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1
Department of Radiology, University Hospital of Graz, Auenbruggerplatz 9,
A-8036 Graz, Austria.
2
Doors to Knowledge, Alte Reichsstr. 9, A-8410 Wildon, Austria.
Received July 10, 2000;
accepted after revision December 11, 2000.
Address correspondence to A. J. Ruppert-Kohlmayr.
Abstract
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MATERIALS AND METHODS. Forty-five histologically proven focal nodular hyperplasias in 27 patients and 18 hepatocellular adenomas in six patients were examined with helical CT. Quantitative evaluation included the following: attenuation of lesions, scar, and liver parenchyma during unenhanced, arterial (20 sec after injection), and portal venous phases (70 sec after injection); relative enhancement of lesions and liver (the ratio between attenuation in arterial phase and portal venous phase, respectively, and attenuation in unenhanced phase); and the prevalence of scar and its central vessel in focal nodular hyperplasia.
RESULTS. The study showed no significant difference between mean attenuation values of focal nodular hyperplasia (mean ± SD, 51.2 ± 5.9 H) and hepatocellular adenoma (mean ± SD, 56.3 ± 7.8 H) in the unenhanced phase. In the arterial phase attenuation values were significantly higher in focal nodular hyperplasia (mean ± SD, 117.9 ± 15.1 H) than in hepatocellular adenoma (mean ± SD, 80.1 ± 10.5 H). In the portal venous phase no significant differences in attenuation values were detected between focal nodular hyperplasia (mean ± SD, 112.1 ± 20.4 H) and hepatocellular adenoma (mean ± SD, 110.2 ± 12.9 H). For enhancement parameter thresholds separating focal nodular hyperplasia from hepatocellular adenoma, the following were found: the relative enhancement was higher in 100% of the focal nodular hyperplasias and lower than or equal to 1.6 (accuracy, 96%) in 87% of the hepatocellular adenomas.
CONCLUSION. Triphasic helical CT combined with quantitative evaluation of liver lesions offers the possibility of detecting differences in liver lesions that are visually similar on CT. The attenuation and relative enhancement in the arterial phase show significant differences that make accurate differentiation between focal nodular hyperplasia and hepatocellular adenoma possible.
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Focal nodular hyperplasia of the liver is a benign lesion characterized by nodular hyperplasia of the hepatic parenchyma around a central stellate area of fibrosis associated with an anomalous artery. Studies suggest that focal nodular hyperplasia is not a neoplasm but a hyperplastic response of liver parenchyma to the presence of a preexisting vascular malformation [3]. Several vascular anomalies have been described in association with focal nodular hyperplasia, such as teleangiectasies, hemangiomas, and arteriovenous malformations at the hepatic hilum, that support the hypothesis of a vascular origin of focal nodular hyperplasia [3, 4]. In patients with focal nodular hyperplasia, arterial blood flows centrifugally from the anomalous central arteries, with its sources in the branches of the hepatic artery, via the capillaries and into sinusoids adjacent to fibrous septa. The blood in the sinusoids drains into the hepatic vein either directly or via perinodular sinusoids [5, 6].
In contrast to focal nodular hyperplasia, hepatocellular adenoma is a true neoplasm, which is composed of sheets of normal or atypical hepatocytes that are frequently vacuolated and lacking Kupffer's cells and bile ducts. The presence of subcapsular feeding arteries accounts for the centripetal blood flow of the lesion [4].
Compared with previous CT studies [4, 7,8,9] our study is the first one, to the best of our knowledge, that deals with quantitative enhancement parameters of focal nodular hyperplasia and hepatocellular adenoma in a large number of patients using common triphasic CT protocols. The purpose of our study was twofold: first, to quantify and compare attenuation and enhancement patterns of focal nodular hyperplasia, hepatocellular adenoma, and normal liver parenchyma; and second, to determine quantitative parameters that can be used to characterize liver lesions on helical CT.
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Twenty-three patients with 38 focal nodular hyperplasias and five patients with 17 hepatocellular adenomas had undergone triphasic helical CT. Four patients with seven focal nodular hyperplasias and one patient with one hepatocellular adenoma who underwent CT arterioportography were included in the evaluation of morphologic changes but were excluded from attenuation and enhancement measurements. All patients were examined on helical CT because of unknown liver lesions, and all lesions were analyzed histologically after biopsy or surgical removal.
