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A diagnostic is a sentence.

Cirrhosis-associated Hepatocellular Nodules:


Introduction

Correlation of Histopathologic and MR Imaging Features

RadioGraphics 2008;28:747-769

Content Introduction Nodule Classification Nodule Characterization Differential Diagnosis

Introduction
Hepatocellular carcinoma (HCC) is the fifth most common tumor in the world and is the third most common cause of cancer-related death, after lung and stomach cancer. Cirrhosis is the strongest predisposing factor for HCC, approximately 80% of cases of HCC developing in a cirrhotic liver. with

The annual incidence of HCC is 2.0%6.6% in patients with cirrhosis compared with 0.4% in patients without cirrhosis.

Introduction
The incidence of HCC increased from 1.3 per 100 000 in 19811983 to 3.0 per 100 000 in 19961998 (US). In Vietnam

Age-standardized rate (per 100 000) of major cancers in Hanoi (1996) and Ho Chi Minh City (199596). Pham Thi Hoang Anh and Nguyen Ba Duc. Japanese Journal of Clinical Oncology 32:S92-S97 (2002)

Nodule Classification

Liver cirrhosis: irreversible remodeling of the hepatic architecture with bridging fibrosis and a spectrum of hepatocellular nodules. Guidelines nodular hepatocellular lesions (Canada 1995), there are two categories of nodules: (a) regenerative lesions and (b) dysplastic or neoplastic lesions

Lesions in italics are described in this article

Nodule Classification
There are four classes of lesions that characteristically are found in the cirrhotic liver: regenerative nodules, dysplastic foci, dysplastic nodules, and hepatocellular carcinomas. Term: cirrhosis-associated hepatocellular nodules.

Stepwise pathway of carcinogenesis for HCC in cirrhosis: - regenerative nodules may be monoacinar or multiacinar, surrounded by fibrous septa, diameter up to 5cm but rare. - dysplastic and neoplastic nodules: abnormal growth do not satisfy the histologic criteria for malignancy or invasion . - HCC are malignant neoplasms composed of dedifferentiated hepatocytes.

Nodule Classification
Note: The diagnostic differentiation of dysplastic nodules from other cirrhosisassociated hepatocellular nodules may be difficult even at histopathologic analysis, and molecular geneticsbased techniques may be necessary. Although these nodules may transform over time into HCC, but relatively slow. Dysplastic nodules should not be treated or managed as cancers, and patients with known or suspected dysplastic nodules should not be monitored more aggressively than patients without such nodules (American Association for the Study of Liver Diseases). Siderotic Nodules.- The term was coined by radiologists to describe cirrhosis-associated nodules (regenerative or dysplastic) with high levels of endogenous iron. Siderotic nodules rarely, if ever, are malignant

Nodule Classification
Characteristics of Cirrhosis-associated Hepatocellular Nodules in Comparison with Parenchyma

Nodule Characterization
1. Size As a general rule, lesions with a diameter of less than 2 cm are more likely to be benign than malignant and, if malignant, are usually well differentiated. 2. Importance of Clinical History and Laboratory Testing (table) The diagnostic value of imaging is greatest when the images are interpreted with consideration given to the available clinical and laboratory data.

Nodule Characterization
3. Vascularity The major shift in angiogenesis typically occurs during the transition from lowgrade to high-grade dysplasia.

Changes of intranodular blood supply (shaded bars = hepatic arterial supply, open bars = portal supply, hatched bars = abnormal arterial supply) in hepatocellular nodules associated with liver cirrhosis. RN = regenerative nodule, low-DN = lowgrade dysplastic nodule, high-DN = high-grade dysplastic nodule, wd-HCC = well-differentiated HCC, mpHCC = moderately or poorly differentiated HCC. Asterisks indicate isodense on CT during hepatic arteriography.

