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Mri The Liver

Fig. 6a-d. Atypical hemangioma. Patient with history of renal cell carcinoma. The precontrast CT scan (a) shows a large, slightly hypo-dense lesion (arrows) located in segment VIII of the right liver lobe. In the arterial phase of the dynamic study after contrast medium administration (b) the hemangioma demonstrates an irregular and marked enhancement with progressive but incomplete filling in the portal-venous (c) and equilibrium (d) phases

Fig. 6a-d. Atypical hemangioma. Patient with history of renal cell carcinoma. The precontrast CT scan (a) shows a large, slightly hypo-dense lesion (arrows) located in segment VIII of the right liver lobe. In the arterial phase of the dynamic study after contrast medium administration (b) the hemangioma demonstrates an irregular and marked enhancement with progressive but incomplete filling in the portal-venous (c) and equilibrium (d) phases a

Mri Liver Hemangioma Protocol
Fig. 7a, b. Hemangioma. On the unenhanced GE T1-weighted MR image (a), the hemangioma is seen as a well-defined hypointense mass. Conversely, on the T2-weighted image (b), the lesion (arrowhead) is markedly hyperintense
Hemangioma

Fig. 8a-d. Hypervascular hemangioma after Gd-BOPTA .The lesion is markedly hyperintense (arrow) on the Turbo SE T2-weighted image (a) and hypointense on the GE Tl-weighted image (b). Rapid enhancement on images acquired during the arterial phase (c) after the bolus injection of Gd-BOPTA is noted, which persists and becomes homogeneous during the portal-venous phase (d)

Fig. 8a-d. Hypervascular hemangioma after Gd-BOPTA .The lesion is markedly hyperintense (arrow) on the Turbo SE T2-weighted image (a) and hypointense on the GE Tl-weighted image (b). Rapid enhancement on images acquired during the arterial phase (c) after the bolus injection of Gd-BOPTA is noted, which persists and becomes homogeneous during the portal-venous phase (d)

Fig. 9a-e. Cavernous hemangioma after Gd-BOPTA. The mass (asterisk) is het-erogeneously hyperintense on the SE T2-weighted image (a) and hypointense on the precontrast GE T1-weighted image (b). During the arterial phase (c), multiple focal areas of nodular enhancement (arrows) that are isointense with the aorta are seen in the periphery. Centripetal filling-in has occurred when the equilibrium phase is reached (d). During the delayed liver-specific phase after Gd-BOPTA (e), the lesion appears slightly heterogeneously hypointense imaging of the liver, is a very useful discriminating feature for the differential diagnosis of heman-giomas and metastases [59]. The third pattern of enhancement includes lesions that enhance homogeneously and thus may be difficult to differentiate from hypervascular metastases, which may demonstrate similar enhancement behavior. For these lesions, the combination of T2-weighted and serial dynamic post-contrast T1-weighted images facilitates a confident diagnosis of hemangioma (Fig. 10) [94].

Liver-specific contrast agents have also been evaluated for the characterization of heman-giomas. As in the case of purely extracellular Gd agents, a "nodular" centripetal pattern of enhancement on dynamic imaging after Gd-BOPTA and Gd-EOB-DTPA administration is considered highly specific for hemangioma in a manner sim ilar to the finding of rim enhancement in the case of liver metastases. In the delayed liver-specific phase, hemangiomas tend to be isointense or hy-pointense compared to the surrounding liver parenchyma, and often contain low intensity areas indicative of fibrotic or cystic components. While contrast agent pooling of intralesional components may be seen a peripheral wash-out as observed in metastases is not observed in heman-giomas.

Superparamagnetic iron oxide (SPIO) contrast agents have also been evaluated for the characterization of hemangiomas, especially when these appear atypical on other imaging modalities. After administration of SPIO, hemangiomas appear hy-perintense on post-contrast T1-weighted images compared to surrounding liver parenchyma, the reverse of their appearance on pre-contrast T1-

Atypic Fnh Mri

Fig. 10a-e. Capillary hemangioma. On the unenhanced T2-weighted TSE image (a) the capillary hemangioma (arrow) is markedly hyperintense, whereas on the GRE Tl-weighted image (b) it is hypointense. During the dynamic study after contrast agent administration, rapid, almost complete filling-in is seen in the arterial phase (c) which persists, completely and homogeneously, into the portal-venous (d) and equilibrium (e) phases

Fig. 10a-e. Capillary hemangioma. On the unenhanced T2-weighted TSE image (a) the capillary hemangioma (arrow) is markedly hyperintense, whereas on the GRE Tl-weighted image (b) it is hypointense. During the dynamic study after contrast agent administration, rapid, almost complete filling-in is seen in the arterial phase (c) which persists, completely and homogeneously, into the portal-venous (d) and equilibrium (e) phases

Mri Contrast
Fig. 11a, b. Hemangioma after SPIO. On the unenhanced GE Tl-weighted image the hemangioma appears hypointense (a). On the post-contrast Tl-weighted image after SPIO administration (b) the lesion shows increased signal intensity compared to the surrounding liver tissue (T1 effect)

Fig. 12a-c. Hemangioma after USPIO. The same case as shown in Fig. 11. A hypointense lesion (arrowhead) is seen on the unenhanced Tl-weighted image (a). During the dynamic phase after the bolus injection of SHU 555 A (b, c), the hemangioma (arrows) demonstrates weak nodular peripheral enhancement that progresses with time weighted images. This signal enhancement is caused by a T1 effect due to low SPIO concentration in the vascular channels of hemangiomas. However, this effect can only be observed on T1-weighted delayed phase images, which are not routinely acquired after administration of SPIO (Fig. 11) [35].

With the use of ultrasmall superparamagnetic iron oxide (USPIO) contrast agents, which are ultimately cleared by the reticuloendothelial system but which reside in the intravascular compartment immediately after injection, hemangiomas enhance on T1-weighted dynamic images and appear hyperintense compared with the normal liver parenchyma (Fig. 12). On T2-weighted scans the lesions decrease in signal intensity and, at higher doses of USPIO, may become isointense with the liver [90].

Hemangiomas usually do not contain significant amounts of Kupffer cells or normal hepato-cytes and therefore do not take up SPIO particles or Mn++ after the infusion of mangafodipir trisodi-um. Specifically, on delayed phase T2-weighted images after SPIO administration, hemangiomas appear hyperintense, whereas on T1-weighted images in the hepatobiliary phase after administration of mangafodipir trisodium hemangiomas generally appear hypointense.

Focal Nodular Hyperplasia

FNH is a benign tumor-like lesion of the liver which is considered to be the result of a hyperplastic response of the hepatocytes to the presence of a pre-existing vascular malformation. It is thought that increased arterial flow hyperperfuses the local parenchyma leading to secondary hepatocellular hyperplasia [111].

