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DOI: 10.1148/rg.266065014
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MR Contrast Agents for Liver Imaging: What, When, How1

Sunil N. Gandhi, MD, Michèle A. Brown, MD, James G. Wong, MD, Diego A. Aguirre, MD2 and Claude B. Sirlin, MD

1 From the Department of Radiology, UCSD Medical Center, 200 W Arbor Dr, San Diego, CA 92103. Recipient of a Certificate of Merit award for an education exhibit at the 2004 RSNA Annual Meeting. Received February 6, 2006; revision requested March 16 and received May 5; accepted May 8. All authors have no financial relationships to disclose.

Figure 1
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  		Figure 1a.  T1 shortening due to gadolinium in a 42-year-old woman with focal nodular hyperplasia. (a) Axial T1-weighted spoiled GRE image, obtained before the administration of gadolinium, shows no visible lesion. (b) Axial T1-weighted spoiled GRE image, obtained during the late hepatic arterial phase after gadolinium administration, shows enhancement of a liver lesion (arrow), a finding suggestive of focal nodular hyperplasia.

 

Figure 1
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  		Figure 1b.  T1 shortening due to gadolinium in a 42-year-old woman with focal nodular hyperplasia. (a) Axial T1-weighted spoiled GRE image, obtained before the administration of gadolinium, shows no visible lesion. (b) Axial T1-weighted spoiled GRE image, obtained during the late hepatic arterial phase after gadolinium administration, shows enhancement of a liver lesion (arrow), a finding suggestive of focal nodular hyperplasia.

 

Figure 2
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  		Figure 2a.  Predominant T2 shortening due to gadolinium in a 58-year-old man. (a) Axial T2-weighted echo-train spin-echo image, obtained before the administration of gadolinium, depicts high signal intensity throughout the bladder. (b) Axial gadolinium-enhanced T2-weighted echo-train spin-echo image shows a dependent area with low signal intensity (arrow), a feature indicative of T2 shortening in the bladder because of a high concentration of excreted gadolinium chelate.

 

Figure 2
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  		Figure 2b.  Predominant T2 shortening due to gadolinium in a 58-year-old man. (a) Axial T2-weighted echo-train spin-echo image, obtained before the administration of gadolinium, depicts high signal intensity throughout the bladder. (b) Axial gadolinium-enhanced T2-weighted echo-train spin-echo image shows a dependent area with low signal intensity (arrow), a feature indicative of T2 shortening in the bladder because of a high concentration of excreted gadolinium chelate.

 

Figure 3
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  		Figure 3a.  Effect of gadolinium when used with a STIR sequence in a 37-year-old woman. (a) Axial T2-weighted STIR image, obtained before gadolinium administration, shows fluid-sensitive signal hyperintensity in the kidneys and to a lesser extent in the liver. The fat signal was intrinsically nulled by the short inversion time (180 msec). (b) Axial T2-weighted STIR image, obtained after gadolinium administration, depicts nulling of signal (arrows) both in fat and in gadolinium-enhanced tissue in the kidneys.

 

Figure 3
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  		Figure 3b.  Effect of gadolinium when used with a STIR sequence in a 37-year-old woman. (a) Axial T2-weighted STIR image, obtained before gadolinium administration, shows fluid-sensitive signal hyperintensity in the kidneys and to a lesser extent in the liver. The fat signal was intrinsically nulled by the short inversion time (180 msec). (b) Axial T2-weighted STIR image, obtained after gadolinium administration, depicts nulling of signal (arrows) both in fat and in gadolinium-enhanced tissue in the kidneys.

 

Figure 4
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  		Figure 4.  Diagram shows the procedure used to calculate the delay from gadolinium (Gd) injection to peak aortic enhancement for pulse sequences with 3D sequential k-space encoding. The authors routinely add 4 seconds to the calculated delay to account for the transit of contrast material from the aorta to the target tissue (eg, liver tumor). AT = acquisition time, IT = injection time, TTP = time to peak aortic enhancement.

