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Fig. 1a-e. Typical focal nodular hyperplasia. On the pre-contrast HASTE T2-weighted (a) and GRE T1-weighted (b) images the lesion (arrows in a) appears homogeneously slightly hyperintense and slightly hypointense, respectively, compared to the surrounding normal liver parenchyma. Conversely, the central scar (arrowhead in a) is hyperintense on the HASTE image and hypointense on the GRE image. On the arterial phase image (c) of the dynamic series of acquisitions after administration of Gd-BOPTA, the lesion demonstrates marked enhancement, with a hypointense central scar. Rapid wash-out occurs during the portal-venous phase (d) resulting in an almost isointense appearance in the subsequent equilibrium phase (e). The central scar during these phases is hypointense and hyperintense, respectively

Fig. 2a, b. Typical focal nodular hyperplasia after Gd-BOPTA. Same case as Fig. 1. On the pre-contrast GRE T1-weighted image (a) the lesion appears homogeneously slightly hypointense compared to the normal liver parenchyma. In the hepatobiliary phase after Gd-BOPTA administration (b), the lesion appears hyperintense due to the uptake of Gd-BOPTA by normal hepatocytes. Conversely, the central scar is still hypointense (arrow)

Fig. 2a, b. Typical focal nodular hyperplasia after Gd-BOPTA. Same case as Fig. 1. On the pre-contrast GRE T1-weighted image (a) the lesion appears homogeneously slightly hypointense compared to the normal liver parenchyma. In the hepatobiliary phase after Gd-BOPTA administration (b), the lesion appears hyperintense due to the uptake of Gd-BOPTA by normal hepatocytes. Conversely, the central scar is still hypointense (arrow)

Fig. 3a, b. Typical focal nodular hyperplasia after Mn-DPDP. Same case as Fig. 1 and 2. On the pre-contrast GRE T1-weighted image (a) the lesion appears homogeneously slightly hypointense. In the hepatobiliary phase after Mn-DPDP administration (b), the lesion appears isointense with a hypointense central scar, similar to the appearance after Gd-BOPTA administration

Fig. 3a, b. Typical focal nodular hyperplasia after Mn-DPDP. Same case as Fig. 1 and 2. On the pre-contrast GRE T1-weighted image (a) the lesion appears homogeneously slightly hypointense. In the hepatobiliary phase after Mn-DPDP administration (b), the lesion appears isointense with a hypointense central scar, similar to the appearance after Gd-BOPTA administration

Fig. 4a-e. Typical focal nodular hyperplasia after SH U 555 A. Same case as Fig. 1, 2 and 3. The lesion is homogeneously slightly hypointense on the pre-contrast GRE T1-weight-ed image (a). Slight enhancement of the cellular components can be seen during the T1-weighted dynamic evaluation after SH U 555 A administration (b-d), while the scar appears hypointense. During the reticuloendothelial phase (e) the nodule shows a discrete signal drop due to the uptake of iron oxide particles by Kupffer cells within the lesion not contain Kupffer cells and is therefore usually seen as a hyperintense central stellate area that corresponds to the high signal area seen on pre-contrast T2-weighted images. The possibility of performing dynamic phase T1-weighted imaging is an added advantage of the USPIO agents (Fig. 4).

A recent intraindividual comparison of Gd-BOPTA and ferumoxides in 50 patients with 83 FNH revealed that whereas all 83 (100%) FNH were seen during the examination with Gd-BOP-TA, only 62 FNH were seen during the examination with ferumoxides [8]. Importantly, Gd-BOPTA detected, and was able to diagnose correctly, all 17 FNH in 12 patients with previous neoplasia, while ferumoxides was able to detect only nine of these 17 lesions (52.9%) and to accurately characterize only seven (Fig. 5).

