DOI:10.2214/AJR.05.1998
AJR 2007; 188:W459-W463
© American Roentgen Ray Society
Focal Nodular Hyperplasia-Like Nodules in Alcoholic Liver Cirrhosis: Radiologic-Pathologic Correlation
Young Han Lee1,
Seong Hyun Kim1,2,
Mee-Yon Cho3,
Kwang Yong Shim4 and
Myung Soon Kim1
1 Department of Radiology, Wonju Christian Hospital, Wonju College of Medicine,
Yonsei University, 162 Ilsan-dong, Wonju, Gangwon-do 220-701, South
Korea.
2 Present address: Department of Radiology and Center for Imaging Science,
Samsung Medical Center, Sungkyunkwan University School of Medicine, 50
Ilwon-dong, Gangnam-gu, Seoul 135-710, South Korea.
3 Department of Pathology, Wonju Christian Hospital, Wonju College of Medicine,
Yonsei University, Wonju, Gangwon-do 220-701, South Korea.
4 Department of Oncology, Wonju Christian Hospital, Wonju College of Medicine,
Yonsei University, Wonju, Gangwon-do 220-701, South Korea.
Received November 14, 2005;
accepted after revision March 15, 2006.
Address correspondence to S. H. Kim.
WEB This is a Web exclusive article.
Abstract
OBJECTIVE. The purpose of this study was to describe our experience
with three patients who had pathologically proven focal nodular hyperplasia
(FNH)-like nodules that radiologically mimicked hepatocellular carcinoma
(HCC).
CONCLUSION. FNH-like nodules may radiologically mimic HCC, appearing
as hypervascular masses on contrast-enhanced CT images and as
high-signal-intensity masses on superparamagnetic iron oxide-enhanced MR
images. Pathologically, there is the presence of a high number of unpaired
arteries and sinusoidal capillarization, which may mimic HCC. Thus, it is
important to differentiate FNH-like nodules radiologically, pathologically,
and clinically from HCC.
Keywords: cirrhosis • focal nodular hyperplasia • hepatocellular carcinoma • liver disease
Introduction
With the remarkable improvements in MDCT, a greater number of
hypervascular nodules are being detected in the liver. In patients with liver
cirrhosis, hypervascular nodules seen in the early phase of contrast
enhancement are usually considered to be representative of hepatocellular
carcinoma (HCC).
Several investigators
[1-6]
have recently reported focal nodular hyperplasia (FNH)-like nodules in the
cirrhotic liver. These nodules are macroscopically, microscopically, and
immunohistochemically identical to FNH seen in the noncirrhotic liver.
FNH-like nodules in the cirrhotic liver are usually hypervascular, and they
can mimic HCC. To the best of our knowledge, radiographic findings using MDCT
and superparamagnetic iron oxide (SPIO)-enhanced MRI for detecting FNH-like
nodules in the cirrhotic liver have not been previously reported in the
radiologic literature. We describe the unique features of pathologically
proven FNH-like nodules using MDCT or ferucarbotran-enhanced MRI with
pathologic correlation.
Materials and Methods
The study was approved by our institutional review board. From September
2003 to February 2005, three patients were diagnosed as having HCC on the
basis of imaging findings; one patient underwent hepatic segmentectomy and two
underwent percutaneous liver biopsy. All three patients were pathologically
confirmed as having FNH-like nodules in alcoholic liver cirrhosis. The three
patients were all men, and they were 39, 40, and 43 years old. Hepatitis virus
markers were negative in all three. The serum level of 
-fetoprotein was
within the normal limits. The tumors ranged from 1.2 to 4.5 cm in diameter
(mean diameter, 2.4 cm).
Sonography was performed for all patients with a 2- to 5-MHz convex-array
transducer using either an HDI 5000 (Advanced Technology Laboratories) or iU22
(Philips Medical Systems) scanner. For two tumors, a sonography-guided
percutaneous biopsy using an 18-gauge (Gunbiopsy Needle, M.I. Tech) automated
biopsy gun was performed. Tissue was obtained from the tumor centers and
margins with a minimum of three biopsies per lesion. For the two patients with
the diagnosis of FNH-like nodules confirmed by percutaneous liver biopsy, the
followup duration was 6 and 8 months, respectively.