A helical CT scanner (Somatom Plus S4; Siemens, Erlangen, Germany) and an identical examination protocol were used in all patients. A total of 150 mL of contrast agent with a concentration of 300 I mg/mL (Ultravist 300; Schering, Erlangen, Germany) was administered with a flow rate of 4 mL/sec using a motor injector (Medrad, Indianola, PA). During each examination the contrast agent was injected via a 19-gauge venous line into the right antecubital vein.
The CT examination consisted of a triphasic helical CT protocol that included obtaining unenhanced scans of the upper abdomen, with a field of view from the diaphragm to the iliac crest; obtaining arterial phase scans 20 sec after injection; and obtaining portal venous phase scans 70 sec after injection. During the arterial and portal venous phases, the field of view covered the entire liver. We used the following technical parameters for imaging: section collimation, 8 mm; pitch, 1.5; reconstruction interval, 4 mm; 120 kVp; and 290 mAs. All examinations were evaluated on a work-station (Sparc 10 CT/MR or Sienet Magic View 1100; Siemens, Erlangen, Germany) by two radiologists who were unaware of the diagnosis.
Morphology
Abdominal scans were investigated for a multiplicity of lesions and the
presence of other focal lesions, such as hemangiomas or angiomyolipomas, or
calcifications within the lesions. Other features that were evaluated included
the vascularity (the absence or presence of feeding vessels) and the perfusion
of the lesions (amount of blood flowing through the lesion corresponding to
the enhancement). Homogeneity and subjective visible density (hypo-, iso-, or
hyperdensity) of the lesions relative to the liver density were assessed.
Measurement Parameters: Attenuation
Three attenuation values of the lesions and the liver were obtained during
each phase. Mean values with a single standard deviation were then calculated.
When evaluating scars, only a single attenuation value could be assessed in
each lesion because of the small size of these structures.
To exclude the influences of external factors, such as IV access and the patient's weight and cardiac function, on parenchymal or lesion enhancement, we used a special method. The idea was that different amounts of contrast agent are in the supplying vessel at the scan time because of external factors especially cardiac output. Therefore, the blood and contrast material supply to the organ and a lesion in this organ are different in each patient, a fact that influences the liver and lesion enhancement. Therefore, we wanted to find a method to equalize these conditions for each patient. The simplest way was to equalize the attenuation in the aorta at the level of the celiac trunk during the arterial and portal venous phases for each patient. If we suppose that all patients have the same attenuation in the supplying vessel, we can also suppose that the contrast enhancement conditions in the liver and in liver lesions are the same for each patient. We chose as the standard value in the aorta at the level of the celiac trunk the mean aortic attenuation value of our patient cohort. Then we calculated the ratio between the standard value and the measured aortic attenuation value to get a correction factor and multiplied the result by the measured attenuation in liver or lesion. The formulas for our enhancement-correcting method are listed in Table 1. For example, a patient has a liver lesion showing a measured attenuation value (Ma) of 110 H and celiac trunk attenuation (Ca) of 280 H during the arterial phase. The mean aortic attenuation (mCa) of our study cohort during the arterial phase was 250 H and that during the portal venous phase was 130 H. For the patient, the corrected attenuation in the lesion during the arterial phase (cMa) would be 98.2 H (110 x [250/280] = 98.2).
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Calculated Parameters: Enhancement
Relative lesion enhancement was determined from the standardized
attenuation values. It represents the enhancement 20 and 70 sec after contrast
injection, respectively. This parameter was calculated for lesions and liver
parenchyma as the differences in attenuation between the unenhanced and
arterial phase and the unenhanced phase and portal venous phase, respectively.
The formulas for this parameter are listed in
Table 1.
All inducted parameters were also statistically assessed for two subgroups
of lesions, small (
3 cm) and large (>3 cm).
For statistical analysis, Kolmogorov-Smirnov tests of the attenuation parameter of each phase were carried out. A p value less than 0.05 was considered statistically significant at the 95% confidence interval.
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Neither in focal nodular hyperplasia nor in hepatocellular adenoma were calcifications present (0%). On helical CT, 36 (95%) of 38 focal nodular hyperplasias and none of the hepatocellular adenomas (0%) showed homogenous enhancement during the arterial phase.
Central scars were detected in 65% of all focal nodular hyperplasias and in
none of the hepatocellular adenomas (0%). Scars were present in five (29%) of
17 small (3 cm) focal nodular hyperplasias and in 23 (82%) of 28 large
(>3 cm) focal nodular hyperplasias. Arterial vessels within the scar could
be detected in 17 (45%) of the 38 focal nodular hyperplasias exhibiting scar
formation (Figs.
