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Gastrointestinal Imaging |
20-mm) Enhancing Lesions Seen Only during the Hepatic Arterial Phase at MR Imaging of the Cirrhotic Liver: Evaluation and Comparison with Whole Explanted Liver1
1 From the Departments of Radiology (A.E.H., E.M.H., W.Y.H., D.C.K., J.S.B., V.S.L., G.A.K.) and Pathology (A.B.W.), New York University Medical Center, New York, NY. Received August 6, 2004; revision requested October 12; revision received December 29; accepted February 1, 2005. Address correspondence to A.E.H., Department of Radiology, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, New York, NY 10021.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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20 mm in diameter) hepatic arterial phase–enhancing (HAPE) lesions that are occult during portal and/or equilibrium phases and at unenhanced T1- and T2-weighted magnetic resonance (MR) imaging and to determine the gross pathologic diagnosis with whole-liver explant comparison. MATERIALS AND METHODS: This retrospective study was approved by the institutional review board and compliant with HIPPA. Forty-six patients with cirrhosis who underwent MR imaging and transplantation within 90 days were evaluated with breath-hold T2-weighted and volumetric three-dimensional gadolinium-enhanced gradient-echo MR imaging in the hepatic arterial, portal venous, and equilibrium phases at 1.5 T. Three readers, who were blinded to the pathologic results, retrospectively reviewed the MR images in consensus for small HAPE nodules that were occult at T2-weighted and portal and/or equilibrium phase MR imaging. Only patients with nodules that enhanced during the arterial phase were included in the final study group, which included 16 patients (12 men and four women) aged 18–66 years (median age, 51.5 years). Explanted livers were serially sliced into 5–8-mm-thick sections to evaluate dysplastic nodules and hepatocellular carcinomas (HCCs). The Fisher exact test was performed to determine whether there was a relationship between HCC and the presence of a neoplastic HAPE-only lesion. The Mann-Whitney test was used to determine if patients with at least one neoplastic HAPE-only lesion had a larger number of non–HAPE-only lesions.
RESULTS: The 16 patients had 45 HAPE-only lesions; three (7%) of which were neoplastic, including one overt HCC, one HCC arising in a dysplastic nodule, and one dysplastic nodule. None of the remaining 42 HAPE-only lesions (93%) had correlative pathologic findings. All three neoplastic lesions seen only during the arterial phase were found in eight patients with concomitant HCC, who also had an additional 13 pathologically proved nonneoplastic HAPE-only lesions. In eight patients without HCC, none of the HAPE-only lesions were neoplastic. A concomitant non–HAPE-only neoplastic lesion was not a significant (P = .2) predictor for the presence of at least one neoplastic HAPE-only lesion. There was a preliminary but insignificant (P = .13) indication that the number of non–HAPE-only lesions tends to be higher in patients with neoplastic HAPE-only lesions.
CONCLUSION: The majority (93%) of HAPE-only lesions that are occult at T2-weighted and portal and/or equilibrium phase MR imaging are nonneoplastic, even in patients with pathologically proved HCC.
© RSNA, 2005
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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2 cm), dysplastic nodules, and multiacinar regenerative nodules (8–10) at unenhanced MR imaging, the diagnosis of HCC is often made when unequivocal arterial phase enhancement is present (especially when the lesion is iso- or hypointense relative to the liver at T2-weighted MR imaging). However, because some dysplastic nodules (11,12) and focal nodular hyperplasias (13,14) also enhance during the hepatic arterial phase, its presence is not specific for malignancy. In addition, arterial phase enhancement can be seen with hemangiomas, arterial-portal venous shunts, and aberrant venous drainage (15,16).
The importance and management of small (2 cm) hepatic arterial phase–enhancing (HAPE) lesions that are occult during the portal and/or equilibrium phase and at unenhanced T1- and T2-weighted imaging is unknown. Kanematsu et al (15) and Jeong et al (17) performed studies in which they specifically evaluated these lesions. Although in both studies a histopathologic diagnosis was proved for nodules that were suspicious for HCC, many lesions that were thought to be benign had no histopathologic confirmation, and their benign nature could only be assumed owing to the lack of growth at follow-up studies. Ideally, the use of whole explant pathologic correlation would help further characterize many of these lesions.