Contrast-enhanced triple-phase CT was performed for the three patients
using a 16-MDCT scanner (LightSpeed Pro 16, GE Healthcare). The scanning
parameters were 120 kVp, 180-200 mAs, 5-mm slice thickness, and 18.75 mm/s
(pitch, 0.938) table speed during a single breath-hold helical acquisition of
8-10 seconds (depending on the liver size). The images were obtained in the
craniocaudal direction and reconstructed every 5 mm to provide contiguous
sections. With a bolus-triggered technique, the arterial phase of scanning
started 20-35 seconds after the start of an IV injection of 120 mL of nonionic
iodinated contrast material ([iopamidol] Iopamiro 370, Bracco Diagnostics)
with a power injector (OP 100, Medrad) through an antecubital vein at a rate
of 4 mL/s. The portal phase of scanning began 70 seconds after the start of
the contrast material injection. The delayed phase of scanning began 180
seconds after the start of the contrast material injection.
MRI was performed on two patients using a 1.5-T unit (Gyroscan NT, Philips
Medical Systems) within 10 days after CT. All the images were obtained in the
transverse plane using a body coil. For all the pulse sequences, a 6- to 8-mm
section thickness (according to the liver volume) was used with a 2-mm
intersection gap, a field of view of 30-32 cm, and a 256 x 256 matrix.
The dose of ferucarbotran (Resovist, Schering) was 1.4 mL in patients with a
body weight of 60 kg or more, and 0.9 mL was used in patients with a body
weight of less than 60 kg (dose range, 8.0-12.0 µmol of iron/kg). The
contrast agent was manually administered by IV through a 5-µm in-line
specific filter with a rapid bolus given in 1 second, immediately followed by
a 10-mL saline solution flush. The entire procedure was performed in
approximately 5 seconds.
Before injection of the contrast agent, we acquired a fat-suppressed
respiratory-triggered turbo spin-echo series with two TEs (proton
density-weighted and T2-weighted images) (TR/TE first echo, TE second-echo,
1,800/9, 90; echo-train length, 12), a T2*-weighted gradient-echo
series (TR/TE, 157/9.2; flip angle, 10°), and a breath-hold in-phase
T1-weighted gradient-echo series (15/4.2; flip angle, 25°) with the fast
field-echo sequence. After the unenhanced images, contrast-enhanced images of
the same sequences were obtained 10 minutes after the injection of the
contrast agent. The unenhanced and contrast-enhanced dynamic T1-weighted
gradient-echo images (207/2.3; flip angle, 80°) were also obtained with
delays of 20 seconds and 1, 3, and 5 minutes after injection of the contrast
agent. Twenty transverse images were obtained during each pulse sequence.
Hepatic angiography was performed in two patients. In one of these two
patients, transcatheter arterial chemoembolization was performed. However,
this patient was not followed up until 8 months after the transcatheter
arterial chemoembolization, at which time a percutaneous liver biopsy was
performed with ferucarbotran-enhanced MRI and follow-up CT.
The resected and biopsied liver tissues were fixed in 10% formalin,
prepared as paraffin-embedded specimens, and cut into slices 4-5 µm thick.
The specimens were histologically examined by staining with H and E, Masson
trichrome, and Prussian blue. Immunostaining for CD34, CD68, CK7, CK19, Ki-67,
and p53 was performed. All the histopathologic specimens were reviewed by an
experienced pathologist to confirm the diagnoses.
Results
Table 1 shows the imaging
findings of the nodules. The nodules were hypoechoic or hyperechoic, with or
without a peripheral halo on the sonography images. All of the nodules were
located in the right liver. In all cases, contrast-enhanced triple-phase MDCT
showed hypervascular nodules during the arterial phase (Figs.
1A,
1B,
1C,
1D,
2A,
2B,
2C,
2D,
2E,
2F,
3A,
3B,
3C,
3D), followed by iso- or
hypoattenuation relative to the surrounding liver with a washout pattern
during the delayed phase (Fig.
