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Gastrointestinal Imaging |
1 From the Departments of Radiology (G.A.K., V.S.L., J.C.W., N.M.R.), Pathology (N.D.T.), and Transplant Surgery (T.D., L.W.T.,) and the Kaplan Comprehensive Cancer Center (G.A.K.), New York University Medical Center, 530 First Ave, New York, NY 10016. Received August 14, 2000; revision requested September 20; revision received October 4; accepted November 9. Supported by an RSNA Research Grant and an award from the Society of Computed Tomography and Magnetic Resonance. Address correspondence to G.A.K. (e-mail: glenn.krinsky@med.nyu.edu)
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Seventy-one patients without a known history of HCC who underwent MR imaging and subsequent transplantation within 90 days were examined. Breath-hold turbo short inversion time inversion-recovery and/or T2-weighted turbo spin-echo MR images were obtained. Dynamic two- or three-dimensional gadolinium-enhanced gradient-echo MR images were obtained in the hepatic arterial, portal venous, and equilibrium phases. Prospective MR image interpretations were compared directly with explanted liver pathologic results.
RESULTS: Eleven (15%) of 71 patients had hepatic malignancies; MR imaging enabled diagnosis of tumor in six (54%) of 11 patients. On a lesion-by-lesion basis, MR imaging depicted 11 of 20 hepatic neoplasms, for an overall sensitivity of 55%. MR imaging depicted four (80%) of five lesions larger than 2 cm, six (50%) of 12 lesions 1–2 cm, and one (33%) of three lesions smaller than 1 cm. MR imaging depicted only nine (15%) of 59 DNs. The specificities of MR imaging for detection of HCC and DNs on a per patient basis were 60 (86%) of 70 patients and 53 (85%) of 62 patients, respectively.
CONCLUSION: MR imaging is insensitive for the diagnosis of small (<2-cm) HCCs and DNs.
Index terms: Liver, cirrhosis, 761.794 • Liver, nodules, 761.3198 • Liver, transplantation, 761.459 • Liver neoplasms, 761.31, 761.321, 761.323 • Liver neoplasms, MR, 761.121411, 761.121412, 761.121413, 761.121415, 761.12143
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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3 cm). It is therefore critical to detect nodules that contain HCC at an early stage both to control tumor burden while awaiting transplantation and to distinguish those patients who may have favorable long-term results with transplantation from those who will not, because cadaveric organs are in short supply.
The magnetic resonance (MR) imaging literature is limited by its lack of complete correlation between pathologic and imaging findings. Most published studies have relied on biopsy or surgical resection specimens to evaluate the accuracy of imaging detection and characterization of cirrhotic nodules, with the resulting bias being toward the positive studies. In addition, in many studies the diagnosis of HCC is known prior to MR imaging and is based on the results of other radiologic studies or markedly elevated 
-fetoprotein levels; these factors further compound the bias. Finally, many earlier MR studies involved imaging strategies that are no longer considered state of the art—for example, conventional T1- and T2-weighted spin-echo imaging performed with a body coil and without dynamic contrast material enhancement. It is now well established that imaging of the cirrhotic liver during the hepatic arterial phase (HAP) with computed tomography (CT) or MR increases the diagnostic yield for HCC (6–12), and, in some cases, tumors are seen only during this phase (9–12).
The purpose of our study was to assess the diagnostic sensitivity and specificity of state-of-the-art MR imaging of HCC and dysplastic nodules in the cirrhotic liver, by using thin-section whole-explant correlation following transplantation, in patients in whom the diagnosis of HCC was not known before imaging.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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The causes of cirrhosis in the 71 patients are listed in Table 1. All patients, except those with primary sclerosing cholangitis, had Child-Pugh class B or C cirrhosis. Eight patients had transjugular intrahepatic portosystemic shunts at the time of MR imaging. Institutional review board approval was obtained for this study, and informed consent was obtained from all patients. During the same 52-month study period, 41 patients with HCC who were deemed poor candidates for transplantation on the basis of excessive tumor burden diagnosed at MR imaging, advanced age, and/or substantial comorbid disease were treated with palliative care.