In support of this theory, FNH has been found in association with cavernous hemangioma and in some cases FNH has been associated with vascular malformations of various other organs and with neoplasms of the brain (Fig. 13) [111].

In frequency, FNH is the second most common benign hepatic tumor after hemangioma and has been shown to constitute about 8% of primary hepatic tumors at autopsy. It usually occurs in women of childbearing- and middle-age, but cases have been reported in men and children as well. Most investigators agree that oral contraceptives are not the causal agents of FNH [9]. However estrogens could have a trophic effect on FNH by increasing the size of nodules and contributing to the vascular changes [111].

Clinically, this tumor is usually an incidental finding at autopsy, elective surgery or on diagnos

Fig. 13a-f. Focal nodular hyperplasia (FNH) / Hemangioma. Unenhanced T2-weighted images (a) show a slightly hyperintense lesion with a small hyperintense central scar (arrow) compressing the gallbladder. An additional subcapsular lesion (arrowhead) with homogeneous high signal intensity (light-bulb phenomenon indicative of hemangioma) can be seen. On the unenhanced T1-weighted GE echo image (b), the suspected hemangioma appears homogeneously hypointense with distinct borders while the lesion compressing the gallbladder shows isointense signal intensity and lobulation. On arterial phase images after the bolus administration of Gd-BOPTA (c), the lesion located near the gallbladder shows strong hyperintensity with a central hypointense scar. On portal-venous phase images (d), this lesion is still hyperintense and clearly delineated and the central scar is still hypointense. The second lesion demonstrates nodular peripheral enhancement typical of hemangioma. Imaging during the equilibrium phase 5 min after Gd-BOPTA administration (e) reveals enhancement of the central scar, a typical enhancement pattern of pseudoscar formation in FNH. The second lesion shows homogeneous contrast agent uptake. In the hepatobiliary phase (f), the lesion close to the gallbladder appears isointense compared to the surrounding parenchyma, indicating a lesion consisting of functioning hepatocytes able to take up Gd-BOPTA. The imaging pattern is consistent with that of an FNH. The second lesion is again hypointense and the imaging pattern is consistent with that of a hemangioma

Mri The Liver

Fig. 13a-f. Focal nodular hyperplasia (FNH) / Hemangioma. Unenhanced T2-weighted images (a) show a slightly hyperintense lesion with a small hyperintense central scar (arrow) compressing the gallbladder. An additional subcapsular lesion (arrowhead) with homogeneous high signal intensity (light-bulb phenomenon indicative of hemangioma) can be seen. On the unenhanced T1-weighted GE echo image (b), the suspected hemangioma appears homogeneously hypointense with distinct borders while the lesion compressing the gallbladder shows isointense signal intensity and lobulation. On arterial phase images after the bolus administration of Gd-BOPTA (c), the lesion located near the gallbladder shows strong hyperintensity with a central hypointense scar. On portal-venous phase images (d), this lesion is still hyperintense and clearly delineated and the central scar is still hypointense. The second lesion demonstrates nodular peripheral enhancement typical of hemangioma. Imaging during the equilibrium phase 5 min after Gd-BOPTA administration (e) reveals enhancement of the central scar, a typical enhancement pattern of pseudoscar formation in FNH. The second lesion shows homogeneous contrast agent uptake. In the hepatobiliary phase (f), the lesion close to the gallbladder appears isointense compared to the surrounding parenchyma, indicating a lesion consisting of functioning hepatocytes able to take up Gd-BOPTA. The imaging pattern is consistent with that of an FNH. The second lesion is again hypointense and the imaging pattern is consistent with that of a hemangioma tic liver imaging performed for other reasons. Less than one third of cases are discovered because of clinical symptoms, usually comprising right upper quadrant or epigastric pain. Although most patients are asymptomatic at discovery, in symptomatic cases pain is usually caused by larger lesions, which expand the Glisson capsule or have a focal mass effect on surrounding organs.

The natural history of FNH is characterized by the absence of complications. Therefore, typical asymptomatic FNH should be managed conservatively in association with the discontinuation of oral contraceptives. Rarely, when symptoms are particularly severe, surgical resection may be indicated.

FNH is usually a solitary, subcapsular nodular mass, but cases with several nodules have been described (Fig. 14). FNH is a homogeneous tumor, which only infrequently demonstrates hemorrhage and necrosis. On cut section the majority of these tumors have a central fibrous scar and although the margin is sharp, generally there is no capsule [19].

Often FNH has a mean diameter of 5 cm at the time of diagnosis, although sometimes it is possible to find neoplasms that replace an entire lobe of the liver, as in the lobar FNH form.

Currently, FNH is divided into two types, classic and non-classic. Classic FNH is characterized by the presence of abnormal nodular architecture, malformed vessels, and cholangiocellular proliferation. The non-classic type comprises three subtypes: a) telangiectatic FNH, b) FNH with cyto-logic atypia and c) mixed hyperplastic and adeno-matous FNH.

Non-classic FNH may lack the nodular abnormal architecture and malformed vessels, which characterize the classic type, but they always show bile ductular proliferation [73].

The gross appearance of classic FNH consists of lobulated contours and parenchyma that is composed of nodules surrounded by radiating fibrous septa originating from a central scar that contains malformed vessels. A classical form of FNH with a stellate scar is seen in about 50% of cases; however, variant lesions are increasingly being detected. These variant lesions are often small with atypical features, such as the absence of a central scar or teleangiectatic changes. The most characteristic microscopic features of classic FNH are fibrous septa and cellular areas of hepatic proliferation. The hepatic plates may be moderately thickened and contain normal hepatocytes. The central scar typically consists of fibrous connective tissue, cholangiocellular proliferation with inflammatory infiltrates and malformed vessels, including tortuous arteries, capillaries and veins.

The arterial blood in FNH, as opposed to that in adenoma, flows centrifugally from the anomalous central arteries. Both classic and non-classic types contain a variable content of Kupffer cells.

In contrast, the gross appearance of non-classic FNH is heterogeneous and globally resembles that of adenoma, with lobulated contours and no macroscopic central scar. The histological findings of non-classic FNH depend on the subtype [9,73]. The teleangiectatic type consists of hepatic plates that frequently appear atrophic. The plates are one cell thick and are separated by dilated sinusoids. Fibrous septa can be found in all cases of teleang-iectatic FNH that contain some degree of bile duct proliferation. In this type of FNH arteries have a hypertrophic muscular media but no intimal proliferation. In contrast to the classic form, these abnormal vessels drain directly into the adjacent sinusoids, while in classic FNH connections to the sinusoids are almost never seen. Necrotic areas and hemorrhage can be found within teleangiectatic FNH; these features are often responsible for the appearance of the tumor and the presence of abdominal pain [73,111]. FNH with cytological atyp-ia have the gross and histological features of classic FNH but contain areas of large cell dysplasia. The mixed hyperplastic and adenomatous form of FNH has two variants, one resembling the teleangiectat-ic type, the other simulating adenoma [73].