 

Figure 5
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  		Figure 5a.  Increased conspicuity of HCC in a 54-year-old man after the administration of SPIO particles and gadolinium, relative to conspicuity with SPIO alone. (a) Axial T1-weighted spoiled GRE image shows a lesion in the right hepatic lobe (arrow), a finding that is difficult to characterize without the use of SPIO particles or gadolinium. (b) Axial T1-weighted spoiled GRE image, obtained after the injection of SPIO particles and before that of gadolinium, shows negative enhancement of the background liver tissue and clearly depicts the lesion (arrow). (c) Axial T1-weighted spoiled GRE image, obtained during the late hepatic arterial phase of enhancement after the administration of SPIO particles and gadolinium, shows increased conspicuity of the lesion (arrow).

 

Figure 5
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  		Figure 5b.  Increased conspicuity of HCC in a 54-year-old man after the administration of SPIO particles and gadolinium, relative to conspicuity with SPIO alone. (a) Axial T1-weighted spoiled GRE image shows a lesion in the right hepatic lobe (arrow), a finding that is difficult to characterize without the use of SPIO particles or gadolinium. (b) Axial T1-weighted spoiled GRE image, obtained after the injection of SPIO particles and before that of gadolinium, shows negative enhancement of the background liver tissue and clearly depicts the lesion (arrow). (c) Axial T1-weighted spoiled GRE image, obtained during the late hepatic arterial phase of enhancement after the administration of SPIO particles and gadolinium, shows increased conspicuity of the lesion (arrow).

 

Figure 5
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  		Figure 5c.  Increased conspicuity of HCC in a 54-year-old man after the administration of SPIO particles and gadolinium, relative to conspicuity with SPIO alone. (a) Axial T1-weighted spoiled GRE image shows a lesion in the right hepatic lobe (arrow), a finding that is difficult to characterize without the use of SPIO particles or gadolinium. (b) Axial T1-weighted spoiled GRE image, obtained after the injection of SPIO particles and before that of gadolinium, shows negative enhancement of the background liver tissue and clearly depicts the lesion (arrow). (c) Axial T1-weighted spoiled GRE image, obtained during the late hepatic arterial phase of enhancement after the administration of SPIO particles and gadolinium, shows increased conspicuity of the lesion (arrow).

 

Figure 6
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  		Figure 6a.  Characterization of a liver mass with the use of SPIO particles and gadolinium in a 52-year-old woman with renal cell carcinoma. (a) Axial 2D T1-weighted GRE image, obtained before the administration of SPIO particles and gadolinium, demonstrates a mass (arrow) with signal isointense to that of liver. (b) Axial 2D T1-weighted GRE image, obtained after the injection of SPIO particles, shows a signal intensity loss in the mass (arrow). (c, d) Axial 3D T1-weighted GRE images, obtained after the administration of SPIO particles and gadolinium, demonstrate homogeneous avid enhancement of the mass during the late hepatic arterial phase (arrow in c) and prompt washout of gadolinium during the portal venous phase (arrow in d). The accumulation of SPIO particles in the mass is suggestive of focal nodular hyperplasia, a diagnosis confirmed by the gadolinium enhancement characteristics, and helps exclude metastasis. Although uptake of SPIO particles is suggestive of focal nodular hyperplasia, the differential diagnosis includes well-differentiated HCC, dysplastic nodule, and hepatic adenoma.

 

Figure 6
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  		Figure 6b.  Characterization of a liver mass with the use of SPIO particles and gadolinium in a 52-year-old woman with renal cell carcinoma. (a) Axial 2D T1-weighted GRE image, obtained before the administration of SPIO particles and gadolinium, demonstrates a mass (arrow) with signal isointense to that of liver. (b) Axial 2D T1-weighted GRE image, obtained after the injection of SPIO particles, shows a signal intensity loss in the mass (arrow). (c, d) Axial 3D T1-weighted GRE images, obtained after the administration of SPIO particles and gadolinium, demonstrate homogeneous avid enhancement of the mass during the late hepatic arterial phase (arrow in c) and prompt washout of gadolinium during the portal venous phase (arrow in d). The accumulation of SPIO particles in the mass is suggestive of focal nodular hyperplasia, a diagnosis confirmed by the gadolinium enhancement characteristics, and helps exclude metastasis. Although uptake of SPIO particles is suggestive of focal nodular hyperplasia, the differential diagnosis includes well-differentiated HCC, dysplastic nodule, and hepatic adenoma.