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In all patients, T1-weighted breath-hold spoiled gradient-echo fast low-angle shot (FLASH) images were acquired in the transverse plane with 130–220/4–5 (repetition time msec/echo time msec), a 70°–90° flip angle, a 5–8-mm section thickness, a 0%–10% intersection gap, a 128–192 x 256 matrix, and a rectangular field of view optimized to the patient’s body habitus, with the largest dimension of 30–40 cm. This resulted in a 14–26-second breath hold for 20–26 sections. The same pulse sequence with similar parameters was then performed out of phase (echo time, 2.1–2.5 msec). In five patients, image quality was poor because of the patient’s inability to follow commands or suspend respiration. Therefore, a breath-hold–independent sequence involving magnetization-prepared T1-weighted spoiled gradient-echo imaging—that is, turbo fast low-angle shot (turbo FLASH) (11.0/4.2, 300-msec inversion time, 15° flip angle)— was used. This sequence was then performed out of phase with an echo time of 2.2 msec. The imaging parameters and voxel size were similar to those used in the breath-hold spoiled gradient-echo FLASH sequence.
In 69 of 71 patients, a breath-hold echo train turbo short inversion time inversion-recovery (STIR) sequence (4,000–5,500/58 or 76 [effective], 150–165-msec inversion time, 150°–180° flip angle, echo train length of 33) was performed with an 8-mm section thickness and 2-mm intersection gap. This required two noninterleaved breath-hold acquisitions with 8–10 sections for sufficient anatomic coverage. The matrix and field of view were similar to those used to acquire the previously described T1-weighted images.
In the first 32 patients and in those who were unable to suspend respiration, a T2-weighted echo train turbo spin-echo sequence (3,600–6,000/99 [effective], 180° flip angle, echo train length of 11) was performed in the transverse plane with an 8-mm section thickness, a 2-mm intersection gap, three signals acquired, and a similar matrix and field of view.
All patients underwent dynamic gadolinium-enhanced MR imaging in the HAP, portal venous phase, and equilibrium phase after intravenous administration of 19 mL of gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ) at a rate of 2 mL/sec by means of hand injection (n = 4) or an MR-compatible power injector (Spectris; MedRad, Pittsburgh, Pa) (n = 67). In addition, patients with primary sclerosing cholangitis underwent delayed imaging (10–15 minutes). A test dose of 0.5 or 1.0 mL of gadopentetate dimeglumine with transverse turbo FLASH imaging was performed to optimize HAP imaging in 67 patients (14). The time delay between the start of the injection and the start of the HAP acquisition ranged from 8–24 seconds. In the first 36 patients who were capable of breath holding, the previously described in-phase spoiled gradient-echo FLASH sequence also was performed with dynamic gadolinium-enhanced imaging.
In the first four of the 71 patients, imaging began 20 seconds after initiation of contrast material administration and was repeated at 50 and 110 seconds. In the remaining 67 patients, the first acquisition was timed according to the data from the test bolus, and an additional three or four breath-hold acquisitions were spaced 35–45 seconds apart. This allowed the patient at least 10–15 seconds of free breathing between breath holds. The second acquisition encompassed the portal venous phase, and the last acquisition was considered the equilibrium phase study. Breath holding was routinely performed at end expiration to facilitate subtraction imaging.
In five patients who were unable to suspend respiration, dynamic turbo FLASH imaging (11.0/4.2, 300-msec inversion time, 15° flip angle) was performed similarly to FLASH imaging, with five consecutive contrast material–enhanced acquisitions.
In the remaining 30 patients who were capable of breath holding, transverse three-dimensional fat-suppressed spoiled gradient-echo imaging (4.2/1.8, 12° flip angle, bandwidth of 488 Hz per pixel) was performed. The section thickness ranged from 160 to 200 mm to ensure full coverage of the liver, and interpolation in the section-select direction yielded a partition thickness of 2–3 mm with a matrix interpolated to 256 x 256. Nonenhanced acquisition was performed first, followed by an acquisition timed according to the data from the test bolus. The acquisition was then repeated twice at 45-second intervals for portal venous and equilibrium phase imaging.
