor was confined to the liver with no vascular invasion or regional lymph node involvement. It was predominantly composed of bland hepatocytes, though there were areas of scattered cytological atypia. Moreover, the architecture was diffusely pseudoglandular (Fig. 2b) with reticulin staining showing multifocal loss of the normal peri-cellular reticulin framework (Fig. 2c). These latter features were considered diagnostic of a well-differentiated hepatocellular carcinoma (HCC) as opposed to a β-catenin-activated hepatic adenoma (HCA). The patient and his guardian decided against undergoing chemotherapy. The patient is being followed up by the pediatric oncology service, to monitor for possible tumor progression, with periodic surveillance by imaging with MRI. Case 2 A 26-year-old man with history of glycogen storage disease type 1a, and a family history of familial adenomatous polyposis, was referred for evaluation of irondeficiency anemia. He complained only of fatigue. His medical history included hypertension and hyperlipidemia. His surgical history while an infant included gastrostomy for nocturnal feedings at an outside hospital, and liver biopsy; no report of this biopsy was available. His medications included lisinopril and fenofibrate. His father had a history of familial adenomatous polyposis (Gardner syndrome variant). He denied using tobacco, alcohol, or recreational drugs. His physical examination revealed a short stature, mild conjunctival pallor, doll-like facies, and a palpable liver edge, with a heart rate of 110/min. MRI of his abdomen (with and without contrast) showed multiple large arterially enhancing liver lesions within the right and left lobe. The largest lesion (within the right lobe) occupied the majority of segments 5 and 6 and measured approximately 20.2 × 17.7 × 13.5 cm (Fig. 3). The liver was massively enlarged and infiltrated, the right lobe measuring 26 cm, consistent with the known history of glycogen storage disease. Laboratory studies revealed a blood hemoglobin of 12.6 g/dL (normal 13.8–17.2 g/dL), a white blood cell count of 6.4 (4–103/μL), and a platelet count of 529 × 103/μL (150–400 × 103/μL)], with serum concentrations of alanine aminotransferase 92 (14–67 U/L), alkaline phosphatase of 145 (38–150 U/L), and aspartate aminotransferase 82 U/L (6–58 U/L). Serum alpha-fetoprotein (AFP) concentration was 1.1 ng/mL (0–15 ng/mL). Serum iron panel values were * Christina Ling [email protected]