3A,
3B,
3C,
3D). In the delayed phase,
there was no capsular enhancement of the nodules. During arteriography of the
two nodules studied, one showed hypervascular tumor staining and the other
showed no tumor staining. In one hyper-vascular mass treated with
transcatheter arterial chemoembolization, the iodized oil was completely
deposited within the mass. On follow-up CT 8 months later, this mass showed no
change in imaging findings except for a decrease in size compared with its
size before chemoembolization, and there was no iodized oil within the mass
(Fig. 2A,
2B,
2C,
2D,
2E,
2F).
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Fig. 1A —43-year-old man with 1.2-cm-diameter focal nodular hyperplasia
(FNH)-like nodule in right liver (case 1). Contrast-enhanced CT scan obtained
on arterial phase shows hypervascular nodule (arrow) in right liver.
This was followed by faintly hypoattenuated nodule relative to surrounding
cirrhotic liver at delayed phase (not shown) with no characteristic findings
of central scar.
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Fig. 1B —43-year-old man with 1.2-cm-diameter focal nodular hyperplasia
(FNH)-like nodule in right liver (case 1). Superparamagnetic iron oxide
(SPIO)-enhanced T2*-weighted gradient-echo image (TR/TE, 157/9.2;
flip angle, 10°) shows hyperintense nodule (arrow) in surrounding
hypointense liver. There were no characteristic findings of central scar on
unenhanced and contrast-enhanced MR images. This nodule was interpreted as
hepatocellular carcinoma.
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Fig. 1C —43-year-old man with 1.2-cm-diameter focal nodular hyperplasia
(FNH)-like nodule in right liver (case 1). Photomicrograph of resected
specimen shows well-demarcated and complete encapsulation (arrows)
with central stellate, scarlike fibrosis (arrowheads). Hepatocytes
display no atypia. (Masson trichrome, x10)
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Fig. 1D —43-year-old man with 1.2-cm-diameter focal nodular hyperplasia
(FNH)-like nodule in right liver (case 1). Immunohistochemistry image shows
marked increase of Kupffer cells (arrowheads) in FNH-like nodule (N)
compared with surrounding cirrhotic liver (S). Asterisk = fibrous capsule.
(CD68 immunostain, x200)
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Fig. 2A —40-year-old man with hypervascular mass that showed interval
decrease in size during 8 months of followup (case 2). Contrast-enhanced CT
scan obtained on arterial phase shows 4.5-cm-diameter hypervascular mass
(arrow) in right liver. Mass was initially interpreted as
hepatocellular carcinoma, and transcatheter arterial chemoembolization was
performed (not shown).
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Fig. 2B —40-year-old man with hypervascular mass that showed interval
decrease in size during 8 months of followup (case 2). Contrast-enhanced CT
scan obtained at arterial phase 8 months after initial CT examination
(A) and after transcatheter arterial chemoembolization shows interval
decrease in size of mass to 2.5 cm (arrow) and hypervascular
enhancement same as A with no iodized oil within mass in right
liver.
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Fig. 2C —40-year-old man with hypervascular mass that showed interval
decrease in size during 8 months of followup (case 2). Unenhanced
T2*-weighted gradient-echo image (TR/TE, 157/9.2; flip angle,
10°) obtained 8 months after initial CT examination (A) and after
transcatheter arterial chemoembolization shows very hypointense
2.5-cm-diameter nodule with faintly hyperintense area within nodule
(arrow).
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Fig. 2D —40-year-old man with hypervascular mass that showed interval
decrease in size during 8 months of followup (case 2). Superparamagnetic iron
oxide-enhanced T2*-weighted gradient-echo image (157/9.2; flip
angle, 10°) obtained 8 months after initial CT examination (A) and
after transcatheter arterial chemoembolization shows hypointense nodule
(arrow), same as that shown on unenhanced image (C), with no
contrast difference between nodule and surrounding hypointense liver.
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Fig. 2E —40-year-old man with hypervascular mass that showed interval
decrease in size during 8 months of followup (case 2). Photomicrograph of
biopsied specimen obtained 8 months after initial CT examination (A)
and after transcatheter arterial chemoembolization shows thick-walled blood
vessel (arrows) and sinusoidal dilatation (arrowheads).