Nodule Characterization
4. Hepatocellular Function Regenerative nodules generally have normal hepatocellular function and therefore demonstrate avid uptake of hepatocellular contrast agents. As dedifferentiation proceeds, the number of expressed organic ion transporters decreases, with a resultant progressive reduction in the uptake of hepatocellular agents. 5. Kupffer Cell Density The density of Kupffer cells within regenerative lesions = surrounding nonneoplastic hepatic parenchyma. The cell density is visible at contrastenhanced imaging because Kupffer cells avidly accumulate particulate agents through phagocytic mechanisms. According to empirically derived values reported in the literature, dysplastic nodules and well-differentiated HCCs have variable Kupffer cell densities, ranging from diminished to elevated levels. Moderately and poorly differentiated HCCs tend to have a diminished Kupffer cell density.

Nodule Characterization
6. Usefulness of MR Imaging A critical role is the depiction of early-stage HCC. Other roles: staging of HCC, differentiation of neoplastic lesions from regenerative lesions, planning and guidance of therapy, and assessing the response to therapy. Unenhanced Acquisitions. The pulse sequences most commonly used: T1, T2, and T2* weighting. Chemical fat-saturation sequences and gradient-recalled echo (GRE) sequences with out-of-phase and in-phase image acquisitions are helpful for assessing hepatic or intralesional steatosis. Diffusion-weighted sequences are used at some institutions to evaluate hepatocellular nodules. Contrast-enhanced Acquisitions. Three classes of MR contrast agents: gadolinium chelates with low molecular weight, hepatocellular agents, and superparamagnetic iron oxide (SPIO) particles.

Nodule Characterization
6. Usefulness of MR Imaging: Contrast-enhanced Acquisitions (cont). Low-molecular-weight gadolinium chelates: extracellular agents generate T1 shortening, provide information about tissue vascularity. T1W, volumetric (3D) fat-saturated spoiled GRE sequences are well suited for this purpose. The hepatic arterial phase is critical: acquisition of the center of k-space coincides with the peak arterial perfusion of hepatic nodules. Portal venous phase: 2030 seconds after gadolinium administration. Recently, acquiring delayed venous phase and equilibrium phase images 180240 seconds after contrast agent injection, to better assess venous washout. The disadvantages of gadolinium: precise timing and patient cooperation are critical because gadolinium-related enhancement is transient. Well-differentiated HCCs and some dysplastic nodules may be portally perfused and hypoenhanced or isoenhanced during the arterial phase, thus evading detection. Benign cirrhotic tissue may be hyperenhanced because of altered hemodynamics and may obscure underlying HCCs. In addition, benign arteriovenous shunts and active inflammation may cause early enhancement mimicking that in HCC

Nodule Characterization
6. Usefulness of MR Imaging: Contrast-enhanced Acquisitions (cont).

Calculating the Delay for Hepatic Arterial Phase Imaging with a Test Bolus. Note: AT = acquisition time, IT = injection time, TTP = time to peak aortic enhancement.

Nodule Characterization
6. Usefulness of MR Imaging: Contrast-enhanced Acquisitions (cont).

Mixed extracellular and hepatocellular agents: a specific subcategory of gadolinium chelates. They are useful not only for evaluating lesion vascularity, but also for assessing hepatocellular function on images acquired with an appropriate delay. Two such agents have been manufactured commercially: gadobenate dimeglumine (Gd-BOPTA) and gadoxetic acid disodium (Gd-EOB-DTPA). Up to 5% of the dose of gadobenate is selectively taken up by functioning hepatocytes and excreted into the bile. Although initial biliary excretion of the agent is noticeable on delayed T1W images at 5 minutes after injection, reliable characterization of hepatocellular function in the cirrhotic liver usually requires delays of 30120 minutes. Thus, although a single injection of gadobenate permits assessment of lesion vascularity and hepatocellular function, two imaging sessions are typically required if both types of data are desired.