Finally, in 67 patients, a flow-sensitive breath-hold gradient-echo sequence (20–200/9–20, 20°–45° flip angle) was performed, first with selective presaturation above and then with presaturation below the imaging sections to assess the patency and direction of portal venous flow. The voxel size was similar to that in the T1-weighted gradient-echo pulse sequence, but only four sections per breath hold were acquired. All patients were able to complete the examinations without untoward side effects, and all studies were of diagnostic quality.
Image Interpretation
The MR studies were prospectively reviewed in consensus by one of three attending radiologists (N.M.R., G.A.K., V.S.L.) and two fellows by using film hard-copy images from all the available pulse sequences described. The three-dimensional T1-weighted data sets—both nonenhanced and three-phase gadolinium enhanced—were evaluated at a commercially available workstation (Siemens Medical Systems). Because of the difficulty in determining the enhancement of lesions that are hyperintense on nonenhanced T1-weighted images, this data set was subtracted from the HAP acquisition. This facilitated the qualitative recognition of lesion enhancement (15). Quantitative measurements of enhancement were not performed.
The criteria for malignancy were as follows: a mass demonstrating homogeneous, heterogeneous, or ring enhancement during the HAP (excluding the classic peripheral, transient hepatic signal intensity difference [16–19]) and/or moderate hyperintensity on T2-weighted turbo spin-echo and/or turbo STIR images. Lesions that were markedly hyperintense on T2-weighted turbo spin-echo and/or turbo STIR images and not enhancing after contrast material administration were considered to be cysts, and hemangiomas were diagnosed on the basis of previously described enhancement patterns (20).
Nodules that were hyperintense and substantially larger than the background regenerative nodules at T1-weighted pulse sequences but did not demonstrate arterial phase enhancement or T2 hyperintensity were considered to be dysplastic (21,22). All other nodules were presumed to be regenerative. The size, signal intensity characteristics, enhancement patterns, lesion locations, and diagnoses were recorded in a database and in the dictated clinical report.
Pathologic Analysis
One of two pathologists (N.D.T.) cut the explanted livers sequentially into 5–8-mm sections that corresponded as closely as possible to the MR imaging planes. Dysplastic and HCC nodules were identified grossly as those that were distinct from the surrounding regenerative nodules in terms of size, texture, color, and/or degree of bulging beyond the cut surface of the liver (23). All livers were photographed, and all lesions other than ordinary regenerative nodules were sampled.
By using the diagnostic criteria from the International Working Party’s "Terminology of Nodular Hepatocellular Lesions" (23), nodules were classified as follows: regenerative nodule, dysplastic nodule-low grade, dysplastic nodule-high grade, small HCC (<2 cm), or HCC (>2 cm). There were no absolute size criteria, as described by the International Working Party, to diagnose or distinguish regenerative nodules from dysplastic nodules; a dysplastic nodule could be as small as 1 mm, and a regenerative nodule could be as large as 5 cm (23). Low-grade dysplastic nodules were defined as those showing normal architecture and cytologic features or diffuse large cell changes (23). High-grade dysplastic nodules were defined on the basis of the presence of one of the following: diffuse small cell changes, pseudogland formation, nodule-in-nodule lesions with small cell dysplasia, iron resistance in siderotic nodules, fatty change, clear cell change, or Mallory body clustering (23). HCCs were classified as well, moderately, or poorly differentiated.
Statistical Analyses
A two-tailed Student t test was performed to compare the size differences between HCCs detected and HCCs not seen and the size differences between dysplastic nodules detected and dysplastic nodules not seen. A P value of less than .05 was used to define statistical significance.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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In the subset of 30 patients who underwent thin-section (2–3-mm) three-dimensional fat-suppressed T1-weighted imaging, both with and without contrast material, only two patients had hepatic neoplasms—cholangiocarcinoma (Fig 1) in one patient and HCC in the other—and both were detected prospectively by using MR imaging.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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The sensitivity for the detection of hepatic malignancies (55%) that we achieved is comparable also to those in two explantation studies involving the use of CT after intraarterial administration of iodized oil: The sensitivities were 53% (30) and 58% (31), which are slightly lower than the 68% sensitivity achieved in a nonhelical contrast-enhanced CT study (32) with 200 consecutive patients who underwent transplantation. In a more recent explantation study (33) involving three-phase helical CT, a sensitivity of 71% for HCC detection was reported. However, compared with our study, in most prior explantation studies, the diagnosis of HCC was known or clinically suspected in some patients.
