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1 Both authors: Department of Radiology, NYU Medical Center, 530 First Ave., Basement Schwartz Bldg., New York, NY 10016.
Received June 17, 2002;
accepted after revision September 10, 2002.
Address correspondence to G. A. Krinsky.
Abstract
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MATERIALS AND METHODS. Two observers retrospectively evaluated in-phase (4–5 msec), opposed-phase gradient-echo (2.0–2.4 msec), and turbo short tau inversion recovery (STIR) MR images in 68 patients with cirrhosis—but without dysplastic nodules or hepatocellular carcinoma—who underwent MR imaging at 1.5 T within 150 days before liver transplantation. The size, number, signal characteristics, and arterial enhancement pattern of nodules that appear hyperintense on T1-weighted gradient-echo images were evaluated as well as the presence or absence of signal loss on opposed-phase imaging. These imaging findings were correlated with pathologic findings of whole explanted livers.
RESULTS. Eleven (16%) of 68 patients had at least one nondysplastic nodule that was hyperintense on T1-weighted MR imaging. Three patients had diffuse nondysplastic hyperintense nodules (>10 nodules) measuring less than 0.5 cm, and the remaining eight patients had 22 nondysplastic hyperintense nodules ranging in size from 0.5 to 2.5 cm (mean, 1.2 cm), of which 13 were isointense and nine were hypointense on turbo STIR images. No lesion lost signal on opposed-phase imaging or enhanced during the hepatic arterial phase.
CONCLUSION. In cirrhotic patients undergoing liver transplantation, nondysplastic nodules that are hyperintense are common findings on T1-weighted gradient-echo MR imaging and do not lose signal intensity on opposed-phase imaging or enhance during the hepatic arterial phase. These nodules may be indistinguishable from dysplastic nodules.
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In a recent review article, the authors stated that "it is probably appropriate to consider hyperintense regenerative nodules to be dysplastic" [4]. We have recognized many hyperintense nodules on T1-weighted gradient-echo imaging that ultimately have proven to be regenerative—not dysplastic. Therefore, the purpose of this study was to determine the frequency with which nodules appear hyperintense on T1-weighted gradient-echo imaging that are not dysplastic (nondysplastic) in a large cirrhotic population with whole-liver explant correlation. In addition, we sought to determine whether T1-weighted hyperintensity is caused by steatosis by comparing the signal intensity of these nodules on in- and opposed-phase imaging. Finally, we evaluated dynamic gadolinium-enhanced MR imaging to determine whether nondysplastic nodules that are hyperintense on T1-weighted gradient-echo imaging enhance during the hepatic arterial phase.
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The cause of cirrhosis in these 68 patients was as follows: hepatitis C
(n = 20 patients [nine with concomitant ethanol abuse]; ethanol abuse
(n = 12); primary sclerosing cholangitis (n = 11);
cryptogenic (n = 7); hepatitis B (n = 6); autoimmune
(n = 5); and hepatitis C and primary biliary cirrhosis, hepatitis B
and ethanol abuse, hepatitis B and C, 
1-antitrypsin
deficiency, Wilson's disease, hemochromatosis, and Budd-Chiari syndrome (one
patient each). Institutional review board approval and patient informed
consent were obtained for this study.
MR Imaging Technique
All patients underwent MR imaging in a 1.5-T system (Magnetom Vision;
Siemens, Erlangen, Germany) with high-performance gradients (25-mT/m maximum
gradient strength and 600-msec rise time) and a torso phased array
multicoil.
After a three-plane localizer was used, all patients underwent axial T1-weighted spoiled gradient-echo fast low-angle shot imaging during breath-holding with a TR range/TE range of 130–220/4–5, a slice thickness of 5–8 mm, an interslice gap of 0–10%, a matrix of 128–192 x 256, and a rectangular field of view optimized for each patient's body habitus with the largest dimension of 30–40 cm. This pulse sequence resulted in a 14- to 26-sec breath-hold for 20–26 slices. The same pulse sequence with similar parameters was then performed out-of-phase (TE range, 2.1–2.5 msec).