Nodule Characterization
6. Usefulness of MR Imaging: Contrast-enhanced Acquisitions (cont). SPIO particles (mean diameter of 25250 nm), are phagocytosed by Kupffer cells in the liver and spleen. At MR imaging, SPIO particles cause shortening of T2* and, to a lesser degree, T2. In the cirrhotic liver, they accumulate in tissues that contain Kupffer cells (eg, in regenerative nodules, some dysplastic nodules, and regions of surrounding liver parenchyma), causing signal loss in those regions on T2W images and T2*W images. Most HCCs lack Kupffer cells, do not accumulate SPIO particles, and therefore appear hyperintense relative to the liver parenchyma on T2W images and T2*-weighted images obtained after the administration of SPIO

Nodule Characterization
6. Usefulness of MR Imaging: Contrast-enhanced Acquisitions (cont). SPIO particles may be used alone or in combination with gadolinium. Contrast-enhanced MR imaging with the use of SPIO particles should be performed with T2- or T2*W sequences. However, this technique has important intrinsic disadvantages. First, lesion characterization is limited because most lesions do not exhibit SPIO uptake and thus appear hyperintense on T2W images. Second, well-differentiated HCC may accumulate SPIO particles and thus appear invisible against the normal liver background. To overcome these limitations, some institutions advocate double contrastenhanced MR imaging in which both SPIO particles and a gadolinium are administered sequentially. A shortcoming of double contrast-enhanced imaging is that it is logistically more difficult than contrast-enhanced imaging with the use of a single agent. It also exposes the patient to two drugs and, thus, to a greater risk of adverse effects. A potential technical limitation of SPIO is that, in addition to shortening the T2* of liver tissue, it shortens T1 and therefore reduces the effectiveness of the subsequent gadolinium injection at dynamic T1W imaging.

Differential Diagnosis
Table: MR Imaging based Differential Diagnosis Cirrhosis-associated Hepatocellular Nodules Note.Most HCCs detected at surveillance imaging are small and show no evidence of intralesional fat, a tumor capsule, or aggressive behavior. Thus, the absence of these features does not necessarily imply benignity.

Differential Diagnosis
1. Regenerative Nodules Gross Pathologic and Histologic Features Although most d < 2 cm, regenerative nodules with d > 2 cm have been observed in patients with long-standing Budd-Chiari syndrome and in patients with cirrhosis due to autoimmune hepatitis. The largest nodules are usually located near major vessels. Regenerative nodules characteristically are surrounded by regions of bridging fibrosis (Fig 1). In the early stages of cirrhosis, the liver may contain nonregenerative nodules of hepatocellular tissue carved out by bridging fibrosis. Such nodules may resemble regenerative nodules at gross pathologic evaluation; however, because they lack regenerative features, they are not classified as regenerative.

Differential Diagnosis
1. Regenerative Nodules Gross Pathologic and Histologic Features

Figure 1. a 54 y/o/m with HCV-induced cirrhosis. (ac) Axial 2D T2*W spoiled GRE images obtained at 3 T with a TE of 5.8 msec. (a) Unenhanced image shows minimal heterogeneity of the liver parenchyma, with faintly visible nodules of various sizes (arrows). (b) Image obtained after SPIO administration shows a marked loss of signal intensity because of the phagocytic uptake of SPIO particles in the nodules (arrows), which appear dark and sharply circumscribed.

Differential Diagnosis
1. Regenerative Nodules Gross Pathologic and Histologic Features

Figure 1. (c) Double contrast-enhanced image obtained after the intravenous administration of a gadolinium-based contrast agent shows fibrotic reticuli with high signal intensity due to extracellular accumulation of the low-molecular-weight agent. The enhancement of fibrotic tissue further increases the visibility of the innumerable nodules (arrows). (d) Photograph of explanted liver from a 67-year-old woman with HCV-induced cirrhosis shows an outer surface studded with regenerative nodules of various sizes.