Hepatocytes in nodule display slight cellular atypia with irregular trabecular
pattern and marked intracellular hemosiderin deposits. (H and E,
x400)
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Fig. 2F —40-year-old man with hypervascular mass that showed interval
decrease in size during 8 months of followup (case 2). Photomicrograph of
biopsied specimen obtained 8 months after initial CT examination (A)
and after transcatheter arterial chemoembolization shows marked iron
deposition in hepatocytes and Kupffer cells (arrowheads) in nodule
compared with surrounding cirrhotic liver. (Prussian blue, x400)
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Fig. 3B —39-year-old man with hypervascular nodule with macrovesicular
steatosis (case 3). Contrast-enhanced CT scan obtained on arterial phase shows
hypervascular nodule (arrow) in right liver.
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Fig. 3C —39-year-old man with hypervascular nodule with macrovesicular
steatosis (case 3). Contrast-enhanced CT scan obtained on delayed phase shows
hypoattenuated nodule (arrow) at same level as B with washout
pattern. Nodule was interpreted as hepatocellular carcinoma.
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Fig. 3D —39-year-old man with hypervascular nodule with macrovesicular
steatosis (case 3). Photomicrograph of biopsied specimen shows macrovesicular
steatosis (arrowheads) in nodule (N) compared with surrounding
cirrhotic liver (S). Asterisk = fibrous capsule. (H and E, x100)
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In the two cases that were examined with SPIO-enhanced MRI, one nodule was
hyperintense on the unenhanced T1-weighted gradient-echo, proton density- and
T2-weighted MR images. It was isointense on the unenhanced
T2*-weighted gradient-echo images and hyperintense on all
SPIO-enhanced MR images (Fig.
1A,
1B,
1C,
1D). SPIO-enhanced MRI of the
other nodule (Fig. 2A,
2B,
2C,
2D,
2E,
2F) was obtained 8 months
after transcatheter arterial chemoembolization, and this nodule was very
hypointense on all unenhanced and SPIO-enhanced MR images, particularly on the
T2*-weighted gradient-echo images, with hyperintense areas noted
within the nodule. One nodule appeared hyperintense and the other nodule
appeared hypointense on all of the unenhanced and SPIO-enhanced dynamic MR
images.
The resected (Fig. 1A,
1B,
1C,
1D) and biopsied (Figs.
2A,
2B,
2C,
2D,
2E,
2F and
3A,
3B,
3C,
3D) specimens showed nearly
the same histologic features. The surrounding liver tissue of all the nodules
showed micronodular cirrhosis. All specimens showed a clear demarcation from
the surrounding cirrhotic liver by a thin rim of fibrous tissue, a moderate
increase in cell density with a mildly irregular trabecular pattern, scarlike
fibrosis, thick-walled blood vessels, unpaired arteries with no portal tract,
and diffuse sinusoidal capillarization with or without sinusoidal dilatation
(Figs. 1A,
1B,
1C,
1D,
2A,
2B,
2C,
2D,
2E,
2F,
3A,
3B,
3C,
3D). In the resected specimen
(Fig. 1A,
1B,
1C,
1D), central stellate scarlike
fibrosis, one of the important findings for FNH-like nodules, was clearly
shown in the nodule. However, the nodule showed no evidence of a central scar
on imaging findings. The other two nodules with scarlike fibrosis on biopsied
specimens also showed no evidence of a central scar on the imaging
findings.
The nodules showed mild or marked iron deposits in the hepatocytes and
Kupffer cells (Fig. 2A,
2B,
2C,
2D,
2E,
2F), and there was a marked
increase in the number of Kupffer cells compared with the surrounding
cirrhotic liver (Fig. 1A,
1B,
1C,
1D). One resected specimen
showed ductal proliferation along the interface of the scarlike fibrosis with
a neutrophil-predominant inflammatory cell infiltration (Fig.
1A,
1B,
1C,
1D). Only one case showed
slight cellular atypia (Fig.
2A,
2B,
2C,
2D,
2E,
2F). Macrovesicular fatty
infiltration was shown in one nodule, and this was accompanied by fatty
infiltration of the surrounding liver (Fig.
3A,
3B,
3C,
3D). Labeling indexes of Ki-67
were rarely found, and overexpression of p53 was not observed in any of the
specimens.