 

Figure 6
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  		Figure 6c.  Characterization of a liver mass with the use of SPIO particles and gadolinium in a 52-year-old woman with renal cell carcinoma. (a) Axial 2D T1-weighted GRE image, obtained before the administration of SPIO particles and gadolinium, demonstrates a mass (arrow) with signal isointense to that of liver. (b) Axial 2D T1-weighted GRE image, obtained after the injection of SPIO particles, shows a signal intensity loss in the mass (arrow). (c, d) Axial 3D T1-weighted GRE images, obtained after the administration of SPIO particles and gadolinium, demonstrate homogeneous avid enhancement of the mass during the late hepatic arterial phase (arrow in c) and prompt washout of gadolinium during the portal venous phase (arrow in d). The accumulation of SPIO particles in the mass is suggestive of focal nodular hyperplasia, a diagnosis confirmed by the gadolinium enhancement characteristics, and helps exclude metastasis. Although uptake of SPIO particles is suggestive of focal nodular hyperplasia, the differential diagnosis includes well-differentiated HCC, dysplastic nodule, and hepatic adenoma.

 

Figure 6
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  		Figure 6d.  Characterization of a liver mass with the use of SPIO particles and gadolinium in a 52-year-old woman with renal cell carcinoma. (a) Axial 2D T1-weighted GRE image, obtained before the administration of SPIO particles and gadolinium, demonstrates a mass (arrow) with signal isointense to that of liver. (b) Axial 2D T1-weighted GRE image, obtained after the injection of SPIO particles, shows a signal intensity loss in the mass (arrow). (c, d) Axial 3D T1-weighted GRE images, obtained after the administration of SPIO particles and gadolinium, demonstrate homogeneous avid enhancement of the mass during the late hepatic arterial phase (arrow in c) and prompt washout of gadolinium during the portal venous phase (arrow in d). The accumulation of SPIO particles in the mass is suggestive of focal nodular hyperplasia, a diagnosis confirmed by the gadolinium enhancement characteristics, and helps exclude metastasis. Although uptake of SPIO particles is suggestive of focal nodular hyperplasia, the differential diagnosis includes well-differentiated HCC, dysplastic nodule, and hepatic adenoma.

 

Figure 7
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  		Figure 7a.  TE-dependent negative contrast enhancement effect of SPIO particles in a 56-year-old man with cirrhosis and HCC. (a) Axial 2D T1-weighted GRE image, obtained with a TE of 2.2 msec after the administration of SPIO particles, depicts a mild signal intensity loss in liver tissue and consequent mild enhancement of contrast between the liver and HCC (arrow), which does not accumulate SPIO particles. The effect was increased on images obtained with a TE of 6.6 msec (b) and 8.8 msec (c).

 

Figure 7
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  		Figure 7b.  TE-dependent negative contrast enhancement effect of SPIO particles in a 56-year-old man with cirrhosis and HCC. (a) Axial 2D T1-weighted GRE image, obtained with a TE of 2.2 msec after the administration of SPIO particles, depicts a mild signal intensity loss in liver tissue and consequent mild enhancement of contrast between the liver and HCC (arrow), which does not accumulate SPIO particles. The effect was increased on images obtained with a TE of 6.6 msec (b) and 8.8 msec (c).

 

Figure 7
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  		Figure 7c.  TE-dependent negative contrast enhancement effect of SPIO particles in a 56-year-old man with cirrhosis and HCC. (a) Axial 2D T1-weighted GRE image, obtained with a TE of 2.2 msec after the administration of SPIO particles, depicts a mild signal intensity loss in liver tissue and consequent mild enhancement of contrast between the liver and HCC (arrow), which does not accumulate SPIO particles. The effect was increased on images obtained with a TE of 6.6 msec (b) and 8.8 msec (c).

 

Figure 8
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  		Figure 8a.  Effect of SPIO particles in a 72-year-old man with cirrhosis and severe liver dysfunction. (a) Axial 2D T1-weighted GRE image, obtained with a TE of 4.4 msec after the administration of SPIO particles, shows an MR imaging analog of "colloid shift": The signal loss in the spleen (arrow) is greater than that in the liver. SPIO particles accumulate in the spleen because of Kupffer cell dysfunction in the setting of severe liver disease. (b) Axial 2D T1-weighted GRE image, obtained with a TE of 8.8 msec after the administration of SPIO particles, shows increased contrast between the liver and spleen (arrow).