Baron and Oliver (34) screened 1,000 patients with cirrhosis and without known HCC, 195 of whom underwent transplantation, by using predominantly dual-phase helical CT. HCC was present in 32 (16%) of 195 patients and detected in 19 (59%) of the 32 patients. These data are similar to those in our study and representative of findings in a population of patients with late-stage cirrhosis who undergo transplantation. However, on a lesion-by-lesion basis, CT depicted only 23 (36%) of 63 HCCs in the study by Baron and Oliver (34). The poor sensitivity was likely due in part to the fact that 52 (82%) of the 63 HCCs were 2 cm or smaller. Detection of these lesions is of great clinical importance, because the tumor doubling time can be as short as 90 days (13) and the wait for a cadaveric liver can be as long as 2 years. Therefore, if a 2-cm HCC is not detected and the patient undergoes imaging on a yearly basis, there is a possibility that the lesion may be 8 cm by the time it is diagnosed; this size may preclude transplantation at some centers. The detection of small HCCs and subsequent nonsurgical treatment may control the tumor burden while the patient awaits cadaveric or living donor liver transplantation.
The results of previous MR imaging studies (7–9,12,24,25) have demonstrated the importance of imaging during the HAP, especially for detection of small HCCs, because these may be occult at other pulse sequences and on portal venous and equilibrium phase images. Our study results confirm these findings: Eight HCCs demonstrated uniform enhancement during the arterial phase; one (0.7 cm) of these lesions was seen during only the HAP (Fig 2). To optimize HAP imaging, we performed a test bolus examination in 67 patients, because in some patients, empiric delays can result in suboptimal studies owing to variations in circulation times (14).
In our study, a large number of cases (15 lesions in 10 patients) were false-positive for neoplasm. Three patients had four regions of poorly marginated confluent hepatic fibrosis that could not be confidently distinguished from infiltrative neoplasms. In a large CT explantation study, Miller et al (32) reported similar problems in distinguishing confluent hepatic fibrosis from infiltrative neoplasms. In that study, only two of the 10 ill-defined infiltrating lesions were due to neoplasms. Although the MR imaging features of confluent hepatic fibrosis have been established (35), there remains substantial overlap in the signal intensity and enhancement characteristics of confluent hepatic fibrosis, as compared with infiltrative neoplasm, so a definitive diagnosis of fibrosis may be difficult in many cases. One of the two true-positive infiltrating neoplasms demonstrated irregular ring enhancement, and the other encased the portal vein and inferior vena cava.
Four high-grade dysplastic nodules were detected but incorrectly diagnosed as HCC owing to the presence of arterial phase enhancement. This finding confirms that in a previous case report (36)—that is, these lesions can demonstrate arterial phase enhancement at MR imaging and CT—and thus provides further support that criteria other than arterial phase enhancement should be used to distinguish dysplastic nodules from small HCCs. In the remaining seven lesions that were false-positive for malignant neoplasms at MR imaging, no pathologic diagnosis could be obtained despite meticulous correlation of the findings of MR imaging and pathologic analysis of the explanted specimens. Four of these lesions were seen during only the HAP and appeared as well-circumscribed masses measuring 0.5–2.1 cm. Any of these lesions could have represented a nodular form of a transient hepatic signal intensity difference due to arterioportal shunts (16). This belief is supported by the fact that ordinary regenerative nodules have not been demonstrated previously to have an arterial blood supply at angiography (37), CT hepatic arteriography (38), or triphasic spiral CT (39).