Differential Diagnosis
1. Regenerative Nodules Unenhanced MR Imaging Features. Regenerative nodules are usually innumerable, but they may be difficult to see on radiologic images, depending on the imaging technique used. When they are visible, regenerative nodules appear sharply circumscribed within the liver parenchyma. - On unenhanced T2- and T2*W images, the nodules typically display low signal intensity; their signal intensity on T1-weighted images is variable. - Lipid-containing regenerative nodules display signal loss on out-ofphase GRE images and unenhanced asymmetric spin-echo images in comparison with in-phase images. Steatotic regenerative nodules tend to occur in multiples (Fig 2). A single fatty nodule is suggestive of a dysplastic or malignant process (Fig 3).

Differential Diagnosis
1. Regenerative Nodules Unenhanced MR Imaging Features.

Figure 2. Steatotic regenerative nodules in a 54 y/o/w with cirrhosis secondary to fatty liver disease. (a, b) Comparison of axial unenhanced 2D spoiled GRE out-of-phase (TE, 2.3 msec) (a) and in-phase (TE, 4.6 msec) (b) images obtained at 1.5 T shows a diffuse signal intensity loss in the liver in a because of phase interferenceinduced fat and water signal cancellation (chemical shift of the second kind), a finding indicative of diffuse steatosis. Superimposed on the steatotic background are multiple steatotic nodules (arrows) with a signal intensity that is markedly lower than that of background in a and slightly higher than that of background in b.

Differential Diagnosis
1. Regenerative Nodules Unenhanced MR Imaging Features.

Figure 3. Steatotic HCC in a 48 y/o/m with HCV-induced cirrhosis. (ac) Axial SPIOenhanced 2D spoiled GRE images obtained at 1.5 T with TEs of 2.6 msec (a), 4.8 msec (b), and 6.6 msec (c) show a 15-mm nodule in liver segment VIII (arrow). A loss of signal intensity in the nodule periphery on the out-of-phase images (a, c) in comparison with that on the in-phase image (b) is indicative of intralesional fat.

Differential Diagnosis
1. Regenerative Nodules Unenhanced MR Imaging Features.

Figure 3c. d) Axial gadolinium-enhanced 3D fat-saturated T1-weighted spoiled GRE image shows heterogeneous enhancement of the nodule. (e) Photograph of a section of the liver, which was explanted 45 days after MR imaging, shows a yellowish nodule (arrows) in an anatomic location corresponding to that of the nodule in ad. Histologic analysis showed it to be a moderately differentiated steatotic HCC.

Differential Diagnosis
1. Regenerative Nodules Contrast-enhanced MR Imaging Features.
- Contrast-enhanced imaging features are diagnostically more specific than findings at unenhanced imaging. - After the injection of gadolinium, most regenerative nodules enhance to the same degree as the adjacent liver or show slightly less enhancement. - Uptake and excretion of gadobenate dimeglumine by these nodules is usually preserved. Consequently, on images acquired during the hepatocellular phase after an injection of gadobenate dimeglumine, virtually all regenerative nodules have a similar signal intensity, which gives the liver a homogeneous appearance (Fig 4). - Occasionally, regenerative nodules may have sufficient hepatocellular function to take up the hepatocellular agent but not to excrete it; such nodules show hyperintense signal. - Finally, because most regenerative nodules have a preserved phagocytic function, they are SPIO avid and appear hypointense on SPIO-enhanced T2and T2*W images (Fig 1).

Differential Diagnosis
1. Regenerative Nodules Contrast-enhanced MR Imaging Features.

Figure 4. Regenerative nodules and HCC in a 57 y/o/m with cirrhosis. (a) Axial SPIO-enhanced 2D T2*W (TE, 5.8 msec) spoiled GRE image shows a small hepatocellular carcinoma (arrow), which has higher signal intensity than the regenerative nodules surrounding it, because of its lesser phagocytic uptake of SPIO particles.

Differential Diagnosis
1. Regenerative Nodules Contrast-enhanced MR Imaging Features.