When multiple, FNH lesions tend to be associated with other lesions, such as hepatic heman-gioma, meningioma, astrocytoma, teleangiectasia of the brain, and systemic arterial dysplasia. FNH has also been described in association with hepa-tocellular adenoma and liver adenomatosis. In these cases it appears that FNH lesions may be secondary to systemic and local abnormalities of vascular growth induced by oral contraceptives, tumor-induced growth factors, thrombosis or local arteriovenous shunting [9].

On US images, classic FNH appears as a homogeneous well-demarcated nodule which may be hypoechoic, isoechoic or slightly hyperechoic relative to the normal liver parenchyma (Fig. 15). Displacement of contiguous hepatic vessels may be the only detectable abnormality. Some lesions may show a hypoechoic halo surrounding the lesion; this halo most likely represents compressed hepatic parenchyma and is more evident around nodules with fatty infiltration or which are located in steatotic liver tissue.

The central scar and the fibrous septa are often difficult to visualize on US. However, when apparent, the central scar is usually hyperechoic while the fibrous septa are hypoechoic. Characteristic findings at color Doppler US include the presence of a central feeding artery with a stellate or spoke-wheel pattern, which corresponds to vessels running into the radiating fibrous septa from the central scar (Fig. 16). The spectral analysis may show an intratumoral pulsatile waveform with high di-astolic flow and low resistive index corresponding to malformed arteries, and a continuous waveform which could represent a draining vein of the neoplasm [112]. US in general is a non-specific imaging method for the characterization of non-classic FNH.

The hypervascularity of the lesion is detected using SonoVue-enhanced US. In the arterial phase of the dynamic study the intralesional vessels are typically of the stellate or spoke-wheel configuration and the lesion appears homogeneously hyper-echoic compared to the normal liver parenchyma. In the portal-venous phase, FNH remains hypere-choic and the nodule gradually becomes isoechoic with the adjacent liver in the later phases of dynamic imaging. Conversely the central scar is depicted as a hypo- or anechoic area within the hy-perechoic lesion during both the arterial and portal-venous phases, while it shows uptake of contrast in the later phases (Fig. 17) [57].

On unenhanced CT FNH is usually isoattenuat-ing or slightly hypoattenuating. When the lesion is isoattenuating compared to the normal liver parenchyma, it may be detectable only because of

Liver Lesion

Fig. 14a-j. Multiple focal nodular hyperplasia. Unenhanced axial and coronal T2-weighted images (a, b) reveal several slightly hyperintense liver lesions (arrows) with one lesion in the left liver lobe demonstrating a central scar (arrowhead). On the unenhanced T1-weight-ed image (c) the lesions are slightly hypointense. Arterial phase images acquired after the bolus injection of Gd-BOPTA reveal strong hy-pervascularization of all the lesions (d-f), and a central scar in three of the lesions (arrows). In the portal-venous phase (g) the lesions are slightly hyperintense. In the equilibrium phase (h), the central scar of the lesion in the left liver lobe shows late enhancement (arrow). This is typical for FNH in which the central scar is more an arterio-venous malformation than a true scar. T1-weighted images acquired during the hepatobiliary phase (i), show enhancement of the liver lesions. This is more obvious on T1-weighted fs images (arrows) acquired at the same time point (j) and is indicative of the lesions containing functioning hepatocytes that are able to take up Gd-BOPTA. The fact that the lesions enhance to a higher degree than the surrounding liver tissue is indicative of the benign nature of the lesions and of the fact that the biliary system of FNH is malformed, leading to a slowing of biliary excretion

Focal Nodular Hyperplasia The Liver
Fig.15a, b. Classic focal nodular hyperplasia on US. The ultrasound examination reveals a homogeneous lesion (arrows) that is either hy-poechoic (a) or hyperechoic (b) compared to the surrounding normal liver tissue

Fig. 16a, b. Classic focal nodular hyperplasia on color Doppler US. On ultrasound (a) the lesion (asterisk is isoechoic and only a displacement of the middle hepatic vein is appreciable (arrowhead). Color Doppler US (b) shows vascularization within the lesion, corresponding to vessels running in the radiating fibrous septa, demonstrating a spoke-wheel pattern

Fig. 16a, b. Classic focal nodular hyperplasia on color Doppler US. On ultrasound (a) the lesion (asterisk is isoechoic and only a displacement of the middle hepatic vein is appreciable (arrowhead). Color Doppler US (b) shows vascularization within the lesion, corresponding to vessels running in the radiating fibrous septa, demonstrating a spoke-wheel pattern its mass effect. FNH generally only appears hyper-attenuating to unenhanced liver when there is hepatic steatosis or when the liver is otherwise abnormally decreased in attenuation. However, in rare cases FNH may still be isoattenuating or hy-poattenuating on unenhanced CT in patients with hepatic steatosis when there is fatty infiltration of the FNH itself [67]. In a third of cases, a low-density central area is seen, corresponding to the central scar [95].

During the arterial phase of contrast-enhanced CT, FNH enhances rapidly and becomes hyper-dense compared to normal liver. The low-attenuation scar appears conspicuous against the hyper-dense tissue, and foci of enhancement representing feeding arteries may be seen within the scar. In the portal-venous phase of enhancement, the difference in attenuation between FNH and normal liver decreases and FNH may become isodense with normal liver parenchyma. The central scar is almost always seen as hypoattenuating to the remainder of the FNH on unenhanced and enhanced dynamic phase scans. On delayed scans, however, there is retention of contrast material within the fibrous scar, giving it an isoattenuating or, more frequently, a hyperattenuating appearance (Fig. 18). Detection of the central scar is related to the size of the lesion; while a central scar may be identified in as many as 65% of larger FNH, it may be seen in only about 35% of lesions smaller than 3 cm in diameter [15,19]. 3D multidetector CT angiography is very useful in demonstrating the intratumoral vascularization of FNH which is characterized by hepatic venous drainage and by the absence of portal-venous supply (Fig. 19) [17].

On MR, FNH are considered classic when they appear as homogeneously isointense or slightly hy-perintense on T2-weighted images, and isointense or slightly hypointense on T1-weighted images before contrast agent administration. Typical behavior during the dynamic phase of contrast enhancement is marked and homogeneous signal intensity enhancement during the arterial phase, rapid and homogeneous signal intensity wash-out during the portal-venous phase, and signal isointensity (with the exception of the scar) during the equilibrium phase (Fig. 20). A typical scar appears as a hyper-intense central stellate area on T2-weighted images and as a hypointense area on T1-weighted images. During the dynamic phase of contrast enhancement a typical scar is hypointense during the arterial and portal-venous phases and slightly hyper-intense in the equilibrium phase (Fig. 20).