With the widespread use of higher-spatial-resolution (2–3-mm voxel size), arterial-phase, three-dimensional spoiled gradient-echo MR imaging, it is likely that more lesions seen only during the arterial phase will be encountered in patients with cirrhosis. An erroneous diagnosis of neoplasm may result in inappropriate treatment and/or an increase in the status of patients waiting for a cadaveric liver; conversely, a false diagnosis of benignity may have catastrophic results in patients who do not undergo routine surveillance imaging. Thus, the purpose of this study was to retrospectively assess the importance and imaging appearance of small (20 mm in diameter) nodules that enhance during the arterial phase but are occult during the portal and/or equilibrium phase and at unenhanced T1- and T2-weighted MR imaging (HAPE-only lesions) and to determine their pathologic diagnosis with whole-liver explant comparison.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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The entry criterion was the presence of small (20 mm in diameter) HAPE-only lesions. No HAPE-only lesions were identified in 30 of the 46 patients (65%). Consequently, our study population consisted of 16 patients (12 men and four women) with a median age of 51.5 years (age range, 18–66 years). The cause of cirrhosis was as follows: hepatitis C (n = 8), hepatitis B (n = 1), hepatitis C and B (n = 1), alcohol abuse (n = 2), hepatitis C and alcohol abuse (n = 1), autoimmune hepatitis (n = 1), and drug toxicity (n = 1). In one patient, the cause of cirrhosis was unknown.
Our retrospective study was based on an ongoing prospective lesion detection study, for which there was institutional review board approval; informed consent was obtained from all patients. Informed consent included permission for subsequent retrospective analysis. Our retrospective study was approved by the institutional review board and compliant with the Health Insurance Portability and Accountability Act.
MR Imaging Technique
Imaging was performed with one of three 1.5-T MR imaging systems (Magnetom Vision, Magnetom Vision Plus, or Symphony; Siemens Medical Systems, Erlangen, Germany) with a body phased-array coil. A 20–22-gauge intravenous catheter was inserted into an arm vein before MR imaging was performed.
In all patients, breath-hold T1-weighted spoiled gradient-echo images (fast low-angle shot) were obtained in the transverse plane with 130–220/4–5 (repetition time msec/echo time msec), a 70°–90° flip angle, 5–8-mm-thick sections, 0%–10% intersection gap, 128–192 x 256 matrix, and a rectangular field of view optimized to patient body habitus (with the largest dimension of 30–40 cm). This resulted in a 14–16-second breath hold for 20–26 sections. The same pulse sequence with similar parameters was then used out of phase (echo time, 2.1–2.5 msec). Subsequently, we performed a long echo train turbo short inversion time inversion-recovery (STIR) sequence with breath holding, 2530–5074/76 or 86 (effective echo time), a flip angle of 144°–180°, an echo train length of 33, an inversion time of 150–165 msec, 8-mm-thick sections, 2-mm intersection gap, 99–132 x 256 matrix, and a rectangular field of view optimized to patient body habitus (with the largest dimension of 30–40 cm). It was necessary to perform two interleaved breath-hold acquisitions with eight to 10 sections for sufficient anatomic coverage.
Finally, all patients were imaged by using a transverse volumetric three-dimensional fat-suppressed spoiled gradient-echo acquisition—the so-called volumetric interpolated breath-hold examination (VIBE) (19)—with 4.5/1.9, 12° flip angle, and bandwidth of 488 Hz per pixel. The section thickness ranged from 160 to 200 mm to ensure full coverage of the liver, and a rectangular field of view was used to allow for imaging during breath holding. The preinterpolation partition thickness and matrix were 4.0–4.4 mm and 160 x 160, respectively. Interpolation in the section-select direction yielded a partition thickness of 2.0–2.2 mm, with the matrix interpolated to 256 x 256; interpolation in the section-select direction yielded a partition thickness of 2–3 mm, with a matrix interpolated to 256 x 256. In the subset of five patients who were imaged with the Symphony (Siemens) system, a similar transverse volumetric three-dimensional fat-suppressed spoiled gradient-echo acquisition (also VIBE) was used with slightly different parameters, as follows: 3.3–3.6/1.4–1.6, 12° flip angle, and bandwidth of 490 Hz per pixel. The section thickness ranged from 160 to 200 mm to ensure full coverage of the liver, and a rectangular field of view was used to allow for imaging during breath holding. The preinterpolation partition thickness and matrix were 4.0–4.4 mm and 160 x 160, respectively. Interpolation in the section-select direction yielded a partition thickness of 2.0–2.2 mm, with the matrix interpolated to 256 x 256. In all patients, the VIBE sequence was performed without contrast material and was followed by an acquisition timed according to the data from a test bolus of gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ) with use of the circulation time as the first acquisition (hepatic arterial phase) delay time (20). This acquisition was then repeated twice at 45-second intervals for portal venous and equilibrium phase contrast material–enhanced MR images.