All patients underwent turbo short tau inversion recovery (turbo STIR) MR imaging during breath-holding. The sequence was performed with the following parameters: TR range/effective TE of 4000–5500/58 or 76, a flip angle of 160–180°, an echo-train length of 33, an inversion time of 150–165 msec, a slice thickness of 8 mm, and an interslice gap of 2 mm. This pulse sequence required two noninterleaved breathhold acquisitions with 8–10 slices for sufficient anatomic coverage. The matrix and field of view were similar to those used for the previously described T1-weighted sequence.
All patients underwent dynamic gadolinium-enhanced MR imaging using a two- or three-dimensional gradient-echo technique in the hepatic arterial, portal venous, and equilibrium phases after IV administration of 19 mL of gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ) at a rate of 2 mL/sec using an MR imaging–compatible power injector (Spectris; MedRad, Pittsburgh, PA). For the purpose of this study, only the dynamic hepatic arterial phase images of patients with hyperintense nodules on T1-weighted gradient-echo imaging were evaluated.
Image Analysis
By consensus, two observers retrospectively evaluated hard-copy images of
both in- and opposed-phase T1-weighted gradient-echo MR images to determine
the number and size of hyperintense nodules. Each hyperintense lesion was
measured with calipers. Using the spleen as a reference, the observers
determined qualitatively whether a lesion that appeared hyperintense on
in-phase imaging lost signal on opposed-phase imaging. Turbo STIR images were
evaluated to determine whether the lesions that were hyperintense on
T1-weighted images were hypo-, iso-, or hyperintense. To facilitate detection
of arterial enhancement of lesions that were hyperintense on unenhanced MR
imaging, we used a subtraction technique.
Pathologic Analysis
Explanted livers were sectioned sequentially by one of two pathologists at
5- to 8-mm intervals in either the axial or coronal plane. Dysplastic nodules
and hepatocellular carcinoma nodules were identified grossly as those that
were distinct from surrounding regenerative nodules in terms of size, texture,
color, or degree of bulging beyond the cut surface of the liver
[6]. All livers were
photographed, and all distinctive nodules were sampled.
Using the diagnostic criteria established by the International Working
Party on the Terminology of Nodular Hepatocellular Lesions
[6], the observers classified
the nodules as regenerative nodules (which could be as large as 5 cm);
low-grade dysplastic nodules; high-grade dysplastic nodules; small
hepatocellular carcinomas (
2 cm); or hepatocellular carcinomas (>2 cm).
Low-grade dysplastic nodules were defined as nodules showing normal
architecture and cytology or diffuse large cell change
[6]. High-grade dysplastic
nodules were defined on the basis of the presence of one of the following:
diffuse small cell change, pseudogland formation, nodule-in-nodule lesions
with small cell dysplasia, iron resistance in siderotic nodules, fatty change,
clear cell change, or Mallory's bodies clustering
[6].
Radiologic–pathologic correlation was performed at gross (including photomicrographs of sliced livers) and microscopic examinations and ex vivo MR imaging (n = 23 patients) using a technique previously described [7].
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Imaging
Eleven (16%) of 68 patients had at least one hyperintense nondysplastic
nodule on T1-weighted gradient-echo MR imaging (Figs.
1A,
1B,
1C,
1D,
1E and
2A,
2B,
2C). The cause or causes of
cirrhosis, size of the largest nodule, and number of nodules for these 11
patients are presented in Table
1. Three patients had diffuse hyperintense nodules (>10
nodules) measuring less than 0.5 cm. The remaining eight patients had 22
hyperintense nodules ranging in size from 0.5 to 2.5 cm (mean, 1.2 cm). Of the
22 countable lesions in these eight patients, 13 were isointense and nine were
hypointense relative to the background liver on turbo STIR images. None of the
lesions enhanced during the hepatic arterial phase. Eight (73%) of 11 patients
with hyperintense nondysplastic nodules had viral cirrhosis; of these eight
patients, three had concomitant ethanol abuse.
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No signal loss was identified in any of the hyperintense lesions on opposed-phase imaging. In addition, no areas of steatosis were identified in the explanted livers of the patients with hyperintense nodules on T1-weighted gradient-echo imaging.
