Hepatocellular adenoma

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[edit] Discussion of Hepatocellular adenoma

  • Hepatocellular adenoma is a rare benign lesion that is most often seen in young women with a history of oral contraceptive use.
  • It is typically solitary, although multiple lesions have been reported, particularly in patients with glycogen storage disease and liver adenomatosis.
  • Because of the risk of hemorrhage and malignant transformation, hepatocellular adenomas must be identified and treated promptly.
  • Hepatic adenomas were virtually unknown prior to 1960, the year in which oral contraceptives were introduced.
  • In women who have never used oral contraceptives, the annual incidence of hepatic adenoma is about 1 per million. This increases to 30–40 per million in long-term users of oral contraceptives.
  • Another risk group for hepatocellular adenoma are patients with type I glycogen storage disease. In these patients, the adenomas are also more likely to be multiple and to undergo malignant transformation, although the latter is still quite rare.
  • "Liver adenomatosis" describes multiple (usually >10) adenomas in patients lacking other known risk factors for adenomas.
  • The classic clinical manifestation of hepatic adenoma is spontaneous rupture or hemorrhage, leading to acute abdominal pain and possibly progressing to hypotension and even death.
  • Adenomas are increasingly being encountered as incidental findings in patients who undergo multiphasic CT or MR imaging for unrelated or nonspecific signs or symptoms.

[edit] Treatment

  • Some clinicians have proposed nonsurgical management with cessation of hormone therapy, serial radiologic examinations, and screening for elevated {alpha}-fetoprotein levels, especially in isolated small adenomas.
  • Many surgeons have advocated resection of adenomas due to the recognized risk of rupture and hemorrhage. Others have concluded that resection should be performed only when it is possible to do so with minimal morbidity and mortality.

[edit] Histology

  • Adenomas, which consist of large plates or cords of cells closely resembling normal hepatocytes, with the plates separated by dilated sinusoids.
  • These sinusoids are equivalent to thin-walled capillaries that are perfused by arterial pressure because adenomas lack a portal venous supply and are fed solely by peripheral arterial feeding vessels.
    • Extensive sinusoids and feeding arteries constitute the hypervascular nature of hepatocellular adenoma, and poor connective tissue support, also predisposes to hemorrhage within the adenoma.
  • Because a tumor capsule is usually absent or incomplete, hemorrhage may spread into the liver or abdominal cavity.
  • Kupffer cells are often found in adenomas but in reduced numbers and with little or no function, as reflected by absent or diminished uptake of Tc-99m sulfur colloid.
  • Bile ductules are notably absent from adenomas, a key histologic feature that helps distinguish hepatocellular adenoma from focal nodular hyperplasia.

[edit] Imaging Findings for Hepatocellular adenoma

[edit] US

  • Color Doppler US may demonstrate peripheral peritumoral vessels and intratumoral vessels that typically have a flat continuous or, less commonly, triphasic waveform.
  • These Doppler US features are reported to be absent in the vessels within focal nodular hyperplasia and may be useful in distinguishing the two disease entities.
  • Nevertheless, most adenomas are not specifically diagnosed at US and are usually further evaluated with CT or other imaging modalities.

[edit] CT

  • Fat or hemorrhage can easily be identified on unenhanced images, and delayed-phase images demonstrate the tendency for fibrotic components to enhance and retain contrast material.
  • Because adenomas consist almost entirely of uniform hepatocytes and a variable number of Kupffer cells, most adenomas are nearly isoattenuating relative to normal liver on unenhanced, portal venous–phase, and delayed-phase images.
  • In patients with fatty liver, adenomas are hyperattenuating at all phases of contrast enhancement and on unenhanced images as well.
  • Small hepatocellular adenomas enhance rapidly and are hyperattenuating relative to the liver.
  • Excluding lesions with acute or old tumor hemorrhage and fat deposition, hepatocellular adenoma demonstrated homogeneous or nearly homogeneous enhancement in approx 80% of cases.
    • The enhancement usually does not persist in adenomas because of arteriovenous shunting.
  • Larger hepatocellular adenomas may be more heterogeneous than smaller lesions, and their CT appearance is less specific.

[edit] MRI

  • On T1-weighted MR images, hepatocellular adenomas have been variously described as hyperintense, isointense, and hypointense lesions.
  • It has been reported that 47%–74% of hepatocellular adenomas are predominantly hyperintense relative to liver on T2-weighted images; this is due to prolonged T2 and is consistent with findings in other hepatic tumors.
  • Some lesions are hypointense and isointense on T2-weighted images.
  • Most lesions are heterogeneous, demonstrating a combination of hyper- and hypointensity on T2-weighted images relative to hemorrhage and necrosis.
  • Dynamic gadolinium-enhanced gradient-echo MR imaging, like dynamic CT, can be used to demonstrate early arterial enhancement that reflects the presence of subcapsular feeding vessels.
  • Adenomas usually do not show uptake of superparamagnetic iron oxide particles, resulting in decreased signal intensity on T2-weighted images.
  • After injection of a hepatocellular-specific contrast agent such as gadolinium benzyloxypropionictetraacetate (Gd-BOPTA) there is usually no substantial uptake.

[edit] Nuclear Scintigraphy

  • Compared with normal liver, adenomas usually show absent or decreased uptake of Tc-99m sulfur colloid, reflecting the decreased number or function of Kupffer cells.

[edit] Images

Patient #1: Patient with multiple adenomas

[edit] See Also

[edit] External Links

[edit] References for Hepatocellular adenoma