Sex: female
Age: 43 years
History
Psoriasis for many years. No liver disease.
Laboratory data
No abnormalities found, normal values for CEA, CA 19-9, CA 12-5 and alpha-fetoproteine.
Physical findings
None.
Case text
The patient was admitted for liver surgery due to two focal lesions in the right and left liver lobe as shown by liver sonography. Both lesions appeared as isoechoic with the normal liver. There was some evidence of a thin hypoechogenic rim.
Image 1-3
Contrast-enhanced CT of the liver.
Dual-phase spiral CT, axial section at the level of segment II of the liver; collimation: 5mm; table feed 10mm
Image 1: Unenhanced CT.
Image 2: Contrast-enhanced, arterial phase.
Image 3: Contrast-enhanced, portal venous phase.
Image 4-6
MRI of the liver contrast enhanced.
Image 4: Axial T2w TSE (TR/TE 3200/138ms), 5mm
Image 5: Axial T1w FLASH (TR/TE 170/4,4ms; ( = 80°), 5mm, precontrast
Image 6: Axial T1w FLASH (TR/TE 170/4,4ms; ( = 80°), 5mm, after iv-injection of i.v. contrast.
Image 1-3
1. What is the abnormality present on the precontrast scan?
Ill-defined slightly hypodense lesions peripherally located within segment II.
2. Is there any evidence of calcification or bleeding?
Not detectable.
3. Is there any contrast enhancement related to the different phases of perfusion?
CT image obtained in the arterial phase showing a hypervascular lesion with no distinct borders;
in the portal-venous phase the lesion appears nearly isodense with the normal liver with the centre being slightly hypodense.
4. Is there any other pathology of the liver, i.e. cirrhosis?
Not detectable.
5. What is your diagnosis?
Hypervascular lesion consistent with focal nodular hyperplasia (FNH).
6. What is the differential diagnosis?
1. Hepatic adenoma
2. Fibrolamellar hepatic carcinoma
3. Metastasis
Image 4-6
7. What is the abnormality present on the unenhanced T1- and T2-weighted MRI of the liver?
The T2-weighted sequence reveals an ill-defined slightly hyperintense focal mass of segment II of the liver.
The lesion appears hypointense on the T1-weigthed image with some heterogeneous aspect of the centre. Note some focal hyperintensity at the anterior margin of the lesion due to pulsation artifacts from the abdominal aorta.
8. Does MRI after administration of the hepato- biliary contrast agent TESLASCAN®/ MnDPDP (mangafodipir) -Nycomed Amersham provide any further Information?
Yes, there is some increase of signal intensity within the lesion compared to the strongly enhancing normal liver parenchyma. This indicates most of the tumor cells to be of hepatocellular origin.The centre of the lesion now showing a very low signal indicating a central scar. In addition the tumor now seems to be separated from the adjacent liver by a thin hypointens rim.
9. What is your diagnosis?
Hepatocellular lesion consistent with focal nodular hyperplasia (FNH).
10. What is the differential diagnosis?
1. Hepatic adenoma
2. Fibrolamellar hepatic carcinoma
11. What could be the next diagnostic step?
Hepatobiliary scintigraphy using 99mTc labeled iminodiacetic acid derivatives.
Final diagnosis
Focal nodular hyperplasia.
Differential diagnosis
1. Hepatic adenoma
2. Fibrolamellar hepatic carcinoma
Discussion
Following segmental liver resection focal nodular hyperplasia was histologically proven. A typical central scar was found as preoperatively depicted with MRI after administration of the hepato- biliary contrast agent ( MnDPDP, TESLASCAN®). A second lesion showing identical aspects with CT and MRI was located in the lower segments of the right liver lobe (segment V/VI). Surgical resection confirmed this to be the same type of lesion.
A focal nodular hyperplasia (FNH) is a benign tumorous lesion of the liver consisting of hepatocytes, fibrous tissue, bile ducts and cells of the reticular endothelial system. Most of the lesions found are large and single tumors that cause displacement of the normal hepatic vasculature, but in rare cases lesions may be very small and even multifocal. FNH often appears with a thin pseudocapsule consisting of fibrous bands that traverse the tumor forming a central stellate scar which was well depicted in this case on the T1-weighted image after administration of TESLASCAN® MnDPDP (manga- fodipir). The tumor may be either hyperintense or isointens on T2-weighted images and isointense or slightly hypointense on T1-weighted images sometimes making the depiction very difficult (1). However, due to some hypervascularity FNH may be well depicted during the arterial phase of an iodine- or gadolinium contrast-bolus using fast repetitive single-slice or dual-phase CT and MRI scanning of the liver. Contrast-enhancement is usually restricted to the arterial-phase of liver perfusion. So, if scanning is only performed during the portal-venous-phase when equilibrium with normal liver tissue is reached the tumor may be completely missed. The uptake of MnDPDP within a liver tumor reveals the lesion to be of hepatocellular origin (2). Thus, in this case hypervascular metastasis of any unknown extrahepatic malignant tumor could be reliably excluded. Due to the variability of imaging characteristics of FNH differential diagnosis from hepatic adenoma and hepatocellular carcinoma (HCC) may be very difficult. Both lesions and, in particular, the fibrolamellar variant of HCC may undergo central necrosis mimicking the stellate scar of FNH (3). Unlike in fibrolamellar carcinoma calcifications have never been observed in FNH making this an important factor for the differentiation of both entities.Transient contrast enhancement during the arterial phase may also be seen within adenomas and hepatic carcinomas. The hypervascular character of FNH may be well detected using dynamic hepatobiliary scintigraphy. During the late phase of the hepatobiliary transit which is characterised by progressive clearing of the hepatic tissue trapping of the tracer within the tumor is a normal finding. This can be used to distinguish FNH from other hepatic lesions (4). In case of small tumors or uncertain findings surgical excision is indicated to establish the diagnosis.