Hepatocellular adenoma (HCA) is a benign neoplasm arising from hepatocytes. It has a strong association with oral contraceptive (OCP) use (30-40 fold increased risk in young women). Four molecular subtypes have been defined: HNF1α-inactivated (30-40%, diffuse steatosis), inflammatory (40-50%, sinusoidal dilatation, peliosis), β-catenin-activated (10-15%, highest malignant transformation risk), and unclassified (10%). It carries risk of fat content, hemorrhage, and rarely transformation to HCC. Hypointense appearance in the hepatobiliary phase (gadoxetic acid) — the most important finding distinguishing it from the hyperintense appearance of FNH. Risk of spontaneous hemorrhage increases in lesions >5 cm. Malignant transformation risk is highest in males and β-catenin-activated subtype.
Age Range
15-50
Peak Age
30
Gender
Female predominant
Prevalence
Uncommon
Hepatocellular adenoma is a monoclonal benign neoplasm originating from hepatocytes — unlike focal nodular hyperplasia, it is neoplastic not hyperplastic. Hormone dependence plays a key role in pathogenesis: estrogen stimulates hepatocyte proliferation and risk increases 30-40 fold in OCP users. Each of the four molecular subtypes has different pathogenesis and imaging findings. In HNF1α-inactivated type, hepatocyte nuclear factor 1α mutation activates the lipogenesis pathway → diffuse intracellular fat accumulation in hepatocytes → signal drop on opposed-phase and low density on CT. In inflammatory type, IL-6/JAK-STAT pathway is activated → sinusoidal dilatation, peliosis, inflammatory infiltrate → intense arterial enhancement, hyperintense peripheral ring on T2 ('atoll sign'), persistent delayed enhancement. In β-catenin-activated type, Wnt/β-catenin signaling pathway is activated → increased cell proliferation → 5-10% risk of HCC transformation. The reason for hypointensity in the hepatobiliary phase on imaging is that adenoma hepatocytes do not sufficiently express functional OATP1B1/B3 transporter proteins (especially HNF1α-inactivated and β-catenin types) → gadoxetic acid is not taken up → hypointense. Inflammatory subtype may have partial OATP expression → some inflammatory adenomas may appear isointense or mildly hyperintense in the hepatobiliary phase — this may be confused with FNH.
Hypointense appearance of the adenoma lesion in the hepatobiliary phase with gadoxetic acid — due to insufficient expression of OATP1B1/B3 transporter proteins resulting in no contrast retention. This finding is the most reliable differentiator from FNH (hyperintense). However, partial uptake may occur in the inflammatory subtype and careful correlation is required.
On gadoxetic acid (Eovist/Primovist) hepatobiliary phase, the adenoma lesion appears hypointense relative to surrounding parenchyma. This results from adenoma hepatocytes not sufficiently expressing functional OATP1B1/B3 transporters — gadoxetic acid is not taken up or minimally taken up by the lesion. Hypointensity is most pronounced in HNF1α-inactivated and β-catenin-activated subtypes. In the inflammatory subtype, isointense or mildly hyperintense appearance may occur due to partial OATP expression — this may be confused with FNH and requires careful correlation.
Report Sentence
In the hepatobiliary phase, the lesion demonstrates hypointense appearance relative to surrounding parenchyma reflecting lack of functional hepatocyte transporter expression; hepatocellular adenoma should be primarily considered.
Diffuse opposed-phase signal drop throughout the entire lesion in HNF1α-inactivated type — reflecting intracellular fat accumulation. This is the most characteristic MR finding of this subtype and distinguishes it from other adenomas (60-70% have no fat) and FNH (no fat content). Signal drop is homogeneous and diffuse — unlike focal steatosis, mass morphology is present (round/oval, may cause mass effect).
Report Sentence
Diffuse signal drop is observed throughout the lesion on opposed-phase images consistent with diffuse intracellular fat accumulation; HNF1α-inactivated hepatocellular adenoma subtype should be considered.
The lesion shows homogeneous or heterogeneous hypervascular enhancement in the arterial phase. Enhancement pattern varies by subtype: mild-moderate enhancement in HNF1α-inactivated type (fat content masks contrast), intense enhancement in inflammatory type (sinusoidal dilatation), heterogeneous enhancement in β-catenin-activated type. In portal venous/delayed phases, the lesion may be isodense or mildly hypodense — washout is seen in 30-40% of cases and may mimic HCC.
Report Sentence
Mass demonstrating hypervascular enhancement in the arterial phase with subtype-dependent enhancement pattern, hepatocellular adenoma is considered.
Focal or diffuse hyperintense areas within the lesion on T1-weighted images — related to subacute hemorrhage (methemoglobin) or intracellular fat accumulation. In HNF1α type, diffuse T1 hyperintensity is fat-related. Areas of acute/subacute hemorrhage show marked T1 hyperintensity — paramagnetic effect of methemoglobin shortens T1. Old hemorrhage appears hypointense on T1 and T2 as hemosiderin. Presence of T1 hyperintense areas strongly supports adenoma diagnosis — T1 hyperintensity is not expected in FNH.