1A,1B
and 2), and subcapsular
arteries were detected in none of the 38 focal nodular hyperplasias (0%) and
in seven (39%) of the 18 hepatocellular adenomas (Fig.
3A,3B).
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All feeding vessels of focal nodular hyperplasia and hepatocellular adenoma originated from the right or left hepatic artery according to each lesion's location in the liver. On helical CT only the central or subcapsular feeding vessels could be seen; smaller vessels were not visible. In the unenhanced phase 63% of the focal nodular hyperplasias were hypo-, 37% iso-, and 0% hyperdense, whereas 28% of hepatocellular adenomas were hypo-, 0% iso-, and 72% hyperdense compared with the liver parenchyma. In the arterial phase 100% of the focal nodular hyperplasias and 89% of the hepatocellular adenomas became hyperdense and 11% of hepatocellular adenomas became hypodense compared with the enhancing liver parenchyma. In the portal venous phase 40% of the focal nodular hyperplasias were hyperdense and 60% were isodense, whereas 22% of the hepatocellular adenomas were hypo-, 5% iso-, and 73% hyperdense.
Measurement Parameters: Attenuation
In the unenhanced phase the difference in attenuation between focal nodular
hyperplasia and liver was statistically significant (p < 0.05).
Differences in attenuation between focal nodular hyperplasia and
hepatocellular adenoma or between hepatocellular adenoma and liver, however,
were not significant (p > 0.05). Two hepatocellular adenomas
showed an attenuation value of more than 70 H in the unenhanced phase,
indicating intralesional hemorrhage, which was verified at surgery. The
unenhanced attenuation values of small focal nodular hyperplasia (mean, 50.8
H; range, 40.4-67.7 H) and of large lesions (mean, 51.5 H; range, 44.2-60.9 H)
did not differ significantly (p > 0.05).
In the arterial and portal venous phases all attenuation values were corrected. In the arterial phase, the attenuation values of the focal nodular hyperplasias were significantly higher than those of liver parenchyma and hepatocellular adenomas (p < 0.05) (Table 2). Small lesions (mean, 114.7 H; range, 86.3-138.2 H) exhibited slightly, but not significantly (p > 0.05), lower attenuation values than large focal nodular hyperplasias (mean, 120.2 H; range, 87.9-147.6 H).
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During the portal venous phase no significant difference in attenuation between focal nodular hyperplasia, hepatocellular adenoma, and liver parenchyma (p > 0.05) was detected. In addition, there was also no significant difference between small (mean, 109.7 H; range, 99.5-108.8 H) and large (mean, 113.8 H; range, 61.4-123.8 H) focal nodular hyperplasias during the portal venous phase.
The results of attenuation dynamics of focal nodular hyperplasia, hepatocellular adenoma, and liver are visible on graphs of the time-attenuation curves in Figure 4.
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Calculated Parameters: Enhancement
Relative enhancement of focal nodular hyperplasia and hepatocellular
adenoma for the arterial phase was significantly higher in focal nodular
hyperplasia than in hepatocellular adenoma, and the threshold of 1.6 for
relative enhancement could be used to differentiate focal nodular hyperplasia
from hepatocellular adenoma accurately (accuracy, 96%)
(Fig. 5). All focal nodular
hyperplasias (100%) and only two hepatocellular adenomas (12%) had a higher
relative enhancement than 1.6. In the portal venous phase relative enhancement
could not be considered as an accurate differentiating feature because the
calculated values were not significantly different.
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MR imaging is an important additional diagnostic modality for differentiating liver lesions with a high specificity when applying liver-specific contrast agents [10, 11]. Especially in uncertain cases, combinations of different imaging modalities may improve diagnostic certainty. Dynamic MR imaging can then be used to confirm the diagnosis of focal nodular hyperplasia [12].