Nodular Regenerative Hyperplasia (NRH)

NRH of the liver is not a specific entity but is a secondary and non-specific tissue adaptation to a heterogeneous distribution of blood flow. NRH is characterized by multiple monoacinar regenerative nodules without fibrous septa. The lesions are not usually visible until a confluent macroaggrega-tion of sufficient size has been achieved. NRH occurs in 5-6% of individuals over 80 years of age and with increased frequency in patients with Budd-Chiari syndrome, systemic arthritis, polymyalgia rheumatica, massive tumor infiltration, mineral oil deposition and other disorders of liver blood flow [31,33].

On unenhanced MR imaging, NRH displays a broad spectrum of SI characteristics and may appear hypo-, iso- or hyperintense compared to the normal liver parenchyma on T1- and T2-weighted images [31]. On dynamic phase MR imaging with Gd-BOPTA and other extracellularly-distributed Gd agents, about 90% of these lesions appear hy-perintense during the arterial phase and iso- or slightly hyperintense during the portal venous and equilibrium phases [31].

As in the case of FNH, NRH demonstrates abnormal biliary system drainage, which does not derive from or communicate with that in the surrounding normal liver parenchyma. Consequently, like FNH these lesions appear iso- or hyperintense compared to the surrounding liver parenchyma in the hepato-biliary phase after both Gd-BOPTA and Gd-EOB-DTPA.A peripheral hypointense rim is often seen in the biggest nodules, which represents ischemic areas with focal peripheral steatosis (Fig. 6, 7).

These lesions also appear iso- or hyperintense compared to the surrounding liver parenchyma in the hepatobiliary phase after mangafodipir trisodium (Fig. 8).

The appearance of NRH after SPIO administration has not yet been fully described. However, because NRH typically contains abundant functioning Kupffer cells, its behavior can be expected to be similar to that of FNH (Fig. 9).

Hepatocellular Adenoma (HA)

Hepatocellular adenoma (HA) consists of plates or cords of cells that are larger than normal hepato-cytes and may contain large amounts of glycogen and lipid. Lipid accumulation is responsible for the characteristic yellow appearance of the cut surface of adenomas at pathology, and evidence of lipid on CT or MR imaging can be suggestive in diagnosing HA. The plates are separated by dilated sinusoids, which are thin-walled capillaries perfused by arterial pressure, while a portal venous supply is lacking. A tumor capsule may be present (see Chap. 4, Figs. 40,41).

Kupffer cells are often found in HA but may be reduced in number and function. Even though HA have functioning hepatocytes they lack bile ducts, a key histologic feature that distinguishes these lesions from FNH [20]. For this reason, bilirubin metabolism is blocked within HA, as confirmed by the absence of bile within resected lesions.

The appearance of HA on unenhanced MR imaging has been variously described as hyper-, iso-, and hypointense [1, 24]. Areas of increased SI on T1-weighted MR images can result from fat and hemorrhage while low SI areas correspond to necrosis, old hemorrhage or calcifications [24]. Some 47%-74% of HA are predominantly hyperin-tense on T2-weighted images while the remainder are iso- or hypointense. Most lesions are heterogeneous, demonstrating a combination of hyper- and hypointensity on T2-weighted images due to hemorrhage and necrosis. One third of HA have a peripheral rim corresponding to a fibrous capsule [1] that is typically hypointense on T1- and T2-weighted images.

Dynamic Gd-enhanced MR imaging can reveal early arterial enhancement, which is usually homogeneous and intense in non-complicated and small (< 5 cm) HA. However, in large lesions or in lesions with previous hemorrhage, the arterial enhancement may be heterogeneous (see Chap. 4, Fig. 42). On portal venous phase images, this early enhancement usually fades, revealing an iso- or hypointense lesion.