 

Figure 8
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  		Figure 8b.  Effect of SPIO particles in a 72-year-old man with cirrhosis and severe liver dysfunction. (a) Axial 2D T1-weighted GRE image, obtained with a TE of 4.4 msec after the administration of SPIO particles, shows an MR imaging analog of "colloid shift": The signal loss in the spleen (arrow) is greater than that in the liver. SPIO particles accumulate in the spleen because of Kupffer cell dysfunction in the setting of severe liver disease. (b) Axial 2D T1-weighted GRE image, obtained with a TE of 8.8 msec after the administration of SPIO particles, shows increased contrast between the liver and spleen (arrow).

 

Figure 9
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  		Figure 9a.  T2 shortening predominates with a high concentration of manganese in a 34-year-old woman evaluated because of a history of biliary obstruction. (a) Coronal T2-weighted single-shot echo-train spin-echo image demonstrates high signal intensity in the common bile duct (arrow) and mild biliary dilatation. (b) Coronal T2-weighted single-shot echo-train spin-echo image, obtained after the administration of mangafodipir, shows a signal intensity loss in the common bile duct (arrow), a finding secondary to a high concentration of manganese.

 

Figure 9
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  		Figure 9b.  T2 shortening predominates with a high concentration of manganese in a 34-year-old woman evaluated because of a history of biliary obstruction. (a) Coronal T2-weighted single-shot echo-train spin-echo image demonstrates high signal intensity in the common bile duct (arrow) and mild biliary dilatation. (b) Coronal T2-weighted single-shot echo-train spin-echo image, obtained after the administration of mangafodipir, shows a signal intensity loss in the common bile duct (arrow), a finding secondary to a high concentration of manganese.

 

Figure 10
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  		Figure 10a.  Biliary excretion of manganese in a 42-year-old man. (a) Axial 2D T1-weighted GRE image, obtained before mangafodipir administration, shows low signal intensity in the common hepatic duct. (b–d) Axial contrast-enhanced 2D T1-weighted GRE images, obtained at 5 minutes (b), 10 minutes (c), and 15 minutes (d) after mangafodipir administration, show the common hepatic duct with faint enhancement at 10 minutes (arrow in c) and strong enhancement at 15 minutes (arrow in d). Parenchymal liver enhancement is apparent at 5 minutes (b) and steadily increases with time over the 15-minute observation period.

 

Figure 10
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  		Figure 10b.  Biliary excretion of manganese in a 42-year-old man. (a) Axial 2D T1-weighted GRE image, obtained before mangafodipir administration, shows low signal intensity in the common hepatic duct. (b–d) Axial contrast-enhanced 2D T1-weighted GRE images, obtained at 5 minutes (b), 10 minutes (c), and 15 minutes (d) after mangafodipir administration, show the common hepatic duct with faint enhancement at 10 minutes (arrow in c) and strong enhancement at 15 minutes (arrow in d). Parenchymal liver enhancement is apparent at 5 minutes (b) and steadily increases with time over the 15-minute observation period.

 

Figure 10
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  		Figure 10c.  Biliary excretion of manganese in a 42-year-old man. (a) Axial 2D T1-weighted GRE image, obtained before mangafodipir administration, shows low signal intensity in the common hepatic duct. (b–d) Axial contrast-enhanced 2D T1-weighted GRE images, obtained at 5 minutes (b), 10 minutes (c), and 15 minutes (d) after mangafodipir administration, show the common hepatic duct with faint enhancement at 10 minutes (arrow in c) and strong enhancement at 15 minutes (arrow in d). Parenchymal liver enhancement is apparent at 5 minutes (b) and steadily increases with time over the 15-minute observation period.

 

Figure 10
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  		Figure 10d.  Biliary excretion of manganese in a 42-year-old man. (a) Axial 2D T1-weighted GRE image, obtained before mangafodipir administration, shows low signal intensity in the common hepatic duct. (b–d) Axial contrast-enhanced 2D T1-weighted GRE images, obtained at 5 minutes (b), 10 minutes (c), and 15 minutes (d) after mangafodipir administration, show the common hepatic duct with faint enhancement at 10 minutes (arrow in c) and strong enhancement at 15 minutes (arrow in d). Parenchymal liver enhancement is apparent at 5 minutes (b) and steadily increases with time over the 15-minute observation period.