The present study was designed to investigate qualitative and quantitative parameters of attenuation and enhancement patterns of focal nodular hyperplasia and hepatocellular adenoma. The qualitative assessment of large lesions does not cause many problems. Focal nodular hyperplasia and hepatocellular adenoma showed no intralesion calcifications in the present study; however, Caseiro-Alves et al. [13] reported calcifications in 1% of focal nodular hyperplasia cases. Helical CT has enough spatial resolution to show the feeding arteries of many lesions, but is not able to show the smaller vessels such as capillaries. We found that the typical features of focal nodular hyperplasia were a central scar with a visible feeding artery and homogenous contrast enhancement. Focal nodular hyperplasia is usually hypo- or isodense on unenhanced scans, hyperdense on arterial scans, and isodense on portal venous scans [1, 4, 7]. Hepatocellular adenoma typically shows no central scar, subcapsular feeding arteries, or inhomogeneous contrast enhancement [5, 6]. They often present as iso- or hyperdense on unenhanced scans, iso- or hypodense on arterial phase scans [7], and hyperdense on portal venous phase scans. All these features are easily visible in large lesions.
Smaller lesions are more difficult to assess qualitatively. In these cases, we found the quantitative analysis helpful. The quantitative evaluation of attenuation values in focal nodular hyperplasia and hepatocellular adenoma in the unenhanced scans did not show significant differences. In cases of hepatocellular adenoma, the unenhanced phase can show intralesional hemorrhage when attenuation values are equal to or more than 70 H.
For studies using a contrast agent, an appropriate tool to bypass the different cardiac output and blood flow in patients was used. The results of our measurements of aortic attenuation at the level of the celiac trunk indicated a mean value of 250 H during the arterial phase and 130 H during the portal venous phase. These values were used as standardizing factors. All measured attenuation values of the arterial and portal venous phases, respectively, in liver parenchyma and lesions were related to these values by the formula shown in Table 1.
During the arterial phase focal nodular hyperplasia enhanced significantly more, with a high mean attenuation value, than hepatocellular adenoma. This early enhancement of focal nodular hyperplasia seems to be exclusively caused by arterial vascularization in the lesion from a feeding artery in the central scar, an absent capillary bed, and a high a rate of centrifugal blood flow [14, 15]. Hepatocellular adenoma shows lower enhancement in the arterial phase probably because of the observed subcapsular feeding arteries and the centripetal blood flow. Between the arterial and portal venous phases we saw a high rate of enhancement of the liver and hepatocellular adenoma, whereas the mean attenuation of focal nodular hyperplasia remained equal.
A threshold of 1.6 for relative enhancement of the lesion in the arterial phase seems to be appropriate for differentiating focal nodular hyperplasia from hepatocellular adenoma with an accuracy of 96%. Most hepatocellular adenomas presented with a value less than 1.6, whereas all focal nodular hyperplasias exceeded this value.
For relative enhancement of the lesion in the portal venous phase no reasonable thresholds could be determined because of significant overlap.
In their qualitative evaluation, Choi and Freeny [16] described atypical features of focal nodular hyperplasia that cause problems in differentiating this lesion from other liver lesions. We also found some atypical features such as inhomogeneous enhancement or a missing central scar, but in all these cases of focal nodular hyperplasia we could find typical dynamic enhancement patterns.
Because scars may be subtle in smaller lesions, evaluation of the attenuation of scars was difficult in our study group. The structures are small, so we could not with certainty exclude the influences of partial volume effects on attenuation values. Attenuation measurements of the central arteries were also not possible.
The present study could not confirm the results of Doppler sonography reported by Uggowitzer et al. [14, 15] or the results of Miyayama et al. [17] of missing hyperfusion in small focal nodular hyperplasia. No significant difference in enhancement of small and large focal nodular hyperplasia was found. We also could not detect arteriovenous shunts, which, in a previous study [3], were proclaimed as possible causes of focal nodular hyperplasia. This question might be solved using the new multislice CT technique.
The results of this study are preliminary and need to be verified by additional studies performed with a larger numbers of lesions. We also did not analyze hepatocellular carcinoma and fibrolamellar carcinoma. This analysis will be an interesting challenge and we want to compare the qualitative and quantitative parameters of these malignant tumors with our results presented here in a future study. Another interesting future study might be the investigation of all these liver lesions on multislice helical CT.
In conclusion, triphasic helical CT combined with quantitative evaluation of attenuation measurement offers the possibility of detecting quantitative differences in liver lesions that are visually similar on CT. It is an appropriate diagnostic tool to use to differentiate focal nodular hyperplasia from hepatocellular adenoma. During the arterial phase, attenuation is significantly different between focal nodular hyperplasia and hepatocellular adenoma. If relative enhancement is greater than 1.6 in the arterial phase, then focal nodular hyperplasia is most probable. Otherwise, hepatocellular adenoma can be diagnosed with a high degree of accuracy.
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