Discussion
In general, FNH is a lesion that occurs in noncirrhotic livers
[3]. An FNH lesion is defined
as "a nodule composed of benign-appearing hepatocytes that occurs within
a liver that is otherwise histologically normal or nearly normal"
[7]. Several investigators have
reported the occurrence of FNH-like nodules in chronic liver disease
[1-6].
Quaglia et al. [3] reported
that 12 nodules (5% of the total number of distinctive nodular lesions in
explant cirrhotic livers) had features suggestive of FNH. Libbrecht et al.
[5] reported five FNH-like
nodules in four (8%) of 49 cirrhotic explant livers.
The histologic features of the three present cases were similar to those of
the previous reports
[1-6],
and particularly to those of the Nakashima et al.
[6] report. The histology of
our cases showed fibrous capsules, scarlike fibrosis, thick-walled blood
vessels, unpaired arteries, and sinusoidal capillarization with or without
bile duct proliferation. Portal tracts were not present in any of the nodules.
Unlike the histologic features of FNH in noncirrhotic liver, the FNH-like
nodules in our cases showed unique features including encapsulation, diffuse
sinusoidal capillarization, and iron deposition in the hepatocytes and Kupffer
cells.
The FNH-like nodules in our cases showed hypervascular enhancement in the
arterial phase of the contrast-enhanced CT images, and this was followed by a
washout pattern in the delayed phase, which is a feature generally considered
to be highly suggestive of HCC in liver cirrhosis. Although FNH-like nodules
do not occur with high frequency in cirrhotic livers, they are clinically
important because, as in our cases, most of these nodules detected by imaging
examination are suspected of being HCC. Histologic analyses revealed that the
FNH-like nodules showed many unpaired arteries with thick-walled blood
vessels, and this resulted in hypervascular enhancement that mimicked HCC on
contrast-enhanced CT.
High-grade dysplastic nodules and HCCs in cirrhotic livers contain a large
number of unpaired arteries and capillarized sinusoids compared with the
surrounding cirrhotic liver, and atypical hepatocytes can also be distributed
unevenly in the lesions [8].
Consistent with the report by Nakashima et al.
[6], our one biopsy case showed
slight atypia of the hepatocytes in the nodule. The unique vascular
characteristics and slight hepatocyte atypia in the FNH-like nodule could
erroneously lead to the diagnosis of HCC or highgrade dysplastic nodules,
especially in a needle biopsy specimen of an FNH-like nodule within a
cirrhotic liver. Therefore, hypervascular lesions should not be diagnosed as
dysplastic nodules or HCCs if the features of clear-cut atypical hepatocytes
or the architectural findings are not found.
SPIO has been developed as a liver-specific particulate MR contrast agent.
SPIO is primarily taken up by the Kupffer cells of the liver and also by the
macrophages of the spleen. This results in a loss of signal intensity in the
normal liver tissue because of the susceptibility effects of iron.
SPIO-enhanced MRI is useful for detecting HCC
[9]. A variety of hepatic
tumors, such as hepatocellular adenoma, regenerative nodules, dysplastic
nodules, and even well-differentiated HCC, can show variable uptake of SPIO
particles because these tumors contain a variable number of Kupffer cells
[9-12].
FNH also contains variable amounts of Kupffer cells. Typically, FNH in the
noncirrhotic liver is isointense or slightly hypointense on T1-weighted
sequences and is homogeneous, isointense, or slightly hyperintense on
T2-weighted sequences.
After administration of SPIO, the typical MRI features of FNH on T2- and
T2*-weighted images manifest as marked homogeneous or heterogeneous
reduction of the signal intensity when compared with that seen on unenhanced
images [11,
12]. However, Kupffer cells in
FNH may be present in comparatively small numbers; thus, there may be an
insufficient drop of the signal after SPIO administration to make the accurate
diagnosis of FNH. In one of our cases, even though the nodules contained a
markedly increased number of Kupffer cells compared with the surrounding liver
tissues, the SPIO-enhanced T2*-weighted gradient-echo image showed
high signal intensity against a background of decreased signal intensity of
the surrounding hepatic parenchyma. This resulted in confusing the nodules
with malignant lesions, particularly HCC.
