Update: Radiologic-Pathologic Correlation of Hepatocellular Adenoma

Sadhna Dhingra MD, FCAP; Chakradhar Thupili, MD; Steven Chua, MD, PhD; Kaustubh Shirlakar MD; Srinivasa R Prasad, MD; Venkateswar R Surabhi, MD

Disclosures

Appl Radiol. 2019;48(6):21-29.

Pathology

Gross Evaluation

Hepatocellular adenomas are well-demarcated lesions that can occasionally be encapsulated and range in size from 1–30 cm.^[8] HA may present as a solitary mass or as multifocal, variably sized, soft tissue masses. They typically arise in non-fibrotic liver, however, they may occur in the background of cirrhosis. HAs reported in the setting of cirrhosis are usually of the inflammatory subtype.^[24–26] Rare cases of multiple HNF-1-α mutated HAs has been reported to occur in the background of congenital hepatocellular fibrosis.^[27] The cut surface of HA may be tan-yellow or red-brown depending upon the presence of steatosis or peliosis/hemorrhage/old hemorrhage, respectively. Inflammatory HA shows alternating pale red and dark-red surface.^[8]

Microscopic Evaluation. Hepatocellular adenoma is classically characterized by sheets of benign-appearing hepatocytes with interspersed thin-walled, unpaired arteries. The hepatocyte trabeculae are 1–3 cells thick and the reticulin framework is preserved. Portal tracts containing portal veins or bile ducts are absent. Few randomly distributed pseudo-portal tract areas with thick walled vessels and ductular reaction can be seen in some HAs. Other variable features include steatosis, inflammatory cell infiltrate, sinusoidal dilatation, myxoid changes^[28] and presence of pigments such as bile pigment, lipofuscin or Dubin Johnson-like pigment.^[29,30]

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Table 1. Clinical, Radiologic and Pathologic Features of Subtypes of HCA
Subtype	Frequency	Clinical features and associations	Imaging features	Pathologic features	Complications
Inflammatory HCA (IL6ST mutations)	Most common: 40%–55%	• Obesity • Alcohol use • Hepatic steatosis • Metabolic syndrome	• Can mimic FNH • T2 moderate hyperintensity • Intracellular fat seen occasionally • Variable degree of uptake on hepatobiliary phase	• Pseudo-portal tracts with thick arteries, sinusoidal dilatation, and variable steatosis • Increased expression of inflammatory proteins CRP and SAA on immunostaining	• Bleeding is main complication • 10% also express β-catenin and hence may show malignant transformation
HCA with TCF1 gene mutation	30%–50%	• Hepatic adenomatosis • Maturity-onset diabetes of the young type 3	• Intracellular lipid	• Variable steatosis • Absence of expression of L-fatty acid binding protein on immunostaining	• No significant bleeding risk • No risk for malignant transformation
β-catenin–mutated HCA	10%–18%	• Glycogen storage disease • Male hormone administration	• Not usually steatotic • There can be washout during portal venous phase on non-hepatocellular gadolinium contrast agents	• May have cytologic and architectural atypia • Immunostain for β-catenin is positive in nuclei • Glutamine synthetase shows diffuse and strong cytoplasm expression	• Malignant transformation
Unclassified	10%	• No specific association	• No specific features	• No specific features	• Increased risk of bleeding in the subset with sonic hedgehog activation