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Clinical Observations |
1 Department of Radiology, University Hospital Basel, Basel, Switzerland.
2 Present address: Institute of Radiology, Kantonsspital Aarau, Tellstrasse,
5001 Aarau, Switzerland.
3 Department of Gastroenterology, University Hospital Basel, Basel,
Switzerland.
4 Department of Pathology, University Hospital Basel, Basel, Switzerland.
5 Imamed Radiologie Nordwest, Basel, Switzerland.
Received September 21, 2007;
accepted after revision November 16, 2007.
Address correspondence to O. Giovanoli
(olivier.giovanoli{at}ksa.ch).
Abstract
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CONCLUSION. In all three patients, more than 100 liver adenomas revealed no metabolism of the new liver-specific contrast agent in the delayed phase. Because of absent or strongly reduced intracellular uptake of gadoxetic acid in all adenomas during delayed contrast-enhanced series, differentiation of adenomas from dysplastic or malignant lesions was not possible.
Keywords: abdominal imaging • gadoxetic acid • liver adenomatosis • liver imaging
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Initial radiologic workup may be difficult to evaluate because routine imaging criteria do not allow confident differentiation of this benign entity from malignant or dysplastic liver lesions. Recognition of potential dysplastic transformation of adenomas during follow-up examinations is also difficult because MRI features are not specific even after contrast administration [2, 3].
Gadoxetic acid disodium is a new liver-specific MR contrast agent. In addition to dynamic imaging, gadoxetic acid allows delayed imaging of functional liver tissue because of its highly specific uptake by hepatocytes [5]. Benign lesions containing well-differentiated hepatocytes have been shown to metabolize and take up gadoxetic acid, whereas malignant and dysplastic tumors generally show no uptake [6].
Administration of liver-specific contrast media such as gadoxetic acid may therefore be of use for initial workup of patients with newly discovered liver adenomatosis and for follow-up of these patients in search of potential dysplastic growth of adenomas. We describe the initial findings in gadoxetic acid–enhanced MRI as observed in three patients with liver adenomatosis.
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The second patient was 27 years old (patient 2). She suffered from glycogen storage disease type 1b, had multiple known liver adenomas, and was referred to us for a baseline MRI to rule out potential dysplastic lesions. Two years previously, one large adenoma (> 7 cm in diameter) and several small adenomas had been surgically resected in this patient; no dysplastic cells were found at histologic analysis. Follow-up sonography revealed no en largement of the liver adenomas over 2 years.
The third patient was 53 years old (patient 3). She had multiple known liver adenomas and was referred for routine follow-up MRI of the liver. Two years previously, one hepatic lesion in segment III had been surgically removed; histologic analysis showed a liver adenoma without cytologic atypia. The patient had never taken oral contraceptives or other estrogen-containing medications.
Imaging Techniques
MRI was performed using a 1.5-T unit (Achieva, Philips Medical Systems) and
a phased-array body coil. T1- and T2-weighted sequences were acquired with the
following parameters: T1-weighted fast-field echo (FFE) transverse (TR/TE,
23/4.6), dual T1-weighted FFE in-phase and opposed-phase transverse
(237/opposed-phase 2.3, in-phase 4.6), T2-weighted single-shot trans verse
(391/80) and coronal (587/80), and T2-weighted spectral inversion recovery
transverse (416/80).
After IV injection of 10 mL (0.25 mmol/mL) of gadoxetic acid–based contrast medium (gadoxetic acid disodium [Gd-EOB-DTPA] [Primovist, Bayer Schering Pharma]), T1-weighted trans verse gradient-echo sequences (high-resolution isotropic volume examination [THRIVE] with spectral presaturation inversion recovery [SPIR], 4.3/2.1) were obtained during arterial (25 seconds), portal venous (70 seconds), and delayed (3, 10, and 15 or 20 minutes) phases. Gadoxetic acid was injected manually and flushed with saline solution.
Image Interpretation
Two radiologists with 8 and 3 years of experience in gastrointestinal MRI
reviewed the MR images in consensus. The total number of liver lesions was
counted and the size of each lesion was measured on a PACS workstation
(ProVision, Cerner). Signal intensity of all liver lesions was graded on
T1-weighted, T2-weighted, and contrast-enhanced images as isointense,
hypointense, or hyperintense in relation to normal liver tissue. In the
delayed contrast-enhanced images, signal intensity of the liver parenchyma was
hyperintense compared with unenhanced T1-weighted images because of intra
cellular uptake of gadoxetic acid by normal liver tissue.
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Histology
For patient 1, the resected lesions measured 15 x 11 x 6 cm. An
unencapsulated 7.2 x 5.4 x 4.6 cm pale yellow homogeneous nodule
was identified in the liver. Microscopic examination revealed benign
hepatocytes arranged in thickened cords. Steatosis, cytologic atypia, portal
tracts, and bile ducts were absent.