Report Sentence
Hyperintense areas within the lesion on T1-weighted images consistent with subacute hemorrhage and/or intracellular fat; supporting hepatocellular adenoma diagnosis.
T2 signal intensity varies by subtype. In HNF1α type, isointense or mildly hyperintense (fat content). In inflammatory type, peripheral hyperintense ring (T2 'atoll sign') — due to sinusoidal dilatation and peripheral peliosis. In β-catenin-activated type, heterogeneous signal. Old hemorrhage areas are hypointense on T2 (hemosiderin). Central scar is usually absent — distinguishing from FNH.
Report Sentence
A peripheral hyperintense ring ('atoll sign') is observed in the lesion on T2-weighted images consistent with sinusoidal dilatation; inflammatory hepatocellular adenoma subtype should be considered.
Well-defined mass with variable echogenicity on B-mode US. Hyperechoic in HNF1α type due to diffuse fat; mildly hyperechoic or isoechoic in inflammatory type; hemorrhage areas show heterogeneous echo. Acute hemorrhage is hyperechoic, subacute-chronic hemorrhage may show mixed echogenicity. Capsule or pseudocapsule may sometimes be visible. Color Doppler shows peripheral and intralesional vascularity.
Report Sentence
Well-defined mass with variable echogenicity in the liver on US with hyperechoic areas consistent with fat and heterogeneous areas consistent with hemorrhage; hepatocellular adenoma is considered.
Criteria
HNF1α gene mutation, diffuse intracellular steatosis, 30-40% of all adenomas
Distinct Features
Diffuse signal drop on opposed-phase (pathognomonic). Hypointense in hepatobiliary phase. Low hemorrhage risk. Low malignant transformation risk. May be associated with MODY3 diabetes. Mature hepatocytes, steatotic.
Criteria
IL-6/JAK-STAT pathway activation, sinusoidal dilatation and peliosis, 40-50% of all adenomas
Distinct Features
T2 'atoll sign' (peripheral hyperintense ring). Intense arterial enhancement, persistent in delayed phase. Elevated CRP and SAA. Some may show partial uptake in hepatobiliary phase (may be confused with FNH). Moderate hemorrhage risk.
Criteria
Wnt/β-catenin signaling pathway activation, increased cell proliferation, 10-15% of all adenomas
Distinct Features
Highest HCC transformation risk (5-10%). More common in males. Hypointense in hepatobiliary phase. No specific imaging finding — diagnosis usually made by biopsy. Surgical resection recommended.
Criteria
Does not fit the three subtypes above, uncertain molecular classification, 10% of all adenomas
Distinct Features
Heterogeneous imaging findings. Uncertain malignant transformation risk. Usually requires biopsy and surgical evaluation.
Distinguishing Feature
FNH is hyperintense in hepatobiliary phase (OATP expression present), adenoma is hypointense (no OATP expression). FNH shows central scar, spoke-wheel arterial pattern; adenoma does not show central scar. FNH does not contain fat/hemorrhage; adenoma may contain them.
Distinguishing Feature
HCC usually occurs in cirrhotic liver; adenoma in normal liver in OCP users. HCC may show capsule; adenoma is unencapsulated. Mosaic pattern and portal vein thrombosis may be seen in HCC. Both may show arterial enhancement and washout — absence of cirrhosis and clinical context are differentiating.
Distinguishing Feature
Focal steatosis has geographic margins, no mass effect; HNF1α adenoma shows round/oval mass morphology and may cause mass effect. Both show opposed-phase signal drop but adenoma is distinguished by capsule, enhancement, and mass morphology.
Distinguishing Feature
Hemangioma is very bright on T2 (light-bulb sign), shows peripheral nodular enhancement and centripetal fill-in; adenoma is mildly-moderately hyperintense on T2, may show homogeneous arterial enhancement and washout. Hemangioma shows no restriction on DWI (high ADC).
Urgency
urgentManagement
surgicalBiopsy
NeededFollow-up
6-monthHepatocellular adenoma management depends on subtype and size. In lesions >5 cm, spontaneous hemorrhage risk is increased and surgical resection should be considered. In β-catenin-activated subtype, malignant transformation risk is high (5-10%) — resection is recommended regardless of size. All adenomas in males should be resected (increased malignancy risk). Regression may occur with OCP discontinuation — evaluated after 6-month follow-up. Conservative approach (OCP cessation + follow-up) may be considered in HNF1α type due to low risk. Moderate risk in inflammatory type — decision based on size and growth rate. Gadoxetic acid MRI plays a key role in subtype determination.
OCP discontinuation is recommended. Surgical resection is considered for lesions >5 cm due to hemorrhage and malignant transformation risk. β-catenin mutant subtype has the highest risk of HCC transformation. Can also occur in males and glycogen storage disease.