Figure 4. (b - f) Axial 3D fat-saturated T1W spoiled GRE images acquired at 3 T one week later, before (b) and in three phases after (c - f) an injection of a gadoliniumt. The unenhanced image (b) does not show the small HCC, but the hepatic arterial phase image (c) shows increased signal intensity in the carcinoma (arrow).

Differential Diagnosis
1. Regenerative Nodules Contrast-enhanced MR Imaging Features.

Figure 4. (d, e) Portal venous (d) and equilibrium (e) phase images show washout in the lesion center, which has lower signal intensity than that of the liver parenchyma, while contrast material retained in the lesion rim results in hyperintense signal suggestive of a capsule or pseudocapsule. The innumerable regenerative nodules have signal intensity that is varied in b, isointense to that of the parenchyma in c, and slightly less intense than that of the parenchyma in e.

Differential Diagnosis
1. Regenerative Nodules Contrast-enhanced MR Imaging Features.

Figure 4. (f) Hepatocellular phase image obtained 90 minutes after the injection shows slightly lower signal intensity in the carcinoma because of less active hepatocellular function than in background liver. Because most of the regenerative nodules have taken up some gadolinium, the cirrhotic parenchyma appears more homogeneous than in e. However, the regenerative nodules and fibrous reticuli are most visible in a, the SPIO-enhanced image.

Differential Diagnosis
2. Siderotic Nodules Because of their high iron content, siderotic nodules have low signal intensity on T1- and T2*-weighted unenhanced MR images. These lesions may be either regenerative or dysplastic, and no unenhanced imaging feature (size, number, distribution) permits reliable differentiation between the two. To our knowledge, no studies have yet been performed to assess whether contrast-enhanced imaging helps distinguish regenerative siderotic nodules from dysplastic ones.

Differential Diagnosis
3. Dysplastic Nodules Histologic Features. Dysplastic nodules are characterized histologically by progressive architectural derangement, nuclear crowding, atypia, and a variable number of unpaired arterioles or capillaries. -Low-grade dysplastic nodules closely resemble regenerative nodules histologically. They have a preserved hepatic architecture, as well as normal vascular profile, hepatocellular function, and Kupffer cell density. They have low malignant potential with slow, infrequent progression to HCC. -High-grade dysplastic nodules show some architectural distortion with sinusoidal "capillarization" and an increased density of unpaired arteries (Fig 5). The Kupffer cell density is variable; it may be increased, normal, or diminished. High-grade dysplastic nodules progress to HCC more frequently than low-grade dysplastic nodules. The high-grade nodules closely resemble well-differentiated HCC and are difficult to distinguish histologically, particularly those that are small.

Differential Diagnosis
3. Dysplastic Nodules Unenhanced MR Imaging Features. - As expected on the basis of their histopathologic characteristics, dysplastic nodules have variable appearances on MR images, and their signal intensity characteristics overlap with those of regenerative nodules and welldifferentiated HCCs. -On T2W images, low-grade dysplastic nodules tend to have low signal intensity relative to adjacent liver, whereas high-grade dysplastic nodules tend to have slightly higher signal intensity. -T1W images are not helpful because both low- and high-grade dysplastic nodules display variable (low, intermediate, or high) signal intensity. Contrast-enhanced MR Imaging Features. - On gadolinium- and SPIO-enhanced images, low-grade dysplastic nodules typically are indistinguishable from regenerative nodules, whereas high-grade dysplastic nodules are indistinguishable from well-differentiated HCC (Fig 5). - It is not yet clear whether gadobenate dimeglumineenhanced imaging permits the characterization of dysplastic nodules.

Differential Diagnosis
3. Dysplastic Nodules

Figure 5. Dysplastic nodule in a 45 y/o/w with alcoholic cirrhosis. (a) Axial SPIOenhanced 2D T2*W (TE, 6.6 msec) spoiled GRE image obtained at 1.5 T shows a 10mm nodule in liver segment V (arrow) that has a higher signal intensity than the surrounding parenchyma because of less intranodular uptake of SPIO. (b) Axial gadolinium-enhanced 3D fat-saturated T1W spoiled GRE image obtained during the arterial phase shows nodular enhancement (arrow).