Atypical features of FNH generally consist of le-

Fig. 17a-d. Focal nodular hyperplasia with SonoVue. Precontrast US (a) reveals a well defined isoechoic nodule (arrow) surrounded by a hypoechoic halo. In the arterial phase (b) after SonoVue administration the FNH (arrow) appears homogeneously hyperechoic compared to the normal liver parenchyma. Rapid contrast wash-out occurs in the portal-venous (c) and equilibrium (d) phases

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Fig. 18a-d. Focal nodular hyperplasia on CT. On the unenhanced CT scan (a) the FNH (arrows) is isoattenuating to the liver. During the arterial phase (b) after contrast medium administration, the nodule enhances rapidly and homogeneously while the central scar (arrowhead) remains hypodense. In the portal-venous and equilibrium phases (cand d, respectively) the FNH appears isodense compared to the normal liver parenchyma (arrows in c). In the equilibrium phase (d) the central scar is depicted as hyperattenuating (arrow

Non Enhanced Scar

Fig. 19. Focal nodular hyperplasia on 3D multidetector CT angiography. 3D multidetector CT angiography shows the intratu-moral vascularization, characterized by an arterial vessel leading directly into the lesion (arrowhead) and hepatic venous drainage

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Fig. 20a-f. Focal nodular hyperplasia. On the Turbo SE T2-weighted and HASTE T2-weighted images (a and b, respectively), the nodule (arrows) is isointense compared to the surrounding liver tissue and possesses a hyperintense "stellate" central scar. On the unenhanced T1-weighted image (c), the FNH (arrows) appears as an isointense lesion with a hypointense central scar. This lesion shows intense and homogeneous enhancement during the arterial phase after contrast agent administration (d) and rapid wash-out in the portal-venous phase (e). In the equilibrium phase (f), the lesion is again isointense. The central scar is typically hypointense during the arterial and portal-venous phases. However, it appears hyperintense (arrow) in the equilibrium phase comparable to that seen in CT imaging

Fig. 21a-h. Atypical focal nodular hyperplasia with Gd-DTPA. On the precontrast HASTE T2-weighted image (a) the nodule (arrow) is slightly hyperintense compared to the surrounding normal liver parenchyma, whereas on the GRE Tl-weighted "in-phase" image (b) it appears het-erogeneously isointense (arrow). On the GRE T1-weighted "out-of-phase" image (c) it appears heterogeneously hypointense. In the arterial phase of the dynamic evaluation after contrast agent administration (d) the lesion shows marked enhancement, with persistent uptake of contrast material in the portal-venous (e) and equilibrium (f) phases. On late GRE Tl-weighted "in-phase" (g) and "out-of-phase" (h) images the nodule appears as a well defined, slightly hypointense lesion. This behavior could be related to sinusoidal dilatation

Contrast Agent Enhanced Mri Imaging

Fig. 22a-e. Atypical focal nodular hyperplasia. On the unenhanced T2- and T1-weight-ed images (a and b, respectively), the lesion (aster/skin a) is isointense as compared with the normal liver tissue and is delineated by a thin hypointense rim (arrowheadsin b). During the early arterial (c) and portal-venous (d) phases after contrast agent administration, the lesion (arrowheads) is seen as highly vascularized. The lesion remains slightly hyperintense in the equilibrium phase (e) when a hyperintense peripheral rim can also be seen sion heterogeneity, hyperintensity on T1-weighted images, strong hyperintensity on T2-weighted images and hypointensity in the portal-venous or equilibrium phases. Hyperintensity on T1-weight-ed images may be due to different pathologic changes, including fat deposition, copper accumulation, high protein concentration, blood degradation products or sinusoidal dilatation. Persistent contrast agent uptake in teleangiectatic FNH could be related to sinusoidal dilatation (Fig. 21).

Other atypical features include the absence of a central scar in a lesion greater than 3 cm in size, scar hypointensity on T2-weighted images and scar hypointensity in the equilibrium phase following injection of contrast agent. Finally, the presence of a pseudocapsule, seen as a complete hyperintense perilesional ring during the equilibrium phase can be considered atypical (Fig. 22) [38]. In rare cases, hemorrhage, calcification, or necrosis can be observed in non-classic forms of FNH.

The use of contrast-enhanced dynamic MR imaging provides the greatest diagnostic sensitivity among the imaging techniques in current use, especially when combined with the information available on precontrast T1- and T2-weighted im-

Fig. 23a, b. Focal nodular hyperplasia after mangafodipir trisodium administration. On the precontrast T1-weighted image (a), the FNH is seen as isointense with a stellate hypointense central scar. On the delayed image after mangafodipir administration (b), the lesion is again isointense compared to the surrounding parenchyma

Fig. 23a, b. Focal nodular hyperplasia after mangafodipir trisodium administration. On the precontrast T1-weighted image (a), the FNH is seen as isointense with a stellate hypointense central scar. On the delayed image after mangafodipir administration (b), the lesion is again isointense compared to the surrounding parenchyma

Mri The Liver

Fig. 24a, b. Atypical focal nodular hyperplasia after Gd-BOPTA. The same case as presented in Fig. 22. On the precontrast T1-weighted image (a) the FNH is isointense to partially slightly hypointense compared to the normal liver tissue. During the hepatobiliary phase 3 h after the bolus administration of Gd-BOPTA (b), the lesion is again isointense to the surrounding liver parenchyma, indicating functioning he-patocytes. This enables the diagnosis of FNH

Fig. 24a, b. Atypical focal nodular hyperplasia after Gd-BOPTA. The same case as presented in Fig. 22. On the precontrast T1-weighted image (a) the FNH is isointense to partially slightly hypointense compared to the normal liver tissue. During the hepatobiliary phase 3 h after the bolus administration of Gd-BOPTA (b), the lesion is again isointense to the surrounding liver parenchyma, indicating functioning he-patocytes. This enables the diagnosis of FNH

Fig. 25a-f. Focal nodular hyperplasia after Gd-BOPTA. On the unenhanced T2-weighted HASTE and T1-weighted GE images (a, b) as well as on post-contrast T1-weighted images acquired during the dynamic (c, d, e) and delayed (f) phase after administration of Gd-BOPTA, typical findings of FNH are clearly depicted. Importantly, it is possible to characterize the nodule according to both morphological and functional criteria

Mri The Liver

Fig. 25a-f. Focal nodular hyperplasia after Gd-BOPTA. On the unenhanced T2-weighted HASTE and T1-weighted GE images (a, b) as well as on post-contrast T1-weighted images acquired during the dynamic (c, d, e) and delayed (f) phase after administration of Gd-BOPTA, typical findings of FNH are clearly depicted. Importantly, it is possible to characterize the nodule according to both morphological and functional criteria ages. However, the high frequency of atypical features does not permit the accurate characterization of FNH in every case. In this regard diagnosis on dynamic MR imaging with conventional extra-cellularly-distributed Gd agents relies on the same morphologic and hemodynamic features as helical CT [38].