Since HA lack bile ducts, there is altered hepa-tocellular transport compared to normal hepato-cytes. Thus, while HA may contain functioning he-patocytes able to take up Gd-BOPTA, the absence of an intracellular transport gradient due to the lack of active transport across the sinusoid mem-

Fig. 5a-g. Atypical focal nodular hyperplasia after SH U 555 A and Gd-BOPTA in a patient with breast cancer. The pre-contrast HASTE T2-weighted image (a) and the corresponding GRE Tl-weighted image (b) reveal a large nodule (asterisk in a) in segments IV and II of the liver. The lesion appears homogeneously slightly hyperin-tense on the T2-weighted image and homogeneously slightly hypointense on the Tl-weighted image. The lesion demonstrates atypical nodular hyperintensity on the T2*-weighted images acquired before (c) and after (d) administration of SH U 555 A. The post-contrast appearance is suggestive of a breast cancer metastasis. On the arterial phase image (e) of the dynamic study after Gd-BOPTA administration, the lesion appears characteristically and markedly hyperintense. The enhancement persists into the portal-venous phase (f). In the hepatobiliary phase (g) the lesion is typically isointense to slightly hyperintense, strongly suggesting the presence of a benign lesion

Fig. 6a-h. Nodular regenerative hyperplasia after Gd-BOPTA in a patient with previous testicular cancer. A large slightly hyperintense nodule (arrow) and a smaller round hypointense nodule (arrowhead) are visible on the pre-contrast TSE T2-weighted image (a). On the corresponding pre-contrast GRE T1-weighted "in-phase" image (b), numerous slightly hypointense nodules (arrows) are visible. These lesions appear slightly hyperintense in a diffuse fatty liver on the pre-contrast GRE Tl-weighted "out-of-phase" image (c). The lesions show marked and homogeneous enhancement on the arterial phase image (d) of the dynamic study after Gd-BOPTA administration, followed by rapid wash-out in the portal venous (e) and equilibrium (f) phases. In the hepatobiliary phase (g, h) the lesions appear slightly hyperintense, due to the abnormal biliary system drainage which results in a reduced rate of bile elimination.

Fig. 6a-h. Nodular regenerative hyperplasia after Gd-BOPTA in a patient with previous testicular cancer. A large slightly hyperintense nodule (arrow) and a smaller round hypointense nodule (arrowhead) are visible on the pre-contrast TSE T2-weighted image (a). On the corresponding pre-contrast GRE T1-weighted "in-phase" image (b), numerous slightly hypointense nodules (arrows) are visible. These lesions appear slightly hyperintense in a diffuse fatty liver on the pre-contrast GRE Tl-weighted "out-of-phase" image (c). The lesions show marked and homogeneous enhancement on the arterial phase image (d) of the dynamic study after Gd-BOPTA administration, followed by rapid wash-out in the portal venous (e) and equilibrium (f) phases. In the hepatobiliary phase (g, h) the lesions appear slightly hyperintense, due to the abnormal biliary system drainage which results in a reduced rate of bile elimination.

Fig. 7a-f. Nodular regenerative hyperplasia after Gd-BOPTA. No liver lesions are visible on the pre-contrast TSE T2-weighted image (a). Conversely, the pre-contrast GRE Tl-weighted "in-phase" (b) and "out-of-phase" (c) images reveal numerous slightly hyperintense nodules (arrows) surrounded by a thin hypointense rim. During the dynamic evaluation after Gd-BOPTA administration (d, e) the lesions show weak enhancement, which is more evident in the portal venous phase (e). In the hepatobiliary phase (f), multiple well-defined hyperintense lesions with a thin hypointense peripheral rim can be seen

Fig. 7a-f. Nodular regenerative hyperplasia after Gd-BOPTA. No liver lesions are visible on the pre-contrast TSE T2-weighted image (a). Conversely, the pre-contrast GRE Tl-weighted "in-phase" (b) and "out-of-phase" (c) images reveal numerous slightly hyperintense nodules (arrows) surrounded by a thin hypointense rim. During the dynamic evaluation after Gd-BOPTA administration (d, e) the lesions show weak enhancement, which is more evident in the portal venous phase (e). In the hepatobiliary phase (f), multiple well-defined hyperintense lesions with a thin hypointense peripheral rim can be seen

Fig. 8a, b. Nodular regenerative hyperplasia after Mn-DPDP. Same case as Fig. 7. The pre-contrast GRE Tl-weighted image (a) reveals numerous slightly hyperintense nodules (arrows) surrounded by a thin hypointense rim. In the hepatobiliary phase after Mn-DPDP administration (b), the nodules are homogeneously hyperintense due to uptake of Mn++ into the lesion, similar to the appearance after Gd-BOPTA