Differential Diagnosis
3. Dysplastic Nodules

Figure 5. (c) Photograph of a gross pathologic section of the liver, which was explanted 2 months later, shows a well-defined 12-mm nodule (arrows) in a location corresponding to that in a and b. (d) Photomicrograph (original magnification, x100; H-E stain) shows a well-defined transition between the liver parenchyma (arrowheads) and nodule (arrows). Increased cellular and capillary density, a higher nuclear-cytoplasmic ratio, and moderate architectural distortion in the nodule are indicative of high-grade dysplasia.

Differential Diagnosis
4. Hepatocellular Carcinomas Unenhanced MR Imaging Features. - The signal intensity characteristics of HCCs depend on their size, grade, and biologic features. On T1W images, small HCCs may have variable signal intensity; on T2W images, signal intensity usually is slightly increased. Some well-differentiated HCCs may appear isointense or even hypointense. - Large HCCs have signal intensity alterations caused by intralesional fat, hemorrhage, and necrosis than is seen in smaller lesions. - Steatotic HCCs: a signal intensity decrease on out-of-phase images in comparison with in-phase images (Fig 3), and they are easily identified by comparing fat-saturated images with nonfat-saturated ones. - Hemorrhagic HCCs may have marked high signal intensity on T1W images and low signal intensity on T2- and T2*W images. - Intralesional necrosis typically manifests as one or more areas of low signal intensity on T1W images and high signal intensity on T2W images.

Differential Diagnosis
4. Hepatocellular Carcinomas Contrast-enhanced MR Imaging Features. -Approximately 80%90% of HCCs are hypervascular: intensely enhanced during the arterial phase after a bolus injection of a gadolinium (Fig 4). In delayed imaging phases, hypervascular HCCs undergo washout and typically have low signal intensity ; however, some may appear isointense to the liver parenchyma and therefore may be difficult to see on images obtained during the portal venous phase and later phases. -About 10%20% of HCCs are hypovascular and show contrast enhancement slightly less than that in the surrounding liver on arterial phase images. Typically, hypovascular HCCs are small, well-differentiated tumors. However, poorly differentiated and diffusely infiltrating hypovascular HCCs also may occur. Such lesions may be difficult to detect on gadolinium-enhanced MR images despite their large size and aggressive behavior, but they are usually visible on SPIO-enhanced images.
- Because of their diminished uptake of gadolinium, HCCs appear as unenhanced foci of low signal intensity on hepatocellular phase images (Fig 4).

Differential Diagnosis
4. Hepatocellular Carcinomas Contrast-enhanced MR Imaging Features. Moderately and poorly differentiated HCCs characteristically accumulate less SPIO than the surrounding liver parenchyma and have relatively high signal intensity on T2- and T2*W SPIO-enhanced images. Well-differentiated HCCs may accumulate SPIO and tend to be iso- or hypointense compared with the background liver. Thus, the degree of SPIO uptake may be used as a noninvasive means of grading HCCs. Large HCCs may have nonuniform Kupffer cell density and show heterogeneous accumulation of SPIO particles.

Differential Diagnosis
4. Hepatocellular Carcinomas Structural Variation of Large Hepatocellular Carcinomas. Small HCCs tend to be homogeneous, round or oval, and well defined. By contrast, large HCCs may exhibit a broad spectrum of morphologic features, including a mosaic pattern, a tumor capsule, an intratumoral nodule ("nodulein-nodule" appearance), and extracapsular extension with the formation of satellite nodules. -The mosaic pattern reflects underlying mosaic pathologic features and is defined by the presence of multiple compartments of variable signal intensity at unenhanced T1-, T2-, and T2*W imaging. The compartments are distributed within the mass in a seemingly random manner and enhance to variable degrees after the administration of contrast material (Fig 9).