The availability of liver-specific MR contrast agents increases the potential for accurate lesion characterization. FNH are depicted as either hy-perintense or isointense during the delayed phase after administration of Gd-BOPTA, Gd-EOB-DT-PA or Mn-DPDP, reflecting the abnormal biliary drainage within the lesion (Figs. 23,24).

Gd-BOPTA in particular offers both a dynamic and delayed phase imaging capability, thereby permitting both morphological and functional information to be acquired for the characterization of these lesions (Figs. 25,26) [38].

In the same way, Gd-EOB-DTPA is helpful in the characterization of FNH because FNH contains hepatocytes that take up this agent, resulting in

Eob Dtpa Hepatocytes

Fig. 26a-e. Atypical focal nodular hyperplasia after Gd-BOPTA On the unenhanced SE T2-weighted image (a), the lesion (asterisk) shows lobulated margins, exophytic growth and heterogeneous hyperintensity. On the pre-contrast GE Tl-weighted image (b), the lesion appears with heterogeneous hypointensity. During the arterial phase (c) after Gd-BOPTA administration, the nodule shows intense but heterogeneous enhancement. The lesion remains slightly hyperintense during the equilibrium phase (d). The signal intensity and enhancement pattern are not typical for FNH. On the hepatobiliary phase image (e), however, the lesion appears slightly hyperintense due to the uptake of Gd-BOPTA by normal hepatocytes and subsequent impaired biliary excretion. This finding is consistent with the characterization of FNH

Fig. 27a-d. Focal nodular hyperplasia after Gd-BOPTA. On the pre-contrast T1-weighted image (a) the FNH is seen as isointense compared with surrounding liver tissue. The intense and homogeneous enhancement seen during the arterial and portal-venous phases (band c, respectively), as well as the delayed isointensity demonstrated during the hepatobiliary phase (d), is typical for FNH

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Fig. 27a-d. Focal nodular hyperplasia after Gd-BOPTA. On the pre-contrast T1-weighted image (a) the FNH is seen as isointense compared with surrounding liver tissue. The intense and homogeneous enhancement seen during the arterial and portal-venous phases (band c, respectively), as well as the delayed isointensity demonstrated during the hepatobiliary phase (d), is typical for FNH

iso- or hyperintensity of the lesion compared with the normal liver parenchyma on delayed T1-weighted images; the enhancement pattern is very similar to that which is observed after Gd-BOPTA administration (Figs. 27,28) [62].

On delayed phase T2-weighted images after SPIO administration, typical FNH demonstrate a loss of signal due to uptake of iron oxide particles by Kupffer cells within the lesion (Fig. 29) [34]. The degree of signal loss on SPIO-enhanced T2-weight-ed images is significantly greater than that in other focal liver lesions such as HCC and hepatocellular adenoma; however, overlap may occur due to the lack of function of Kupffer cells in some FNH [75].

In a large series it was demonstrated that only 39% of FNH showed significant signal drop after

SPIO. The remaining 61% of nodules did not show significant signal drop and appeared homogeneously, but more frequently heterogeneously, hy-perintense on T2-weighted images after SPIO (Fig. 30) [39].

On dynamic Tl-weighted images after bolus USPIO administration (SH U 555 A), FNH in many cases demonstrate an initial, moderate signal increase followed by an early decrease of signal intensity due to contrast pooling (Fig. 31). The hy-pervascularity depicted on arterial phase images is generally inferior compared to that observed on Gd-enhanced arterial phase imaging. On dynamic T2-weighted images after USPIO administration, FNH demonstrate a decrease of signal intensity over time [44].

Fig. 28a-d. Focal nodular hyperplasia after Gd-EOB-DTPA. The same case as shown in Fig. 27. The enhancement pattern after Gd-EOB-DTPA is very similar to that observed after Gd-BOPTA; a slightly hypointense lesion on the unenhanced T1-weighted image (a) demonstrates strong hyperintensity during the arterial phase (b) after the administration of Gd-EOB-DTPA. The subsequent portal-venous phase image (c) reveals persistent enhancement typical of FNH. On the hepatobiliary phase image (d) the lesion demonstrates an iso/slightly hypointense appearance compared with the surrounding parenchyma. With this contrast agent the hepatobiliary phase image was acquired after 20 min

Fig. 28a-d. Focal nodular hyperplasia after Gd-EOB-DTPA. The same case as shown in Fig. 27. The enhancement pattern after Gd-EOB-DTPA is very similar to that observed after Gd-BOPTA; a slightly hypointense lesion on the unenhanced T1-weighted image (a) demonstrates strong hyperintensity during the arterial phase (b) after the administration of Gd-EOB-DTPA. The subsequent portal-venous phase image (c) reveals persistent enhancement typical of FNH. On the hepatobiliary phase image (d) the lesion demonstrates an iso/slightly hypointense appearance compared with the surrounding parenchyma. With this contrast agent the hepatobiliary phase image was acquired after 20 min

Hemochromatosis Liver Disease
Fig. 29a, b. Focal nodular hyperplasia before (a) and after (b) SPIO administration. After SPIO administration (b), the FNH (asteriskin a) shows significant signal drop compared with that seen on the pre-contrast image (a)

Fig. 30a, b. Focal nodular hyperplasia before (a) and after (b) SPIO administration. The same case as shown in Figure 26. The FNH (asterisk appears slightly heterogeneously hyperintense on the SE T2-weighted image (a). After SPIO administration (b), the nodule is still heterogeneously hyperintense compared to the surrounding normal liver. Note that compared with the unenhanced image (a), the signal drop in FNH is less pronounced than in normal liver parenchyma

Fig. 30a, b. Focal nodular hyperplasia before (a) and after (b) SPIO administration. The same case as shown in Figure 26. The FNH (asterisk appears slightly heterogeneously hyperintense on the SE T2-weighted image (a). After SPIO administration (b), the nodule is still heterogeneously hyperintense compared to the surrounding normal liver. Note that compared with the unenhanced image (a), the signal drop in FNH is less pronounced than in normal liver parenchyma

Image Nodule Mri Neck

Fig. 31a-g. Focal nodular hyperplasia after SH U 555 A. On precontrast TSE T2-weighted (a) and T1-weighted (b) images, the FNH (arrows) appears as an isointense nodule compared with the normal liver. The lesion is slightly hypointense using a VIBE sequence (c). During the arterial phase (d), after SH U 555 A administration the nodule shows a moderate uptake of contrast agent witch washes out rapidly in the portal-venous phase (e). In the equilibrium phase (f) the lesion appears slightly hypointense. The reticuloendothelial phase (g) reveals a typical, marked signal drop, similar to that observed in the normal liver