Fig. 8a, b. Nodular regenerative hyperplasia after Mn-DPDP. Same case as Fig. 7. The pre-contrast GRE Tl-weighted image (a) reveals numerous slightly hyperintense nodules (arrows) surrounded by a thin hypointense rim. In the hepatobiliary phase after Mn-DPDP administration (b), the nodules are homogeneously hyperintense due to uptake of Mn++ into the lesion, similar to the appearance after Gd-BOPTA

Fig. 9a-f. Nodular regenerative hyperplasia after SH U 555 A. Same case as Fig. 6. The pre-contrast T2*-weighted image (a) reveals numerous slightly hyperintense nodules. Conversely, no lesions are visible on the pre-contrast Tl-weighted VIBE image (b). In the arterial phase (c) of the dynamic study after SH U 555 A administration, numerous well-defined hyperintense lesions are visible. These lesions demonstrate rapid contrast wash-out in the portal venous (d) and equilibrium (e) phases. In the reticuloendothelial phase (f) the nodules show a marked signal drop due to the uptake of iron oxide particles by Kupffer cells, similar to the observation in FNH

Fig. 9a-f. Nodular regenerative hyperplasia after SH U 555 A. Same case as Fig. 6. The pre-contrast T2*-weighted image (a) reveals numerous slightly hyperintense nodules. Conversely, no lesions are visible on the pre-contrast Tl-weighted VIBE image (b). In the arterial phase (c) of the dynamic study after SH U 555 A administration, numerous well-defined hyperintense lesions are visible. These lesions demonstrate rapid contrast wash-out in the portal venous (d) and equilibrium (e) phases. In the reticuloendothelial phase (f) the nodules show a marked signal drop due to the uptake of iron oxide particles by Kupffer cells, similar to the observation in FNH

brane results in these lesions appearing hy-pointense on delayed hepatobiliary phase images against normal enhanced liver parenchyma in which enhancement derives from the presence of Gd-BOPTA in both the hepatocytes and adjacent biliary system. This has proven a highly accurate means of differentiating HA from FNH [7].

HA typically appear iso- or hyperintense on delayed hepatobiliary phase images after man-gafodipir trisodium administration because the Mn++ ion non-specifically enters the HA lesion he-patocytes via ionic channels. Unfortunately, since a similar enhancement pattern is seen with FNH, the accurate differentiation of these lesions is not possible using this contrast agent (Figs. 10,11).

Due to the variable number and activity of Kupffer cells in different HA, variable uptake of SPIO particles occurs, leading to a different appearance on post-contrast T2-weighted images (Figs. 12 , 13) [7]. Uptake of SPIO particles in HA may also be due to pooling of the contrast agent within the peliosis-like dilated vessels.

In liver adenomatosis, which is characterized by the presence of multiple adenomas in the same patient, the lesions may appear small or large, non-complicated or complicated. Moreover, some nodules may appear with fatty metamorphosis while others may have a homogeneous appearance. For these reasons the enhancement behavior typically varies for different lesions (Fig. 14).

Fig. 10a-k. Non-complicated hepatic adenoma after Gd-BOPTA and Mn-DPDP. A large nodule (asterisk), located in the left lobe of the liver, appears slightly hyperintense on the pre-contrast TSE T2-weighted image (a), isointense on the pre-contrast GRE Tl-weighted "inphase" image (b) and homogeneously hypointense on the GRE Tl-weighted "out-of-phase" image (c). The lesion demonstrates homogeneous enhancement in the arterial phase (d) of the dynamic series after administration of Gd-BOPTA, followed by rapid wash-out in the portal venous (e) and equilibrium (f) phases. The lesion is hypointense in the hepatobiliary phase after Gd-BOPTA administration (g, h) due to a decreased hepatocyte uptake of Gd-BOPTA as well as to the absence of bile ductules. Conversely, the lesion is isointense compared to the normal liver parenchyma on hepatobiliary phase images (i, j) after the administration of Mn-DPDP. This is due to the fact that Mn++ ions non-specifically enter the hepatocytes of the lesion via ionic channels. The gross specimen (k) shows a heterogeneous, well-defined, non-hemorrhagic and non-necrotic mass