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Although the one patient in our study who had cirrhosis due to Budd-Chiari syndrome had no focal nodules, distinguishing the nodules seen in this syndrome [14, 15, 16] from those that result from ordinary cirrhosis is important. Both causes of cirrhosis may result in regenerative nodules that are hyperintense on T1-weighted gradient-echo images [14, 15, 16], but the regenerative nodules seen in cirrhosis due to Budd-Chiari syndrome may have a central scar, enhance during the hepatic arterial phase, and resemble focal nodular hyperplasia lesions at pathologic analysis [14, 15, 16].
The detection of dysplastic nodules is made by the pathologist on gross examination, whereas the distinction between low- and high-grade dysplastic nodules is based on microscopic findings. At gross examination, dysplastic nodules are distinct from surrounding regenerative nodules in terms of size, texture, color, or degree of bulging beyond the cut surface of the liver [6]. However, no definite size criterion exists to distinguish dysplastic nodules from regenerative nodules: both may be as small as 0.1 cm or as large as 5.0 cm [6].
Our study confirms that nondysplastic nodules that are hyperintense on T1-weighted gradient-echo MR imaging may have MR imaging characteristics identical to those of dysplastic nodules, according to the MR imaging literature [7, 17], and that these nodules are also commonly seen in explanted cirrhotic livers (16% in this study). None of the hyperintense nodules in our study exhibited enhancement during the hepatic arterial phase. This finding is consistent with those of a previous study in which researchers found that regenerative nodules have a blood supply exclusively from the portal vein [18]. Previous pathology studies have shown that high-grade dysplastic nodules have a greater number of so-called unpaired or nontriadal arteries than background regenerative nodules [19, 20] and dysplastic nodules may exhibit arterial phase enhancement on CT or MR imaging [21]. However, most dysplastic nodules, especially low-grade ones, do not exhibit arterial phase enhancement. Therefore, the MR imaging findings of a nodule that is hyperintense on T1-weighted and hypo- or isointense on T2-weighted images and that does not exhibit arterial phase enhancement cannot be definitively characterized as a dysplastic nodule before biopsy, resection, or transplantation.
The pathologic substrate that makes some nondysplastic nodules hyperintense on T1-weighted gradient-echo images has not been identified. A similar conundrum has been described for dysplastic nodules and hepatocellular carcinomas that are hyperintense on T1-weighted images. Although the cause of the hyperintensity is not the presence of lipid, the cause may be related to an increased amount of copper with respect to the background liver parenchyma [22].
This study has recognized limitations including a retrospective design and
the use of consensus interpretations. In addition, we excluded 52 patients
with hepatocellular carcinoma, dysplastic nodules, or both. Because MR imaging
is insensitive for the diagnosis of small hepatocellular carcinomas and
dysplastic nodules (2 cm)
[5,
23], our goal was to be
certain that a hyperintense nodule seen on T1-weighted gradient-echo images
was neither a hepatocellular carcinoma nor a dysplastic nodule. Even after the
exclusion of these 52 patients, viral and ethanol-induced cirrhosis still
accounted for the cause of cirrhosis in most of the patients in this series
(41/68 [60%]) who are typical of a transplantation population in North
America. We also used the term "nondysplastic nodule" instead of
the specific histologic term "hyperintense regenerative nodule."
This term was chosen because our pathologists could not distinguish the
hyperintense nodules detected on MR imaging from the background regenerative
nodules, thus making it impossible to achieve histologic correlation on a
nodule-by-nodule basis.
Although no visual signal loss was detected on opposed-phase imaging of the hyperintense nodules, small amounts of fat could have been present but not sampled by the pathologist. This possibility exists because if a pathologist does not find a lesion that looks suspicious (dysplastic nodule or hepatocellular carcinoma) at gross examination of the liver, only random samples are obtained from each lobe for pathologic analysis. Finally, we did not perform quantitative comparisons of the signal intensity of the hyperintense nodules on in-phase imaging versus opposed-phase imaging; however, previous work on adrenal adenomas has shown visual inspection to be as accurate as quantitative measurements [24, 25].
In conclusion, in cirrhotic patients undergoing liver transplantation, nondysplastic nodules that are hyperintense on T1-weighted gradient-echo MR imaging are common findings, do not lose signal on opposed-phase imaging, do not enhance during the hepatic arterial phase, and may be indistinguishable from dysplastic nodules.
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