Differential Diagnosis
4. Hepatocellular Carcinomas Structural Variation of Large Hepatocellular Carcinomas.

Figure 9c. HCC with a mosaic pattern of enhancement in a 62 y/o/m with HCVinduced cirrhosis. (a) Axial unenhanced 3D fat-saturated T1W spoiled GRE image obtained at 3 T shows a well-circumscribed mass (arrow) at the junction of liver segments VII and VIII with signal isointense to that of the liver parenchyma but with a lower-signal-intensity periphery (arrowheads) that represents a capsule. (b) Axial gadolinium-enhanced images during the hepatic arterial phase show heterogeneous enhancement of the mass.

Differential Diagnosis
4. Hepatocellular Carcinomas Structural Variation of Large Hepatocellular Carcinomas. - A characteristic but uncommon finding is the nodule-in-nodule appearance, which generally represents a HCC within a larger dysplastic or regenerative nodule. - On arterial phase images obtained after gadolinium administration, the carcinomatous nodule typically appears enhanced, while the surrounding regenerative or dysplastic nodule does not enhance and has lower signal intensity. - On SPIO-enhanced T2- and T2*-weighted images, signal in the carcinoma usually appears hyperintense, while that in the regenerative nodule or dysplastic nodule is hypointense (Fig 5). - At dynamic gadolinium-enhanced imaging, necrotic HCCs that contain nodules of viable tumor tissue also may have a nodule-in-nodule appearance (Fig 11).

Differential Diagnosis
4. Hepatocellular Carcinomas Structural Variation of Large Hepatocellular Carcinomas.

Figure 11. Nodule-in-nodule appearance of HCC in a 56 y/o/w with HCV-induced cirrhosis. (a, b) Axial SPIO-enhanced 2D T2*-weighted spoiled GRE (TE, 6.6 msec) (a) and T2-weighted echo-train spin-echo (TE, 90 msec) (b) images obtained at 1.5 T show a 35-mm heterogeneously hyperintense mass in the right liver lobe (arrows).

Differential Diagnosis
4. Hepatocellular Carcinomas Structural Variation of Large Hepatocellular Carcinomas.

Figure 11. (c) Axial gadolinium-enhanced 3D fat-saturated T1W spoiled GRE image obtained during the hepatic arterial phase shows a markedly enhanced mural nodule (arrowheads) within the largely nonenhanced mass. The lack of enhancement in the mass is suggestive of necrosis. (d) Photograph of a section from the liver, which was explanted 10 weeks after MR imaging, shows two mural nodules (arrows) within the mass. At histologic analysis, the nodules proved to be viable HCC; the rest of the mass consisted of necrotic tissue. Note the multiple regenerative nodules (*) in the surrounding liver parenchyma.

IMAGING TECHNIQUE
The sequences used can vary according to vendor and personal preferences (117), but certain guidelines should be followed: - First, sequences should be performed during suspended respiration or should be respiratory averaged (some T2-weighted sequences). - Second, GRE sequences have replaced spin-echo sequences for T1-weighted imaging. - Third, three-dimensional gadolinium-enhanced GRE sequences are preferred to two-dimensional GRE sequences. - Fourth, contrast agent bolus timing is strongly recommended.

Spoiled Gradient Echo Incoherent or Spoiled Gradient Echo


FLASH (fast low-angle shot): Siemens Medical Solutions SPGR (spoiled gradient echo): GE Medical Systems Background: Spoiled gradient-echo sequences destroy or "spoil" any residual transverse magnetization remaining at the end of each TR. In that way, every RF flip applied in a sequence acts solely on longitudinal magnetization. Features: Used in fast T1-weighted imaging. The short TRs allow 3D and breath-hold 2D acquisitions.

Sensitivity of various imaging tests for detecting hepatocellular carcinoma

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