Fig. 10a-k. Non-complicated hepatic adenoma after Gd-BOPTA and Mn-DPDP. A large nodule (asterisk), located in the left lobe of the liver, appears slightly hyperintense on the pre-contrast TSE T2-weighted image (a), isointense on the pre-contrast GRE Tl-weighted "inphase" image (b) and homogeneously hypointense on the GRE Tl-weighted "out-of-phase" image (c). The lesion demonstrates homogeneous enhancement in the arterial phase (d) of the dynamic series after administration of Gd-BOPTA, followed by rapid wash-out in the portal venous (e) and equilibrium (f) phases. The lesion is hypointense in the hepatobiliary phase after Gd-BOPTA administration (g, h) due to a decreased hepatocyte uptake of Gd-BOPTA as well as to the absence of bile ductules. Conversely, the lesion is isointense compared to the normal liver parenchyma on hepatobiliary phase images (i, j) after the administration of Mn-DPDP. This is due to the fact that Mn++ ions non-specifically enter the hepatocytes of the lesion via ionic channels. The gross specimen (k) shows a heterogeneous, well-defined, non-hemorrhagic and non-necrotic mass

Fig. 11a-i. Coexisting hepatic adenoma and focal nodular hyperplasia after Gd-BOPTA and Mn-DPDP. The pre-contrast TSE T2-weighted image (a) reveals a large lesion (arrows) with heterogeneous signal intensity indicative of two different nodules. On the corresponding pre-contrast GRE T1-weighted "in-phase" (b) and "out-of-phase" (c) images, the lesion is isointense compared to the surrounding liver parenchyma. Unusual enhancement behavior is noted on dynamic phase images after the bolus injection of Gd-BOPTA (d-f). On the arterial phase image (d) the larger nodule (asterisk) appears slightly hyperintense while the smaller nodule (arrowheads) appears strongly hyperintense compared to the normal liver parenchyma. In the portal venous phase (e) both nodules appear homogeneously hyperintense with rapid wash-out of enhancement noted in the equilibrium phase (f). In the hepatobiliary phase after Gd-BOPTA administration (g) the larger nodule is markedly hypointense while the smaller nodule is slightly hyperintense. The enhancement behavior of the two nodules is characteristic for HA and FNH, respectively. In the hepatobiliary phase after Mn-DPDP administration (h), both nodules are isointense compared to the surrounding liver, indicating non-specific entry of Mn++ ions into hepatocytes. The gross specimen (i) confirms the different composition of the lesions: the FNH has a more homogeneous appearance (arrows) while the HA has a heterogeneous appearance due to hemorrhagic areas

Fig. 12a-f. Non complicated hepatic adenoma after SH U 555 A. Same case as shown in Fig. 10. The lesion is isointense compared to the liver on the pre-contrast T2*-weighted image (a) and homogeneously hypointense on the pre-contrast VIBE image (b). The lesion is homogeneously enhanced in the arterial phase (c) of the dynamic evaluation after administration of SH U 555 A. Note the presence of feeding vessels (arrowhead). The lesion appears hypointense in the subsequent portal venous (d) and equilibrium (e) phases. In the reticuloendothelial phase (f) the lesion shows heterogeneous uptake of iron oxide particles characterized by a peripheral drop in signal

Fig. 12a-f. Non complicated hepatic adenoma after SH U 555 A. Same case as shown in Fig. 10. The lesion is isointense compared to the liver on the pre-contrast T2*-weighted image (a) and homogeneously hypointense on the pre-contrast VIBE image (b). The lesion is homogeneously enhanced in the arterial phase (c) of the dynamic evaluation after administration of SH U 555 A. Note the presence of feeding vessels (arrowhead). The lesion appears hypointense in the subsequent portal venous (d) and equilibrium (e) phases. In the reticuloendothelial phase (f) the lesion shows heterogeneous uptake of iron oxide particles characterized by a peripheral drop in signal