Fig. 31a-g. Focal nodular hyperplasia after SH U 555 A. On precontrast TSE T2-weighted (a) and T1-weighted (b) images, the FNH (arrows) appears as an isointense nodule compared with the normal liver. The lesion is slightly hypointense using a VIBE sequence (c). During the arterial phase (d), after SH U 555 A administration the nodule shows a moderate uptake of contrast agent witch washes out rapidly in the portal-venous phase (e). In the equilibrium phase (f) the lesion appears slightly hypointense. The reticuloendothelial phase (g) reveals a typical, marked signal drop, similar to that observed in the normal liver

Hepatocellular Adenoma

Hepatocellular adenoma (HA) is a rare benign tumor of hepatocellular origin which is most common in middle-aged women. The term HA is used to describe a spectrum of lesions associated with different pathological and etiological factors that give rise to a variety of histological forms. A new classification of adenomas has been proposed, according to which anabolic steroid-associated type HA is considered separate from the classical form [55]. This is due to its distinct histologic appearance, which often resembles that of hepatocellular carcinoma. An additional separate form is liver adenomatosis (LA) which is characterized by the presence of ten or more adenomas within an otherwise normal liver, without a history of glycogen storage disease or chronic anabolic steroid use.

Typical HA is defined as a tumor composed of hepatocytes arranged in cords, that only occasionally produces bile. The tumor lacks portal tracts and terminal hepatic veins [65]. Although the precise pathogenic mechanism of HA is unknown, the use of estrogen-containing [110] or androgen-con-taining [98] steroid medications clearly increases their prevalence, number and size within the affected population and often within individual patients. Moreover, this causal relationship is related to dose and duration, with the greatest risk encountered in patients taking large doses of estrogen or androgen for prolonged periods of time [98]. In women who have never used oral contraceptives the annual incidence of HA is about 1 per million. This increases to 30-40 per million in long-term users of oral contraceptives [83]. Withdrawal of estrogen derivates may result in regression of the HA.

Another risk group for HA are patients affected by glycogenosis, in particular, type I glycogen storage disease. In these patients, the possible patho-genetic mechanisms include glucagon/insulin imbalance, cellular glycogen overload, and proto-oncogene activation [8]. The adenomas are also more likely to be multiple and to undergo malignant transformation, although the latter is still quite rare. Patients with diabetes mellitus have decreased circulating insulin levels and elevated serum glucose, therefore they share a similar pathogenetic mechanism as patients affected by glycogenosis.

A recognized association is that of congenital or acquired abnormalities of the hepatic vascula-ture. An association with portal vein absence or occlusion [71] or portohepatic venous shunts [54] has been noted, particularly in patients with LA [37]. Although the adenomas in LA are histologi-cally similar to other adenomas, they are not steroid-dependent, but are multiple, progressive, symptomatic, and more likely to lead to impaired liver function, hemorrhage, and perhaps malignant degeneration [26,37].

Recently, some authors [11,22] have suggested a genetic alteration in the origin of HA. Specifically, a combination of a P-catenin mutation and a deletion locus on chromosome 12 was found in patients with HA.

An association with pregnancy has also been described, probably due to increased levels of endogenous steroid hormones [103]. HA occurs sporadically in patients without known predisposing factors and rarely in children and adult males.

Most patients with only one or few HA are asymptomatic and almost invariably have normal liver function and no elevation of serum tumor markers such as a-fetoprotein. Large HA may cause a sensation of right upper quadrant fullness or discomfort. However, the classic clinical manifestation of HA is spontaneous rupture or hemorrhage, leading to acute abdominal pain and possibly progressing to hypotension and even death [58].

HA is solitary in 70-80% of cases, but it is not unusual to encounter two or three HA in one patient, particularly at multiphasic CT or MR imaging [49,77]. Patients with glycogen storage disease or LA may have dozens of adenomas detected at imaging and even more at close examination of resected specimens [26, 37, 86]. Individual lesions vary in size from less than 1 cm to more than 15 cm. The typical steroid-related adenoma often comes to clinical attention when it reaches about 5 cm in diameter. Large and multiple lesions are more prone to spontanoeous hemorrhage [58]. The propensity to hemorrhage reflects the histo-logical characteristics of HA, in which the cordlike arrangement of cells structured in large plates are separated by dilated sinusoids. Because adenomas lack a portal-venous supply, they are perfused by arterial pressure derived solely from peripheral arterial feeding vessels. The extensive sinusoids and feeding arteries contribute to the hypervascu-lar nature of HA, which together with the poor connective tissue support, predisposes the lesions to hemorrhage. Because a tumor capsule is usually absent or incomplete, hemorrhage may spread into the liver or abdominal cavity [65].

Kupffer cells are often found in adenomas, but in some cases can be reduced in number and with little or no function, as reflected by absent or diminished uptake of technetium (Tc)-99m sulfur colloid [89]. A key histological feature that helps distinguish HA from FNH is the notable absence of bile ductules in HA [13]. Adenoma cells are generally larger than normal hepatocytes and may contain large amounts of glycogen and lipid. Intra- and intercellular lipid may manifest as macroscopic fat deposits within the tumor [49] and are responsible

Mri Feature Fatty Liver

Fig. 32a, b. Hepatocellular adenoma on US. A small, non-complicated adenoma (a) is shown as a homogeneous, isoechoic nodule (asterisk) with a thin, hypoechoic peripheral rim. Larger adenomas are often heterogeneous in echogenicity (b), with both hyperechoic (arrow) and hypoechoic areas (arrowhead), which correspond to areas of hemorrhage, necrosis and fatty infiltration

Fig. 32a, b. Hepatocellular adenoma on US. A small, non-complicated adenoma (a) is shown as a homogeneous, isoechoic nodule (asterisk) with a thin, hypoechoic peripheral rim. Larger adenomas are often heterogeneous in echogenicity (b), with both hyperechoic (arrow) and hypoechoic areas (arrowhead), which correspond to areas of hemorrhage, necrosis and fatty infiltration

Fig. 33a, b. Hepatocellular adenoma on color Doppler US. Color Doppler ultrasound (a) reveals the intratumoral and peripheral vessels characterizing this lesion as hypervascular. A Color Doppler scan (b) reveals the presence of arterial vessels within the lesion, together with a characteristic arterial Doppler-spectrum

Fig. 33a, b. Hepatocellular adenoma on color Doppler US. Color Doppler ultrasound (a) reveals the intratumoral and peripheral vessels characterizing this lesion as hypervascular. A Color Doppler scan (b) reveals the presence of arterial vessels within the lesion, together with a characteristic arterial Doppler-spectrum for the characteristic yellow appearance of the cut surface of adenoma. Evidence of lipid at CT or MR imaging can be helpful in diagnosing HA.