We speculate that this discrepancy between the number of Kupffer cells and
unexpected SPIO-enhancement characteristics occurred because the decreased
Kupffer cell activity in the FNH-like nodule resulted in smaller intracellular
SPIO clusters that were not sufficient to cause loss of signal intensity due
to the susceptibility effects of iron. Another explanation could be that the
Kupffer cells in the nodule may not have phagocytized the SPIO particles
because the Kupffer cells were already saturated with iron, thus resulting in
a functional lack of Kupffer cells.
Because the pathologic specimen was obtained 8 months after transcatheter
arterial chemoembolization in one of our three cases, histologic findings such
as scarlike fibrosis and iron deposits in Kupffer cells may have been
influenced by chemoembolization. However, we believe that other histologic
findings such as marked iron deposits in hepatocytes and an increased number
of Kupffer cells may not have been caused by chemoembolization, and, in
particular, thick-walled blood vessels are one of the unique histologic
features of FNH-like nodules despite chemoembolization.
Histologically, all of the present cases showed marked or mild iron uptake
by hepatocytes and Kupffer cells in the nodules compared with little or no
iron uptake in the surrounding liver tissues. Of these, the one nodule with
the greatest iron uptake by hepatocytes and Kupffer cells appeared hypointense
on all sequences of the unenhanced and SPIO-enhanced MRI. We believe that
preexisting iron taken up in the hepatocytes and Kupffer cells of the nodule
resulted in a loss of signal intensity because of the magnetic susceptibility
effects of iron, irrespective of uptake of SPIO particles in the Kupffer
cells.
It is unclear why an FNH-like nodule in a background of alcoholic liver
cirrhosis tends to accumulate iron. Terada and Nakanuma
[13] and Terada et al.
[14] reported that
approximately 25% of regenerative nodules and 26% of adenomatous hyperplastic
nodules accumulated more iron than the surrounding hepatic parenchyma. Iron
deposition may not be specific to nodules in alcoholic cirrhosis. One
explanation for the iron deposition was suggested by Nakashima et al.
[6]: The arterial over-inflow
and passive congestion in the nodule, particularly within the encapsulation,
are associated with iron deposition in the hepatocytes and Kupffer cells of
the nodules. Another explanation could be that transferrin receptor proteins,
which mediate hepatocellular iron uptake, may be abnormal in the nodules that
have accumulated iron
[15].
Unlike the report by Nakashima et al.
[6], one of our cases showed a
hyperechoic nodule on sonography with prominent macrovesicular steatosis
compared with the surrounding liver tissue. We think that fat infiltration in
the FNH-like nodule may be caused by a nonspecific response of the liver and
the FNH-like nodule to alcohol toxicity in the patient.
One potential explanation for the pathogenesis of the FNH-like nodules in
cirrhosis is that alterations of the hepatic vascular architecture commonly
occur in chronic liver disease, particularly in cirrhosis, and such
alterations may increase the number of arteries by causing local ischemia;
these changes could potentially stimulate localized hyperplastic changes of
the hepatocytes
[1-3,
6].
The natural course of FNH-like nodules is unclear. However, unlike the
dysplastic nodules that are precursor lesions of HCC and carry a considerable
risk for malignant transformation during the subsequent years of follow-up
[5,
6,
8], two of the three cases in
our study were followed up for 6 to 8 months and showed either a decrease or
no change in the size of nodules. They also showed very low Ki-67 labeling
indexes and no expression of p53. As in the study by Nakashima et al.
[6], these observations suggest
that these nodules are benign—that is, there is no premalignant or
malignant potency. Further research at the molecular level is needed to
determine the true nature of the nodules and their pathogenesis.
In conclusion, FNH-like nodules may radiologically mimic HCC as
hypervascular masses on contrast-enhanced CT and may appear as
high-signal-intensity masses on SPIO-enhanced MRI. Pathologically, there is
the presence of a high number of unpaired arteries and sinusoidal
capillarization compared with the surrounding cirrhotic liver. Thus, it is
important that these FNH-like nodules are differentiated radiologically,
pathologically, and clinically from HCC.
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Abstract
Introduction