In patient 2, segmentectomy showed an oval-shaped, well-circumscribed, homogeneous solid mass measuring 5.5 x 4 x 6 cm. However, additional smaller nodules with smooth borders within the liver parenchyma were also easily detected. All nodules were unencapsulated but well demarcated from the adjacent liver parenchyma. Histologically, the nodules consisted of a proliferation of hepatocytes with steatosis. No portal tracts were present within the nodules. There was no cytologic atypia. The histologic features of the remaining liver parenchyma were well compatible with the diagnosis of glycogen storage disease type I.
In patient 3, the histology was typical for a liver cell adenoma and showed neither steatosis nor cellular atypia.
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Liver adenomatosis and solitary hepatic adenomas are similar histologically, with extensive sinusoids and feeding arteries and a lack of biliary ductules [8], although unusual histology of liver adenomatosis has been reported in patients with glycogen storage disease [9]. Three histologic forms of liver adenomatosis have been recently described: steatotic, peliotic, and mixed [3].
On unenhanced MRI and in comparison with normal liver parenchyma, adenomas in liver adenomatosis have been described as hyperintense on T2-weighted images and mostly hyper- to isointense on T1-weighted images, although some lesions can appear hypointense. With extracellular gadolinium-based contrast media, a majority of lesions show arterial phase enhancement; on venous and delayed phases, contrast enhancement differs depending on histologic type, with enhancement of all peliotic adenomas, partial enhancement of mixed adenomas, and minimal or absent enhancement of steatotic adenomas [3]. Our findings match these published data, although contrast behavior on the delayed phase cannot be compared because of liver-specific intracellular uptake of gadoxetic acid.
Gadoxetic acid is a recently developed gadolinium-based MR contrast agent with high intracellular specificity to hepatocytes. It is administered IV and first distributed in the extracellular vascular compartment, allowing dynamic imaging of liver lesions. Uptake of about 50% of injected gadoxetic acid occurs by the anionic transporter protein of hepatocytes and leads to intracellular accumulation and thus increased signal intensity of liver parenchyma on delayed T1-weighted MR images. Intracellular gadoxetic acid is excreted through the bile ducts, in our experience beginning roughly 10 minutes after contrast administration. The remaining 50% of injected gadoxetic acid is excreted renally [6, 10].
Because of its high specificity to liver cells, gadoxetic acid allows distinction of hepatocyte-containing from non–hepatocyte-containing tissue, although only tumors containing highly differentiated hepatocytes have been shown to enhance in delayed phase imaging [6]. Previous reports have described gadoxetic acid enhancement in hepatic adenomas during delayed phases [5, 6, 11]; one atypical adenoma showing no late enhancement has been reported [6]. These findings indicate the potential of gadoxetic acid to reliably diagnose hepatic adenomatosis during initial workup and even allow recognition of potential dysplastic growth during follow-up.
Contrary to these reports, most adenomas in our three patients showed no gadoxetic acid uptake during delayed phase imaging. Only a few adenomas showed weak and diffuse delayed uptake, and three large adenomas showed strong peripheral enhancement. Absence of delayed phase enhancement did not permit confident diagnosis of benign liver adenomas in our patients; instead, we were left with a differential diagnosis that included dysplastic adenomas, metastases, and multifocal hepatocellular carcinoma [6].
On gadobenate dimeglumine–enhanced (MultiHance, Bracco) MRI, Grazioli et al. [8] described identical behavior of solitary hepatic adenomas and adenomas in liver adenomatosis during delayed imaging. Solitary adenomas and adenomas in liver adenomatosis could be reliably differentiated from focal nodular hyperplasia because of a lack of hepatic metabolism. Gadobenate dimeglumine is also partially specific to hepatocytes, but only 3–5% is metabolized as opposed to 50% of gadoxetic acid [6, 8, 10]. The reason for the absence of hepatic metabolism of gadobenate dimeglumine in adenomas is not known. Grazioli et al. discussed two possible explanations. Adenomas may have an altered cell structure compared with normal hepatocytes and therefore a lack of gadobenate dimeglumine uptake. On the other hand, the absence of biliary ductules in adenomas—and therefore reduced biliary excretion mechanisms—may lead to decreased uptake gradients of gadoxetic acid into hepatocytes of adenomas.
In conclusion, we observed absent or strongly reduced intracellular uptake of gadoxetic acid in all adenomas during delayed phase imaging. Lack of metabolism of gadoxetic acid in liver adenomas did not allow differentiation from malignant or dysplastic nodules in all three patients with liver adenomatosis.
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