Dysplastic nodules are neoplastic premalignant nodules (40,41) that are found in 15%–28% of all explanted livers with cirrhosis (42–44). The development of HCC within a dysplastic nodule in as little as 4 months has been documented in longitudinal studies (45). In our study, the overall sensitivity of MR imaging for the detection of dysplastic nodules was poor on both a patient-by-patient (three of 18 [17%]) and a lesion-by-lesion (nine of 59 [15%]) basis. The 15% sensitivity for dysplastic nodule detection is much lower than the 60% sensitivity reported by Horigome et al (46). However, that series did not have explantation correlation and relied on focal resection and 21-gauge fine-needle biopsy findings for pathologic confirmation; these factors probably led to the higher sensitivities. By using the previously published criteria of T1 hyperintensity and T2 hypointensity (21,22), only nine dysplastic nodules were identified in our study. In fact, a lesion that met these signal intensity criteria was more likely to be a regenerative nodule (n = 15) than a dysplastic nodule. Inclusion of arterial phase enhancement as a criterion for dysplastic nodule would have increased the sensitivity to 22% (13 of 59 lesions) at the expense of decreased specificity, because the HCC lesions demonstrated this pattern more frequently.
Earls et al (22) studied explanted livers with high-spatial-resolution MR imaging (256 x 512 matrix, 20–26-cm field of view) in a retrospective nonblinded fashion and achieved a sensitivity of 96% (24 of 25 lesions) for the detection of dysplastic nodules with explantation correlation. However, in vivo MR imaging is subject to patient motion and flow artifacts that may impede the detection of these nodules. Despite the use of thin-section (2–3-mm) three-dimensional fat-suppressed contrast-enhanced T1-weighted imaging in a subset of 30 patients, none of the 31 dysplastic nodules was identified in our series. This implies that increased spatial resolution may not be sufficient to augment the detection of dysplastic nodules in vivo. Further research to determine the optimal imaging strategy for detecting and characterizing dysplastic nodules is needed. Detection of dysplastic nodules in patients without HCC is important because these lesions are premalignant (40,41) and a marker for hepatocarcinogenesis occurring elsewhere in the liver; thus, patients with dysplastic nodules have a higher risk of developing HCC than do patients without dysplastic nodules (43). Therefore, it may be prudent to perform imaging in these patients with greater frequency compared with that in patients with cirrhosis without dysplastic nodules.
In our study, four of the 10 pathologically proved HCCs detected at MR imaging were well-circumscribed masses that were mild to moderately hyperintense at turbo T2-weighted and/or STIR imaging. No dysplastic nodule or regenerative nodule had these signal intensity characteristics. In fact, to our knowledge, only one dysplastic nodule has been reported to be hyperintense at T2-weighted pulse sequences (46). It has also been reported that regenerative nodules in patients with cirrhosis due to Budd-Chiari syndrome (47) and in those who have undergone infarction (48) also may be hyperintense at T2-weighted pulse sequences. In our study, all of the well-circumscribed lesions that were markedly hyperintense at turbo T2-weighted and/or STIR pulse sequences were either cysts or hemangiomas (20).
Despite the fact that four HCCs and the nine dysplastic nodules detected were hyperintense at T1-weighted gradient-echo sequences both in and out of phase, only one lesion—an HCC—proved to be steatotic. In our study, four of five HCCs that were hyperintense on T1-weighted gradient-echo images were well differentiated at pathologic analysis; these findings confirmed those of Ebara et al (49)—that is, increased signal intensity on T1-weighted images correlates with a more well differentiated histologic grade than does isointensity or hypointensity.
This study had recognized limitations. Because the prospective interpretation of lesions was performed by using consensus reading, interobserver variability could not be evaluated. Furthermore, although the MR imaging criteria used to define dysplastic nodule were developed from previous studies (21,22), one of which had explantation correlation (22), they were not perfect. As noted previously, four dysplastic nodules in two patients were incorrectly interpreted as HCC on the basis of arterial phase enhancement. However, HAP enhancement of dysplastic nodules at MR imaging is rare: To our knowledge, the first such case report was published in 1998 (35), 3 years after this study began. In addition, we were unable to diagnose any of the 11 siderotic iron-retentive dysplastic nodules because we did not consider hypointensity at all pulse sequences as a criterion for dysplastic nodule. However, siderotic regenerative nodules may be difficult to distinguish from siderotic dysplastic nodules at MR imaging. Furthermore, we did not prospectively assess for the presence of a capsule. Although this finding is quite specific for HCC, capsules rarely are seen in small HCCs in non-Asian populations. We were unable to compare the accuracy of thin-section (2–3-mm) three-dimensional fat-suppressed contrast-enhanced T1-weighted imaging, which was performed in 30 patients, with that of dynamic two-dimensional imaging, because the three-dimensional imaging group had only two neoplasms. Finally, the overall number of pathologically proved HCCs in this study was small (n = 19). However, this was a direct result of excluding patients with known HCC, who often have a much greater tumor burden.
