Figure 1a: Axial in phase image demonstrates 3 masses with subtle decreased signal intensity in comparison to the liver parenchyma which are difficult to see prospectively.

Figure 1b: When compared to the in phase image, this out of phase T1-weighted image demonstrates
signal drop out with in the three liver masses. This image finding is consistent with the presence of microscopic lipid within these three liver masses. The differential diagnosis for a liver mass with microscopic lipid includes adenoma and hepatocellular carcinoma.

Figure 2: Arterial phase post-contrast VIBE image demonstrates that these liver masses have an early enhancement pattern.

Figure 3: Portal venous phase post-contrast VIBE image demonstrates that these liver masses have some wash-out in comparison to the surrounding liver parenchyma. Noted also are large varices at the splenic hilum (arrow).

Figure 4a: In phase axial image demonstrates a high intensity mass at the level of the hepatic dome (liver
segment 7). The differential diagnosis for a high signal intensity mass lesion on an in phase T1-
weighted image includes fat, hemorrhage, proteinaceous fluid collection, melanin, or accumulated contrast agent.

Figure 4b: Out of phase axial image demonstrates no signal drop-out within this liver dome mass.

Figure 4c: VIBE image with fat saturation also demonstrates no signal drop-out within the liver dome mass. The fact that this high signal mass on in phase imaging (2A) did not demonstrate signal drop-out on the out of phase imaging or with VIBE images with fat saturation proves that the high signal intensity seen on in phase imaging was not due to fat and most likely represents a hemorrhagic mass.

Hepatic adenomatosis.

Hepatic adenoma is a rare benign primary tumor of the liver. Approximately 90% of liver adenomas occur in young women of reproductive age and in these patients it is associated with the use of oral contraceptives. Other patient populations at risk for developing hepatic adenomas include men who use anabolic steroids and infants and children with metabolic disorders including type I glycogen storage (von Gierke’s) disease, type III glycogen storage (Cori’s) disease, tyrosinemia, and familial diabetes mellitus.

Pathologically, adenomas are most often solitary lesions (70-80%) but they can be multifocal. These tumors consist of sheets of normal appearing hepatocytes but lack the normal acinar architecture of the surrounding hepatic parenchyma. The hepatocytes may be rich in fat or glycogen, and Kupffer cells are occasionally present, but bile ducts and portal tracts are absent. These tumors may be partially or completely enclosed by a pseudocapsule derived from the compressed and collapsed hepatic parenchyma. Hepatic adeomas are yellow in color due to their fat content and often contain areas of hemorrhage or infarction. They may also demonstrate focal scar formation which is indicative of remote infarction. They are pedunculated in 10% of cases. Malignant transformation of these benign tumors is rare.

Most patients with hepatic adenoma are asymptomatic and almost invariably have normal liver function tests (unlike in liver adenomatosis) and no elevation of serum tumor markers such as ?-fetoprotein. Large adenomas may cause a sensation of right upper quadrant fullness or discomfort with or without a palpable abdominal mass. However, the classic presentation of hepatic adenoma is spontaneous rupture or hemorrhage leading to acute abdominal pain and possibly progressing to hypotension, shock, and death. Hepatic adenomas have a tendency to undergo spontaneous rupture in 25-50% of cases. In patients with liver adenomatosis hemorrhage can occur in more than 60% of patients.

On T1-weighted MRI images, the signal intensity of adenomas typically varies from hypointense to hyperintense (most often) in comparison to the liver parenchyma. This variation in signal intensity on T1-weighted images reflects the fat content of the tumor. Adenomas can also appear heterogeneous on T1-weighted images due to areas of increased signal intensity resulting from fat and hemorrhage and areas of low signal intensity, corresponding to areas of necrosis, old hemorrhage, or calcification. On T2-weighted images, hepatic adenomas are most often mildly hyperintense to liver parenchyma, although some hypointense and isointense lesions have been reported. The finding of a hyperintense lesion on T2-weighted imaging is not specific for hepatic adenoma and can reflect other hepatic lesions including, hepatocellular carcinoma and metastases. Hepatic adenomas can also be heterogeneous in appearance on T2-weighted imaging, again reflecting areas of hemorrhage and necrosis. A peripheral rim of low signal intensity on T1-weighted images and variable intensity on T2-weighted images can be seen in 17-31% of patients and histologically corresponds to a pseudocapsule.

Dynamic gadolinium enhanced gradient echo MR imaging can be used to demonstrate that most hepatic adenomas have intense enhancement during the early arterial phase and are isointense to liver tissue on delayed imaging. Characteristically, hepatic adenomas have a transient blush immediately after gadolinium administration that fades by 1 minute. Chemical-shift imaging showing homogeneous drop in signal intensity on out-of-phase or fat-suppressed images is a relatively common feature of fat-containing adenomas. However, 40% of hepatocellular carcinoma lesions are known to contain fat and, therefore, the presence of fat does not help differentiate hepatic adenoma from hepatocellular carcinoma. Because adenomas contain hepatocytes, hepatocyte-specific contrast agents can accumulate in these tumors and show contrast enhancement. These hepatocyte-specific agents can be used to help differentiate hepatic adeomas from liver lesions that may not contain hepatocytes, such as metastases and hemangiomas. However, hepatic lesions that do contain hepatocytes such as, focal nodular hyperplasia or hepatocellular carcinoma can not be easily distinguished. Kupffer cell-specific MRI agents such as superparamagnetic iron oxide (SPIO) and ultrasmall superparamagnetic iron oxide (USPIO) generally show no uptake by hepatic adenomas.

Hepatic adenomas secondary to oral contraceptive or steroid use generally regress or completely disappear following withdrawal of the contraceptive therapy or steroid use. However, it is important to distinguish between hepatic adenoma and other benign hepatic lesions, such as focal nodular hyperplasia, because of its propensity to hemorrhage and the possibility of malignant transformation. A confident distinction of hepatic adenoma from other lesions such as, hepatocellular carcinoma, based solely on imaging is not yet clear-cut. Therefore, histological examination is advocated to make a definitive diagnosis..

Hepatic adenomatosis is a separate clinical entity which can be distinguished from isolated hepatic adenoma by the presence of multiple adeomas, usually greater than 10, in patients lacking other known risk factors for adenomas. Although the adenomas in hepatic adenomatosis are histologically similar to isolated hepatic adenomas, they lack association with steroid medication, have almost equal prevalence in men and women, tend to be progressive, symptomatic, are more likely to lead to impaired liver function, and have a higher incidence of hemorrhage and malignant degeneration. Hepatic adenomatosis has to be differentiated from other diseases causing multiple liver lesions including metastatic disease, multifocal hepatocellular carcinoma, focal nodular hyperplasia, and adenomatous hyperplasia.

Surgical resection is generally recommended in patients with solitary symptomatic hepatic adenomas, but may not be possible in patients with hepatic adenomatosis. In patients with hepatic adenomatosis, periodic follow-up is recommended.

References:

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