Hepatocellular adenoma

Grossly hepatocellular adenoma is a well delineated tumour surrounded by a capsule or pseudocapsule which corresponds to abnormal compression of adjacent hepatic parenchyma and mild fibrosis. On cut surface, fatty metamorphosis, infarction with necrosis, and haemorrhage can be found inside the tumours. Typically, a central scar is not present. They are usually solitary but can be multiple. They are normally located in the subcapsular area but can be pedunculated.

Microscopically, HA consist of a proliferation of sheets of normal or nearly normal hepatocytes mimicking normal liver tissue, but with a global abnormal architecture lacking normal portal triads bile ducts and central veins. Because they are neoplasms with unlimited growth potential they may become large and have a tendency for bleeding.

HA may undergo malignant degeneration. Even at histopathological study it may be difficult to differentiate adenoma from well differentiated hepatocellular carcinoma. Bleeding within the tumour or in the peritoneal cavity is a frequent clinical feature which brings the lesion to attention.

Ultrasound

Although the sensitivity of ultrasound for detection of HA is high the ultrasound features are variable and nonspecific. They appear as well-defined solid lesions with variable echogenicity. About 20 - 40% are hypoechoic, and a hyperechoic appearance is seen in about 30% of cases (Fig.1). The remainder are either isoechoic or of mixed echogenicity. The hyperechoic aspect may be related to the presence of fatty elements in the tumour.

Computed tomography

On precontrast CT most HA are homogeneously isoattenuating or slightly hypoattenuating as compared to the adjacent liver (Fig.2a). However, if they are larger than 4-5 cm in diameter an inhomogeneous appearance may be due to focal areas of hypoattenuation caused by necrosis. Approximately 15% of HA will present as hyperattenuating masses due to recent intratumoural haemorrhage (Fig.3). A low attenuation rim around the tumour can be visible and is due to an excess of lipid laden hepatocytes. On contrast enhanced CT following bolus injection of contrast medium strong homogeneous enhancement during the arterial phase (Fig. 2 b,c,d) is observed. During the portal venous phase, however, the lesion rapidly becomes isoattenuating relative to the adjacent liver parenchyma and could therefore easily be missed if scanning is performed during a late phase of contrast enhancement. Multiple HA can occasionally be visualized by dynamic incremental CT if the lesions are situated in contiguous areas of the liver (Fig.4) but can now routinely be visualized by applying spiral CT.

Magnetic Resonance Imaging

HA have a highly variable appearance on MRI because of their varied histological structure. Most are predominantly hyperintense on T2-weighted, whereas, the predominant signal intensity onT1-weighted images are variable (Fig.5). Areas of high signal intensity may be present on T1-weighted images as a result of haemorrhage and fatty change. The capsule may appear hypointense on T2-weighted images and large feeding vessels can occasionally be demonstrated.

The administration of Gadolinium GD contrast reveals the same pattern of enhancement as seen on CT following the injection of iodinated contrast media. Superparamagnetic iron oxide will not be taken up by most adenomas because of the absence of Kupffer cells, and the tumour will be hyperintense compared to the liver. However, in those adenomas where Kupffer cells are present the tumour will show a decrease in signal intensity similar to the adjacent parenchyma.
 
Scintigraphy
HA usually appears as a photopenic defect on technetium-99m sulphur colloid scintigraphy. However, uptake of the radionuclide tracer in HA has been reported in 23% of patients. This uptake is explained by the presence of Kupffer cells in some adenomas, even though these cells are usually reduced in number.

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