In many cases HA is seen as a large, predominantly hypoechoic lesion on US with central ane-choic areas corresponding to areas of internal hemorrhage (Fig. 32) [117].Adenomas may undergo massive necrotic and hemorrhagic changes which give the lesion a complex appearance on US with large cystic components. Non-complicated HA may appear as an iso- or hypoechoic mass with a relatively homogeneous aspect (Fig. 32a). However, fatty components within the lesion may result in focal hyperechogenicity. A peripheral pseudocapsule, which is present in about one third of HA lesions, is seen as a hypoechoic peripheral rim on US.

Color Doppler US reveals peripheral arteries and veins which correlate well with both gross and angiographic findings. In addition, Color Doppler may identify intratumoral arteries. This finding is absent in FNH and may be a useful discriminating feature for HA (Fig. 33) [30]. Contrast-enhanced US allows depiction of the characteristic vascular behavior of HA. During the arterial phase, an early and homogenous enhancement of non-necrotic, non-hemorrhagic portions of the tumor can be seen. Pericapsular feeding blood vessels are best

Fig. 34a-d. Hepatocellular adenoma with SonoVue. The precontrast US examination (a) shows an isoechoic lesion (asterisk) with lobu-lated margins, located in the left lobe of the liver. Dynamic evaluation after SonoVue administration reveals homogeneous enhancement of the nodule in the arterial phase (b) and rapid wash-out in the portal-venous (c) and equilibrium (d) phases

Ultrasonido Mamario

Fig. 34a-d. Hepatocellular adenoma with SonoVue. The precontrast US examination (a) shows an isoechoic lesion (asterisk) with lobu-lated margins, located in the left lobe of the liver. Dynamic evaluation after SonoVue administration reveals homogeneous enhancement of the nodule in the arterial phase (b) and rapid wash-out in the portal-venous (c) and equilibrium (d) phases visualized during the early arterial phase. In the late arterial phase and in the early portal-venous phase, the contrast wash-out of HA is initially faster than the progressive wash-in of the surrounding liver parenchyma; therefore the neoplasm remains slightly hypoechoic. In the late portal-venous and sinusoidal phases, HA generally shows the same behavior as the surrounding liver parenchyma (Fig. 34).

On unenhanced CT, HA may appear as a hypo-dense mass due to the presence of fat and glycogen within the tumor. However, hyperdense areas corresponding to acute or subacute hemorrhage can be noted frequently in large, complicated lesions (Fig. 35). On contrast-enhanced dynamic CT scanning, non-complicated HA generally enhances rapidly and homogeneously and have increased attenuation relative to the liver. A pseudocapsule is frequently seen in larger lesions as a hypodense and hyperdense rim on non-contrast and equilibrium phase CT images, respectively (Fig. 36) [46]. The enhancement in adenomas typically does not persist because of arteriovenous shunting [88]. Larger or complicated HA may have a more heterogeneous appearance than smaller lesions (Fig. 37) [46].

On MR images, HA frequently show heteroge-

Hyperdense Hypodense Lesion
Fig. 35. Hemorrhagic hepatocellular adenoma. The pre-contrast CT scan reveals a large and inhomogeneous hypodense lesion (arrows) with a hyperdense component (asterisk) corresponding to acute hemorrhage
Hepatic Large Adenoma

Fig. 36a, b. Non-complicated hepatocellular adenoma. On the pre-contrast CT scan (a), the mass appears homogeneously hyperdense compared to the surrounding liver tissue, demonstrating fatty changes. During the arterial phase after the administration of contrast medium (b), the density of the lesion markedly increases in a homogeneous manner

Fig. 36a, b. Non-complicated hepatocellular adenoma. On the pre-contrast CT scan (a), the mass appears homogeneously hyperdense compared to the surrounding liver tissue, demonstrating fatty changes. During the arterial phase after the administration of contrast medium (b), the density of the lesion markedly increases in a homogeneous manner

Fatty Liver Scan

Fig. 37a, b. Complicated hepatocellular adenoma. On the precontrast CT scan (a) the mass (asterisks) appears heterogeneously hyperdense due to intratumoral hemorrhage. Associated subcapsular hematoma (arrowheads) can also be seen. Due to the degenerative changes, the lesion shows heterogenous enhancement in the portal-venous phase (b)

Fig. 37a, b. Complicated hepatocellular adenoma. On the precontrast CT scan (a) the mass (asterisks) appears heterogeneously hyperdense due to intratumoral hemorrhage. Associated subcapsular hematoma (arrowheads) can also be seen. Due to the degenerative changes, the lesion shows heterogenous enhancement in the portal-venous phase (b)

neous hyperintensity on unenhanced T2-weighted images and heterogeneous hypointensity on unen-hanced T1-weighted images. Areas of increased signal intensity on T1-weighted images indicate the presence of fat and hemorrhage, while areas of reduced signal intensity indicate necrosis (Fig. 38) [77]. Sometimes HA have a hypointense peripheral rim, corresponding to a fibrous capsule. In most cases, the rim is of low signal intensity on both T1-and T2-weighted images (Fig. 38) [3]. Because non-complicated HA frequently have a homogeneous iso- or slightly hyperintense signal on T2-

weighted images and an iso- or hypointense signal on T1-weighted images they may be hard to distinguish from surrounding normal liver parenchyma (Fig. 39). The presence of glycogen in HA may increase the signal intensity on T1-weighted images. Similarly, the homogeneous or heterogeneous appearance of HA may be determined by the presence of intranodular fat (Fig. 40).