Image Analysis
As part of an ongoing lesion detection study, all MR images were retrospectively reviewed in consensus by three readers (E.M.H., W.Y.H., D.C.K.), all with 2 years of experience in liver MR imaging, by using a commercially available workstation and its software (Leonardo; Siemens Medical Systems). The readers were blinded to the results of pathologic examination. All lesions were recorded on liver maps, and the size of each lesion was measured. Because of the difficulty in determining enhancement of lesions that had high signal intensity at unenhanced T1-weighted MR imaging, the unenhanced data set was subtracted from the hepatic arterial phase acquisition (21).
Small (20 mm in diameter) nodules that demonstrated arterial phase enhancement but were occult on unenhanced T1-weighted, T2-weighted, and portal and/or equilibrium phase images were defined as HAPE-only lesions and measured in two dimensions by using electronic calibers. All other lesions that did not fulfill these criteria were defined as non–HAPE-only lesions.
One investigator (A.E.H.) with 3 years of experience in liver MR imaging, who did not participate in the lesion detection study or any of the prospective image interpretations, retrospectively recorded the morphologic characteristics (oval, which included round, or wedge shaped) of all HAPE-only lesions and the shortest distance from the HAPE-only lesion to the capsule of the liver by using the workstation.
Pathologic Analysis
The explanted livers were cut into 5–8-mm-thick contiguous slices in the transverse or coronal plane by one of two pathologists (A.B.W.), both with 15 years of experience in liver pathology. Dysplastic nodules and HCCs were identified 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 (22). The liver slices were photographed, and all lesions other than regenerative nodules were sampled for histologic examination.
With use of the diagnostic criteria of the International Working Party "Terminology of Nodular Hepatocellular Lesions" (22), the routine hematoxylin-eosin-stained sections from the nodules were classified as follows: regenerative nodule, low-grade dysplastic nodule, high-grade dysplastic nodule, small HCC (<2 cm), or HCC (>2 cm). There were no absolute size criteria, as described by the International Working Party, for diagnosis of a regenerative or dysplastic nodule or for differentiation of a regenerative nodule from a dysplastic nodule: A dysplastic nodule could be as small as 1 mm, and a regenerative nodule could be as large as 5 cm (22). Low-grade dysplastic nodules were defined as nodules showing normal architecture and cytology or diffuse large cell change. 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 body clustering. HCC was classified as well, moderately, or poorly differentiated depending on the component with the poorest differentiation.
In most cases, a radiologist was not present during the slicing of the explanted livers, and the MR images were retrospectively correlated with the gross pathologic descriptions as well as the gross photographs of all the liver slices.
Statistical Analysis
All statistical analyses were performed by a statistician (J.S.B.) by using software (SAS System for Windows version 9.0; SAS Institute, Cary, NC). Results were declared significant only if associated with a two-sided P value of less than .05. The Fisher exact test was performed to determine whether there is a relationship between the presence of at least one non–HAPE-only neoplastic mass (high-grade dysplastic nodule and/or HCC) and whether the patient had at least one HAPE-only neoplastic mass.
Patients with at least one neoplastic HAPE-only lesion were compared with those with no neoplastic HAPE-only lesions in terms of the number of non–HAPE-only lesions per patient, number of concomitant HCCs per patient, and maximum size of concomitant HCCs within each patient. Because of the small sample size (n = 16) and the skewed distribution of the data, these comparisons were performed with the Mann-Whitney test.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Eight of the 16 patients had 15 histologically proved HCCs, two of which (13%) were seen only during the hepatic arterial phase and were occult on unenhanced T1-weighted, T2-weighted, and portal and/or equilibrium phase images. These two HCCs, therefore, fulfilled the HAPE-only criteria. In these eight patients, in addition to the two HAPE-only HCCs, one HAPE-only high-grade dysplastic nodule was found at pathologic examination. These eight patients had a total of 16 HAPE-only lesions. Only three of the 16 HAPE-only lesions were neoplastic, including the two HCCs and one high-grade dysplastic nodule; for the remaining 13 of 16 HAPE-only lesions (81%), there were no correlative findings at pathologic examination of the explanted livers.
