Hepatic adenoma is an uncommon benign liver tumour that is hormone induced. The tumours have a predilection to haemorrhage and must be differentiated from other focal liver lesions. They are usually solitary (70-80% of cases 10) but when multiple the condition is known as hepatic adenomatosis (usually >10 adenomas 9). Multiple lesions are frequently observed in patients with type I glycogen storage disease 10.
It is the most frequent hepatic tumour in young women who are on the oral contraceptive pill. They are also found in a number of other situations including 3:
- oral contraceptive use: most common association
- anabolic steroidsL typically young men
- type I glycogen storage disease: von Gierke's disease
The lesions typically remain asymptomatic until they spontaneously rupture, at which time the patient develops abdominal pain. Occasionally rapid bleeding into the peritoneal cavity can lead to exsanguination and death.
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 of Kupffer cells, although this has been shown not to be the case, with diminished number of Kupffer cells found in many cases 1,3-4. This has important implication in Tc99m sulphur colloid scans (see below)
The lesion is well circumscribed, often subcapsular with a yellow colouration on account of frequently abundant fat and lack of bile. Haemorrhagic change is common. The tumour is surrounded by a fibrous capsule 5.
The tumours are usually solitary and large at the time of diagnosis (5-15cm) 3,13. They are most frequently seen at a subcapsular location in right lobe of liver. Round well defined pseudo-encapsulated mass. Occasional dystrophic calcification may be evident.
The density of these tumours is variable depending on 8:
- fresh haemorrhage: may be hyperdense
- fat content may make the mass hypodense
In general they are well marginated and iso attenuating to liver. On contrast administration they demonstrate transient relaitvely 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 of course appear hyper dense.
Calcification may be seen in areas of old haemorrhage (5-10 % of cases 10) .
Hepatic adenomas are usually a solitary well demarcated heterogeneous mass. Echogenicity is variable 3:
- hypo echoic: 20-40%
- hyper echoic: up to 30% , often due to fat 3,8
A hypo echoic halo of focal fat sparing is also frequently seen. Colour Doppler may show peri lesional sinusoids.
In non-haemorrhagic adenomas, they typically appear as:
- variable and can range from being hyper- iso- to hypo intense
- hyper intense: 35-77% cases 8
- variable and can range from being hyper- iso- to hypo intense
- mildly hyper intense: 47-74% 2,8
in/out of phase:
- presence of fat typically leads to signal drop out on out of phase imaging
T1 C+ (Gd):
- on dynamic gadolinium-enhanced gradient-echo MR images, adenomas show early arterial enhancement and become nearly isointense relative to liver on delayed images 10.
- some report suggest that the enhancement becomes iso-intense to the rest of the liver by 1 minute 6
- T1 C+ (Gd-EOB-DTPA): adenomas usually appear hypo-intense on hepatocellular phase due to reduced uptake of Gd-EOB-DTPA14.
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 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.
- spontaneous rupture
- although uncommon, hepatic adenomas do occasionally degenerate into hepatocellular carcinomas (HCC) 8
Treatment and prognosis
Usually they are benign but there is a very small risk of transformation to hepatocellular carcinoma (HCC).
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 sub capsular, and has typical appearances, some would chose to observe (with imaging and alpha fetoprotein levels) and cease oral contraceptives. In such instances they may regress. In inoperable cases, hepatic arterial embolisation may have a role 7.
General imaging differential considerations include:
hepatocellular carcinoma (HCC)
- washout tends to leave the lesion hypo intense c.f. to rest of liver
- different demographics
- may be difficult to distinguish if well differentiated 7
fibrolamellar hepatocellular carcinoma
- radiating/central scar
- calcification more common 8
- lymph node enlargement common
focal nodular hyperplasia (FNH)
- T2: bright central scars that have late enhancement
liver metastases (hyper vascular)
- usually hypo intense on T1, and very hyperintense on T2
- fat and haemorrhage are less common
- large haemangioma of the liver
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Synonyms & Alternative Spellings
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