Dynamic MR imaging is able to demonstrate the early arterial enhancement that results from the presence of large subcapsular feeding vessels. This finding, however, is not specific for HA; the a

256x 256 Right Kidney Ultrasound

Fig. 38a, b. Complicated hepatocellular adenoma. Diffuse intratumoral hemorrhage within the lesion appears heterogeneously hyperintense on the T2-weighted spin-echo image (a) and heterogeneously hypointense on the corresponding unenhanced T1-weighted spinecho image (b). A peripheral hypointense rim (arrows) representing a fibrous capsule is visible on both images a

Fig. 38a, b. Complicated hepatocellular adenoma. Diffuse intratumoral hemorrhage within the lesion appears heterogeneously hyperintense on the T2-weighted spin-echo image (a) and heterogeneously hypointense on the corresponding unenhanced T1-weighted spinecho image (b). A peripheral hypointense rim (arrows) representing a fibrous capsule is visible on both images

Fig. 39a, b. Non-complicated hepatocellular adenoma. A non-complicated HA (asterisk) located in the left lobe of the liver, appears slightly hyperintense on the unenhanced HASTE T2-weighted image (a) and isointense on the corresponding unenhanced GRE T1-weight-ed image (b)

Fig. 40a-d. Non-complicated hepatocellular adenoma. (a) and (b) represent a case of liver adenomatosis (LA) in which one lesion shows a hyperintense signal (arrow) on the "in-phase" Tl-weighted image (a) because of intronodular fat. On the corresponding "out-of-phase" image (b) the lesion shows a signal drop because of the intranodular fat. Multiple other fat-containing lesions of LA can also be seen (ar-rowsin b). (c) and (d) in contrast demonstrate a case of HA with intranodular glycogen. Due to the T1-effect of intranodular glycogen, the HA (arrow) appears as a slightly hyperintense nodule on the Tl-weighted "in-phase" image (c). On the corresponding "out-of-phase" image (d), in contrast to the case of LA, no signal-drop is visible since the high signal of the nodule is caused by intranodular glycogen, rather than intranodular fat

Images Liver Adenomatoma

Fig. 40a-d. Non-complicated hepatocellular adenoma. (a) and (b) represent a case of liver adenomatosis (LA) in which one lesion shows a hyperintense signal (arrow) on the "in-phase" Tl-weighted image (a) because of intronodular fat. On the corresponding "out-of-phase" image (b) the lesion shows a signal drop because of the intranodular fat. Multiple other fat-containing lesions of LA can also be seen (ar-rowsin b). (c) and (d) in contrast demonstrate a case of HA with intranodular glycogen. Due to the T1-effect of intranodular glycogen, the HA (arrow) appears as a slightly hyperintense nodule on the Tl-weighted "in-phase" image (c). On the corresponding "out-of-phase" image (d), in contrast to the case of LA, no signal-drop is visible since the high signal of the nodule is caused by intranodular glycogen, rather than intranodular fat specific MR appearance of HA is generally that of a fat-containing or hemorrhagic lesion with increased peripheral vascularity. On portal-venous and equilibrium phase images HA generally appear isointense or slightly hypointense, with focal heterogeneous hypointense areas of necrosis, calcification or fibrosis.

On delayed liver-specific phase images after Gd-BOPTA administration, the common appearance is hypointensity of the solid, non-hemor-rhagic components of the lesion (Figs. 41, 42). This is one of the main features that differentiates FNH from HA in non-complicated, but also in calcified lesions. The hypointensity of HA reflects the lack of biliary ducts. This enhancement pattern of HA in the liver-specific phase after injection of Gd-BOPTA is opposite to that observed in FNH. The overall difference in enhancement behavior of FNH and HA on hepatobiliary phase images can be ascribed to the different structural and functional features of the lesions; in HA the absence of biliary ductules within the lesion results in altered hepatocellular transport compared with that occurring in normal hepatocytes. Thus, while the mechanism of entry of Gd-BOP-TA into the hepatocytes of HA may be unaltered, the absence of the intracellular transport gradient due to the lack of any active transport across the sinusoidal membrane manifests as hy-pointensity against enhanced normal liver parenchyma on images acquired in the hepato-biliary phase.

A recent study has highlighted the ability of Gd-BOPTA to accurately differente of FNH from HA [40]: at 1-3 hours after Gd-BOPTA administration almost all FNH appeared hyper- or isointense, while all HA appeared hypointense.

Conversely, after mangafodipir trisodium administration HA appear iso- or slightly hyperin-tense, similar to the appearance of FNH (Figs. 41, 42). This limits the possibility to make a correct differential diagnosis.

Dynamic T1-weighted imaging after USPIO administration can reveal slight arterial enhancement which in some cases is better seen at the periphery of the lesion and corresponds to the prominent vascular portion of the adenoma. The uptake of SPIO in the accumulation phase depends on the amount and functional status of the Kupffer cells in the tumor as well as in the periphery of the lesion (Fig. 43) [44].

Adenomas in some cases may take up SPIO, re-

Difference Weighted Mri Lesions

Fig. 41a-g. Hepatocellular adenoma: Gd-BOPTA versus Mn-DPDP. A lesion (arrows) appears isointense compared to surrounding liver tissue with intratumoral hyperintense areas on the HASTE T2-weighted image (a) and heterogeneously isointense on the pre-contrast T1-weighted image (b). During the arterial phase after the bolus injection of Gd-BOPTA the lesion demonstrates heterogeneous enhancement (c). On the subsequent portal-venous and equilibrium phases (d and e, respectively) the lesion appears mainly isointense compared to the liver. In the liver specific phase after administration of Gd-BOPTA (f) the lesion is seen as hy-pointense but shows some internal hyperintense peliotic areas. This may be caused by reduced uptake of Gd-BOPTA into the hepatocytes in HA as well as by the absence of bile ductules in HA: in normal liver tissue contrast agent in the hepatocytes as well as in the bile ductules contributes to the increased signal intensity. Conversely, on delayed phase images acquired after the administration of mangafodipir (Mn-DPDP) (g) the lesion demonstrates non-specific uptake of Mn++ and thus appears isointense compared to normal liver tissue

Fig. 41a-g. Hepatocellular adenoma: Gd-BOPTA versus Mn-DPDP. A lesion (arrows) appears isointense compared to surrounding liver tissue with intratumoral hyperintense areas on the HASTE T2-weighted image (a) and heterogeneously isointense on the pre-contrast T1-weighted image (b). During the arterial phase after the bolus injection of Gd-BOPTA the lesion demonstrates heterogeneous enhancement (c). On the subsequent portal-venous and equilibrium phases (d and e, respectively) the lesion appears mainly isointense compared to the liver. In the liver specific phase after administration of Gd-BOPTA (f) the lesion is seen as hy-pointense but shows some internal hyperintense peliotic areas. This may be caused by reduced uptake of Gd-BOPTA into the hepatocytes in HA as well as by the absence of bile ductules in HA: in normal liver tissue contrast agent in the hepatocytes as well as in the bile ductules contributes to the increased signal intensity. Conversely, on delayed phase images acquired after the administration of mangafodipir (Mn-DPDP) (g) the lesion demonstrates non-specific uptake of Mn++ and thus appears isointense compared to normal liver tissue

Difference Weighted Mri Lesions

Fig. 42a-i. Complicated hepatocellular adenoma: Gd-BOPTA versus Mn-DPDP. HASTE T2-weighted (a) and Turbo SE T2-weighted images (b) reveal a large heterogeneous hyper-hypointense mass (asterisk) in the right lobe. This lesion is seen as heterogeneously hypointense on the unenhanced GE T1-weighted image (c). T1-weighted imaging during the arterial (d), portal-venous (e) and equilibrium (f) phases after the bolus in

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