Twenty-nine HAPE-only lesions were seen in the eight patients without HCC; at histopathologic examination of the explanted livers, no correlative lesions other than normal background regenerative nodules were found. Hence, neoplastic HAPE-only lesions were found only in patients with concomitant HCC. Table 3 demonstrates the sizes and pathologic diagnoses of all lesions found in the eight patients with HAPE-only lesions and concomitant HCC. With use of the Fisher exact test, the presence of a concomitant neoplastic non–HAPE-only lesion (dysplastic nodule and/or HCC) was not a statistically significant predictor of the presence of at least one HAPE-only lesion being neoplastic (P = .2).
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No relationship was found between the maximum size or the number of concomitant HCCs and the presence of a neoplastic HAPE-only mass.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Although many HCCs demonstrate arterial phase enhancement and moderate T2 hyperintensity (1–7), some small HCCs are seen only during the hepatic arterial phase (3,6–9,17,27,28). This poses a diagnostic dilemma, and three studies were published in which the clinical importance of such lesions was evaluated (15,17,29).
In our study, the prevalence of HAPE-only lesions in patients with severe cirrhosis before transplantation was 35% (16 of 46 patients). Only three of the 45 HAPE-only lesions (7%) were neoplastic (two HCCs and one high-grade dysplastic nodule); the majority of HAPE-only lesions (42 of 45 [93%]) had no correlative pathologic findings, were benign, and may have represented regenerative nodules or arterial-portal venous shunts. Furthermore, two of the 15 histologically proved HCCs (13%) were HAPE-only lesions. Our findings are similar to those of Jeong et al (17), who evaluated 68 hepatic nodules smaller than 2 cm that were seen only during the hepatic arterial phase in patients with cirrhosis. In their series, nine of 68 lesions (13%) were HCCs; 59 (87%) of the HAPE-only lesions were benign.
In our study, 28 of the 42 benign HAPE-only lesions (67%) were oval and 14 (33%) were wedge shaped; the three neoplastic HAPE-only lesions were oval. Kanematsu et al (15) reported similar findings about the morphologic characteristics of benign early enhancing lesions by using two-dimensional gradient-echo MR imaging; in their series, most lesions (54%) were round.
Tsuchiyama et al (29) retrospectively evaluated tiny staining spots at computed tomography (CT)–assisted hepatic angiography in patients with hepatitis C. Histopathologic confirmation of the diagnosis was present for only one of the 80 tiny staining spots; the remaining lesions were followed-up with serial imaging. Lesions that grew were considered to be suspicious for HCC. The authors concluded that tiny staining spots in patients without primary HCC were unlikely to be HCC and those in patients with primary HCC had a comparatively high possibility of being HCC. Although all three neoplastic HAPE-only lesions in our study were found in patients with concomitant HCC, these patients were also found to have 13 HAPE-only lesions for which there were no correlative neoplastic findings at pathologic examination.
Furthermore, Tsuchiyama et al (29) found no substantial differences with respect to size, position, and morphologic characteristics between lesions that were deemed suspicious for HCC and those that were not. This result is in concordance with our findings because we found no relationship between the maximum size of a HAPE-only lesion and a histologic diagnosis of HCC or dysplastic nodule.
There are a number of explanations for the fact that some early enhancing lesions smaller than 2 cm were not seen at T2-weighted imaging. Some investigators (9) have raised the possibility that artifacts from ascites or breathing may be a reason for nonvisualization of lesions. In our study, however, T2-weighted MR imaging was performed during breath holding, and readers believed the image quality was diagnostically adequate.
A possible explanation for nonvisualization of lesions on T2-weighted images in our study may be the discrepancy in section thickness between the contrast-enhanced three-dimensional images and the T2-weighted images. The interpolated section thickness of the three-dimensional MR images was approximately 2–3 mm, which is thinner than the 8-mm-thick sections used for T2-weighted images.