Although we used gadopentetate dimeglumine as the contrast material in this study, other agents have been used to detect and characterize hepatic masses in the cirrhotic liver. Although it was beyond the scope of this article to review these other agents and the studies performed with them, the combination of reticuloendothelial agents (ie, ferumoxides) and extracellular gadolinium chelates shows promise (50,51) by improving contrast at T2-weighted imaging while still enabling dynamic imaging. The use of ferumoxide-enhanced imaging alone, however, has been shown to be inferior to breath-hold gadolinium-enhanced imaging (26).
In conclusion, MR imaging is insensitive for detection of small (<2-cm) HCCs and dysplastic nodules, but it may be useful in detecting HCCs larger than 2 cm. Multiinstitutional prospective trials with much larger patient cohorts are needed to further validate the results of this study.
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FOOTNOTES |
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Abbreviations: FLASH = fast low-angle shot, HAP = hepatic arterial phase, HCC = hepatocellular carcinoma, STIR = short inversion time inversion recovery
Author contributions: Guarantor of integrity of entire study, G.A.K.; study concepts, G.A.K., N.M.R.; study design, G.A.K.; literature research, G.A.K.; clinical studies, all authors; data acquisition, G.A.K., V.S.L.; data analysis/interpretation, G.A.K., V.S.L., N.M.R., J.C.W.; statistical analysis, V.S.L.; manuscript preparation, definition of intellectual content, editing, revision/review, and final version approval, all authors.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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 E Caturelli, L Solmi, M Anti, S Fusilli, P Roselli, A Andriulli, F Fornari, C Del Vecchio Blanco, and I de Sio Ultrasound guided fine needle biopsy of early hepatocellular carcinoma complicating liver cirrhosis: a multicentre study Gut, September 1, 2004; 53(9): 1356 - 1362. [Abstract] [Full Text] [PDF]
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 J A Guthrie Cirrhosis and focal liver lesions: MRI findings Imaging, September 1, 2004; 16(4): 351 - 363. [Abstract] [Full Text] [PDF]
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K T T Fung, F T W Li, M L Raimondo, D Maudgil, A Mancuso, J M Tibballs, A A Watkinson, D Patch, and A K Burroughs Systematic review of radiological imaging for hepatocellular carcinoma in cirrhotic patients Br. J. Radiol., August 1, 2004; 77(920): 633 - 640. [Abstract] [Full Text] [PDF]
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C. Valls, M. Cos, J. Figueras, E. Andia, E. Ramos, A. Sanchez, T. Serrano, and J. Torras Pretransplantation Diagnosis and Staging of Hepatocellular Carcinoma in Patients with Cirrhosis: Value of Dual-Phase Helical CT Am. J. Roentgenol., April 1, 2004; 182(4): 1011 - 1017. [Abstract] [Full Text] [PDF]
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H. K. Hussain, I. Syed, H. V. Nghiem, T. D. Johnson, R. C. Carlos, W. J. Weadock, and I. R. Francis T2-weighted MR Imaging in the Assessment of Cirrhotic Liver Radiology, March 1, 2004; 230(3): 637 - 644. [Abstract] [Full Text] [PDF]
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I. E. Steingruber, A. Mallouhi, B. V. Czermak, P. Waldenberger, E. Gassner, F. Offner, A. Chemelli, A. Koenigsrainer, W. Vogel, and W. R. Jaschke Pretransplantation Evaluation of the Cirrhotic Liver with Explantation Correlation: Accuracy of CT Arterioportography and Digital Subtraction Hepatic Angiography in Revealing Hepatocellular Carcinoma Am. J. Roentgenol., July 1, 2003; 181(1): 99 - 108. [Abstract] [Full Text] [PDF]