Fig 13a-f. Coexisting hepatic adenoma and focal nodular hyperplasia after SH U 555 A. Same case as Fig. 11. The lesion appears isointense on the pre-contrast T2*-weighted image (a), while on the VIBE image (b) the smaller nodule appears isointense at the periphery and hypointense in the central portion (arrow). On the arterial phase image (c) of the dynamic series after the administration of SH U 555 A, the bigger nodule appears slightly heterogeneously hyperintense while the smaller nodule is homogeneously hyperintense. In the portal venous (d) and equilibrium (e) phases the FNH (smaller nodule) appears hypointense, while the HA remains heterogeneously slightly hyperintense. In the reticuloendothelial phase (f) both lesions show a signal drop due to the presence of Kupffer cells, however the signal drop is less pronounced in the smaller FNH nodule

Fig. 14a-h. Liver adenomatosis and FNH after Gd-BOPTA, Mn-DPDP and SPIO. The pre-contrast TSE T2-weighted image (a) and the GRE Tl-weighted "in-phase" image (b) reveal a small, round, hypointense lesion (arrowhead) located in segment II of the liver. In segment I an isointense nodule (arrow/) with a hyperintense (T2-weighted image) and hypointense (Tl-weighted image) central scar is visible. On the pre-con-trast GRE Tl-weighted "out-of-phase" image (c) the small nodule in segment II appears hyperintense while two other hyperintense lesions (arrowheads) are visible in the right lobe. The lesion located in segment I appears slightly hyperintense. During the arterial phase after Gd-BOPTA administration (d) the nodules (arrows) in segments II and I appear markedly hyperintense; conversely the two nodules located in the right lobe are isointense. In the portal venous phase (e) all the lesions appear isointense. On the hepatobiliary phase image (f) acquired after Gd-BOPTA administration, several hypointense nodules, suggestive of HA, are visible. The nodule in segment I of the liver appears isointense, which is suggestive of FNH. After Mn-DPDP administration (g) some hyperintense nodules are visible in the right lobe of the liver, while the nodules located in segments II and I appear isointense. On the reticuloendothelial phase image (h) after SPIO administration all the nodules are isointense compared to the normal liver, due to the presence of Kupffer cells within the lesions. This case illustrates that HA is more easily differentiated from FNH with Gd-BOPTA

Fig. 14a-h. Liver adenomatosis and FNH after Gd-BOPTA, Mn-DPDP and SPIO. The pre-contrast TSE T2-weighted image (a) and the GRE Tl-weighted "in-phase" image (b) reveal a small, round, hypointense lesion (arrowhead) located in segment II of the liver. In segment I an isointense nodule (arrow/) with a hyperintense (T2-weighted image) and hypointense (Tl-weighted image) central scar is visible. On the pre-con-trast GRE Tl-weighted "out-of-phase" image (c) the small nodule in segment II appears hyperintense while two other hyperintense lesions (arrowheads) are visible in the right lobe. The lesion located in segment I appears slightly hyperintense. During the arterial phase after Gd-BOPTA administration (d) the nodules (arrows) in segments II and I appear markedly hyperintense; conversely the two nodules located in the right lobe are isointense. In the portal venous phase (e) all the lesions appear isointense. On the hepatobiliary phase image (f) acquired after Gd-BOPTA administration, several hypointense nodules, suggestive of HA, are visible. The nodule in segment I of the liver appears isointense, which is suggestive of FNH. After Mn-DPDP administration (g) some hyperintense nodules are visible in the right lobe of the liver, while the nodules located in segments II and I appear isointense. On the reticuloendothelial phase image (h) after SPIO administration all the nodules are isointense compared to the normal liver, due to the presence of Kupffer cells within the lesions. This case illustrates that HA is more easily differentiated from FNH with Gd-BOPTA

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