In our study, we demonstrated a preliminary but insignificant (P = .13) indication that the number of non–HAPE-only lesions tends to be higher in patients with neoplastic HAPE-only lesions. This would mean that the number of non–HAPE-only masses a patient has may possibly be used as a predictor of whether the patient has at least one HAPE-only lesion that is either a dysplastic nodule or HCC. The three patients with one neoplastic HAPE-only lesion had an average (and median) of four non–HAPE-only lesions.
Although we found that the presence of a concomitant HCC (non–HAPE-only) nodule was not a statistically significant predictor for a HAPE-only lesion being neoplastic, all three patients with neoplastic HAPE-only lesions had at least one concomitant HCC. Hence, there may be a trend that patients with a neoplastic HAPE-only mass also have at least one concomitant HCC (non–HAPE-only) mass.
Although we hypothesize that there may be a trend that neoplastic HAPE-only lesions are preferentially found in patients with concomitant HCC, it should be noted that in our study we did not find a way to differentiate neoplastic HAPE-only lesions from nonneoplastic HAPE-only lesions. The ability to definitively characterize these multiple lesions in patients with HCC before therapy is crucial to avoid the ablation of benign lesions and the performance of transplantation in patients who may not meet the strict criteria of Mazzaferro et al (30).
Although we evaluated HAPE-only lesions, the value of T2-weighted MR imaging in the diagnosis of HCC has recently been questioned. Hussain et al (9) demonstrated that T2-weighted MR imaging has limited value in the detection and characterization of nodular lesions in the cirrhotic liver because of reduced lesion conspicuity and the overlap in signal intensity characteristics between benign and malignant nodules.
Our study has recognized limitations, including its retrospective design and small number of patients. Although an effort was made to match the in vivo MR images with the whole explanted livers, precise lesion-by-lesion correlation was extremely difficult owing to variations in size and position of the organ in situ and after explantation. It is possible that some of the HAPE-only lesions were focal nodular hyperplasias, as described in the literature (13,14). Finally, because we did not perform digital subtraction angiography, CT-assisted hepatic angiography, or CT portography, we could not definitively diagnose arterial-portal venous shunts or aberrant venous drainage as a cause of nonneoplastic HAPE-only lesions. This is important because authors of a previous CT report with explant correlation claimed that regenerative nodules were a common cause of HAPE-only lesions (31); however, because regenerative nodules do not have an arterial blood supply and arterial-portal venous shunt creation and/or aberrant venous drainage cannot be seen in explanted liver specimens, we believe this statement may be incorrect.
In conclusion, we believe our study is the first to provide explant correlation for HAPE-only lesions seen at thin-section gadolinium-enhanced three-dimensional MR imaging. With use of this technique, the prevalence of HAPE-only lesions in a pretransplantation cohort with severe cirrhosis was 35% (16 of 46 patients). The majority (93%) of HAPE-only lesions were nonneoplastic, even in patients with pathologically proved HCC. In patients without HCC, all HAPE-only lesions were benign. There was also no relationship between the maximum size or number of concomitant HCCs and a histologic diagnosis of HCC in HAPE-only lesions. Finally, there may be a trend that neoplastic HAPE-only lesions are preferentially found in patients with concomitant HCC. Further studies are needed to determine the optimal imaging interval in patients with cirrhosis and HAPE-only lesions.
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FOOTNOTES |
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Abbreviations: HAPE = hepatic arterial phase enhancing • HCC = hepatocellular carcinoma • STIR = short inversion time inversion recovery • VIBE = volumetric interpolated breath-hold examination
2 Current address: Department of Radiology, Georgetown University Hospital, Washington, DC 
3 Current address: East River Medical Imaging, New York, NY
Authors stated no financial relationship to disclose.
Author contributions: Guarantor of integrity of entire study, A.E.H.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; approval of final version of submitted manuscript, all authors; literature research, A.E.H.; clinical studies, A.E.H., E.M.H., W.Y.H., D.C.K., V.S.L., A.B.W., G.A.K.; statistical analysis, A.E.H., J.S.B.; and manuscript editing, A.E.H., E.M.H., W.Y.H., D.C.K., A.B.W., G.A.K.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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