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R. C. Carlos, H. M. Kim, H. K. Hussain, I. R. Francis, H. V. Nghiem, and A. M. Fendrick Developing a Prediction Rule to Assess Hepatic Malignancy in Patients with Cirrhosis Am. J. Roentgenol., April 1, 2003; 180(4): 893 - 900. [Abstract] [Full Text] [PDF]
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G. Brancatelli, R. L. Baron, M. S. Peterson, and W. Marsh Helical CT Screening for Hepatocellular Carcinoma in Patients with Cirrhosis: Frequency and Causes of False-Positive Interpretation Am. J. Roentgenol., April 1, 2003; 180(4): 1007 - 1014. [Abstract] [Full Text] [PDF]
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G. A. Krinsky and G. Israel Nondysplastic Nodules That Are Hyperintense on T1-Weighted Gradient-Echo MR Imaging: Frequency in Cirrhotic Patients Undergoing Transplantation Am. J. Roentgenol., April 1, 2003; 180(4): 1023 - 1027. [Abstract] [Full Text] [PDF]
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B. Bhartia, J. Ward, J. A. Guthrie, and P. J. Robinson Hepatocellular Carcinoma in Cirrhotic Livers: Double-Contrast Thin-Section MR Imaging with Pathologic Correlation of Explanted Tissue Am. J. Roentgenol., March 1, 2003; 180(3): 577 - 584. [Abstract] [Full Text] [PDF]
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S. A. Teefey, C. C. Hildeboldt, F. Dehdashti, B. A. Siegel, M. G. Peters, J. P. Heiken, J. J. Brown, E. G. McFarland, W. D. Middleton, D. M. Balfe, et al. Detection of Primary Hepatic Malignancy in Liver Transplant Candidates: Prospective Comparison of CT, MR Imaging, US, and PET Radiology, February 1, 2003; 226(2): 533 - 542. [Abstract] [Full Text] [PDF]
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A. Shimizu, K. Ito, S. Koike, T. Fujita, K. Shimizu, and N. Matsunaga Cirrhosis or Chronic Hepatitis: Evaluation of Small (<=2-cm) Early-Enhancing Hepatic Lesions with Serial Contrast-enhanced Dynamic MR Imaging Radiology, February 1, 2003; 226(2): 550 - 555. [Abstract] [Full Text] [PDF]
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B. K. Kang, J. H. Lim, S. H. Kim, D. Choi, H. K. Lim, W. J. Lee, and S. J. Lee Preoperative Depiction of Hepatocellular Carcinoma: Ferumoxides-enhanced MR Imaging versus Triple-Phase Helical CT Radiology, January 1, 2003; 226(1): 79 - 85. [Abstract] [Full Text] [PDF]
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K. Mori, J. Scheidler, T. Helmberger, N. Holzknecht, R. Schauer, C. A. Schirren, I. Bittmann, M. Dugas, and M. Reiser Detection of Malignant Hepatic Lesions Before Orthotopic Liver Transplantation: Accuracy of Ferumoxides-Enhanced MR Imaging Am. J. Roentgenol., October 1, 2002; 179(4): 1045 - 1051. [Abstract] [Full Text] [PDF]
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G. L. Bennett, G. A. Krinsky, R. J. Abitbol, S. Y. Kim, N. D. Theise, and L. W. Teperman Sonographic Detection of Hepatocellular Carcinoma and Dysplastic Nodules in Cirrhosis: Correlation of Pretransplantation Sonography and Liver Explant Pathology in 200 Patients Am. J. Roentgenol., July 1, 2002; 179(1): 75 - 80. [Abstract] [Full Text] [PDF]
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Y. Y. Jeong, D. G. Mitchell, and T. Kamishima Small (<20 mm) Enhancing Hepatic Nodules Seen on Arterial Phase MR Imaging of the Cirrhotic Liver: Clinical Implications Am. J. Roentgenol., June 1, 2002; 178(6): 1327 - 1334. [Abstract] [Full Text] [PDF]
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R. L. Baron and M. S. Peterson From the RSNA Refresher Courses: Screening the Cirrhotic Liver for Hepatocellular Carcinoma with CT and MR Imaging: Opportunities and Pitfalls RadioGraphics, October 1, 2001; 21(90001): S117 - 132. [Abstract] [Full Text] [PDF]
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