Hepatic adenoma

Hepatic adenomas, also referred as hepatocellular adenomas, are benign liver tumours generally hormone induced. The tumours are usually solitary, have a predilection for haemorrhage, and must be differentiated from other focal liver lesions.

The incidence of hepatic adenomas is unknown, with studies showing migration from the classically described female predominance related to the use of oral contraceptives to an increased prevalence in men, particularly recognising that obesity and metabolic syndrome are emerging risk factors for adenomas 18

It is traditionally referred as the most frequent hepatic tumour in young women on the oral contraceptive pill.

They are found in some situations, including 3:

The lesions usually remain asymptomatic until they spontaneously rupture, resulting in abdominal pain. Occasionally rapid bleeding into the peritoneal cavity can lead to exsanguination and death.

Hepatic adenomas are usually solitary (70-80% of cases 10) and large at the time of diagnosis (5-15 cm) 3,13. They are most frequently seen at a subcapsular location in the right lobe of liver and are often round, well-defined pseudo-encapsulated masses. Occasional dystrophic calcification may be present. 

When multiple, usually >10 adenomas 9, the term hepatic adenomatosis is used. Multiple lesions are frequently observed in patients with type I glycogen storage disease.

The lesion is well circumscribed, often subcapsular with a yellow colouration on account of frequently abundant fat and lack of bile. Haemorrhagic change is frequent. The tumour may be surrounded by a fibrous pseudocapsule 15.

Histologically, hepatic adenomas are characterised by proliferation of pleomorphic hepatocytes without normal lobular architecture. These cells frequently have abundant glycogen (thus the von Gierke's disease link) 5. They are traditionally described as being devoid of bile ducts and Kupffer cells, although this has been shown not to be the case, with a diminished number of Kupffer cells found in many cases 1,3-4. This has important implication in Tc99m sulphur colloid scans (see below). 

According to the original 2006 Bordeaux classification, there are four subtypes of hepatic adenomas 17:

A hepatic adenoma usually presents as a solitary well-demarcated heterogeneous mass. Echogenicity is variable 3:

  • hypoechoic: 20-40%
  • hyperechoic: up to 30%, often due to fat 3,8

A hypoechoic halo of focal fat sparing is also frequently seen. 

  • colour Doppler: may show perilesional sinusoids
  • contrast-enhanced ultrasound 16
    • arterial phase
      • hypervascular (similar to FNH, although adenomas are usually less enhancing)
    • portal venous and delayed phases
      • centripetal filling in (opposite of FNH which shows centrifugal filling)

The attenuation of these tumours is variable, depending on 8:

  • fresh haemorrhage: maybe hyperattenuating
  • fat content may make the mass hypoattenuating

In general, they are well marginated and isoattenuating to the liver. On contrast administration, they demonstrate transient relatively homogenous enhancement returning to near isodensity on portal venous and delayed phase image 8,10.

If the rest of the liver shows diffuse fatty infiltration, then they will appear hyperattenuating.

Calcification may be seen in areas of old haemorrhage (5-10% of cases 10).

In non-haemorrhagic adenomas, they typically appear as:

  • T1
    • variable and can range from being hyper-, iso-, to hypointense
      • hyperintense: 35-77% cases 8
  • T2
    • mildly hyperintense: 47-74% 2,8
  • in/out-of-phase
    • the presence of fat typically leads to signal drop out on out-of-phase imaging
  • contrast studies
    • T1 C+ (Gad)
      • on the dynamic postcontrast sequence, adenomas show early arterial enhancement and become nearly isointense about liver on delayed images 10
      • some reports suggest that the enhancement becomes isointense to the rest of the liver by 1 minute 6
    • T1 C+ (hepatocyte-specific): adenomas usually appear hypointense on hepatobiliary phase (20 mins after injection) due to reduced uptake of Gd-EOB-DTPA/Eovist 14 (c.f. FNH which appears iso- to hyperintense)

If haemorrhagic, then blood products may lead to significant heterogeneity in signal on all sequences.

Although classically described as a focal photopenic lesion on Tc99m sulphur colloid scans with a surrounding rim of increased uptake, uptake may be seen in up to 23% of cases 1. This is accounted for by the presence of Kupffer cells in many adenomata, even though they may be reduced in number.

Usually has increased activity on a HIDA scan, but does not take up gallium on a gallium scan.

In general, and if feasible, adenomas are resected, both to eliminate the risk of spontaneous rupture and to conclusively confirm the diagnosis 7. In cases where the lesion is small and not subcapsular and has a typical appearance, some would choose to observe (with imaging and alpha-fetoprotein levels) and cease oral contraceptives. In such instances, the adenoma may regress. In inoperable cases, hepatic arterial embolisation may have a role 7

General imaging differential considerations include:

Hepatobiliary pathology
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Article information

rID: 1440
Synonyms or Alternate Spellings:
  • Liver adenoma
  • Hepatic adenomas
  • Adenoma of liver
  • Hepatocellular adenoma
  • Liver adenomas
  • Hepatic adenomata
  • Adenoma: liver

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Cases and figures

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    Hepatic Adenoma H...
    Figure 1: H and E stain
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    Case 1: on ultrasound
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    Hepatic Adenoma H...
    Figure 2: reticulin stain
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    Case 1: on CT arterial
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    Case 2: MRI out of phase
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    Case 3: inflammatory
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    Case 4: pedunculated
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    Case 6
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    Case 7
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    Case 8: with haemorrhage
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    Case 9: with early arterial enhancement
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