 

Figure 11
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  		Figure 11a.  Renal excretion of manganese after mangafodipir administration in a 51-year-old man with liver dysfunction. Axial (a) and sagittal oblique (b) 3D T1-weighted spoiled GRE images demonstrate the renal excretion of mangafodipir (arrow) in the setting of liver failure. The liver appears less enhanced than normal, a result of hepatocyte dysfunction. Variable enhancement of the renal cortex, adrenal gland, and gastric mucosa is normal and is due to the nonspecific uptake of dissociated manganese ions.

 

Figure 11
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  		Figure 11b.  Renal excretion of manganese after mangafodipir administration in a 51-year-old man with liver dysfunction. Axial (a) and sagittal oblique (b) 3D T1-weighted spoiled GRE images demonstrate the renal excretion of mangafodipir (arrow) in the setting of liver failure. The liver appears less enhanced than normal, a result of hepatocyte dysfunction. Variable enhancement of the renal cortex, adrenal gland, and gastric mucosa is normal and is due to the nonspecific uptake of dissociated manganese ions.

 

Figure 12
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  		Figure 12a.  Positive contrast enhancement due to manganese in a 46-year-old woman with focal nodular hyperplasia. (a) Axial 2D T1-weighted GRE image, obtained before mangafodipir administration, shows an ill-defined mass (arrows) in the liver. (b) Axial 2D T1-weighted GRE image, obtained after mangafodipir administration, demonstrates positive contrast enhancement due to manganese uptake in the liver lesion (arrows). This finding helps confirm the presence of hepatocytes within the lesion and, thereby, exclude the presence of a metastasis.

 

Figure 12
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  		Figure 12b.  Positive contrast enhancement due to manganese in a 46-year-old woman with focal nodular hyperplasia. (a) Axial 2D T1-weighted GRE image, obtained before mangafodipir administration, shows an ill-defined mass (arrows) in the liver. (b) Axial 2D T1-weighted GRE image, obtained after mangafodipir administration, demonstrates positive contrast enhancement due to manganese uptake in the liver lesion (arrows). This finding helps confirm the presence of hepatocytes within the lesion and, thereby, exclude the presence of a metastasis.

 

Figure 13
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  		Figure 13a.  Negative enhancement characteristics of focal nodular hyperplasia and hemangioma after mangafodipir administration. (a, b) Axial 2D T1-weighted spoiled GRE images obtained in a 45-year old woman. Image obtained before mangafodipir administration (a) demonstrates an ill-defined hepatic mass (arrow). Image obtained after mangafodipir administration (b) shows enhancement of contrast between normal liver tissue and the mass (arrow), which was known to represent focal nodular hyperplasia. Note the absence of uptake in the central region of scar tissue, which lacks hepatocytes. (c, d) Axial 2D T1-weighted spoiled GRE images obtained in a 38-year-old woman. Image obtained before mangafodipir administration (c) demonstrates a low-signal-intensity hepatic mass (arrow). Image obtained after mangafodipir administration (d) depicts enhancement of the liver parenchyma and an absence of manganese uptake in the mass (arrow), a nonspecific feature that could be indicative of either a metastasis or a hemangioma. Dynamic gadolinium-enhanced images (not shown) helped confirm the diagnosis of a hemangioma.

 

Figure 13
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  		Figure 13b.  Negative enhancement characteristics of focal nodular hyperplasia and hemangioma after mangafodipir administration. (a, b) Axial 2D T1-weighted spoiled GRE images obtained in a 45-year old woman. Image obtained before mangafodipir administration (a) demonstrates an ill-defined hepatic mass (arrow). Image obtained after mangafodipir administration (b) shows enhancement of contrast between normal liver tissue and the mass (arrow), which was known to represent focal nodular hyperplasia. Note the absence of uptake in the central region of scar tissue, which lacks hepatocytes. (c, d) Axial 2D T1-weighted spoiled GRE images obtained in a 38-year-old woman. Image obtained before mangafodipir administration (c) demonstrates a low-signal-intensity hepatic mass (arrow). Image obtained after mangafodipir administration (d) depicts enhancement of the liver parenchyma and an absence of manganese uptake in the mass (arrow), a nonspecific feature that could be indicative of either a metastasis or a hemangioma. Dynamic gadolinium-enhanced images (not shown) helped confirm the diagnosis of a hemangioma.

 

Figure 13
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  		Figure 13c.  Negative enhancement characteristics of focal nodular hyperplasia and hemangioma after mangafodipir administration. (a, b) Axial 2D T1-weighted spoiled GRE images obtained in a 45-year old woman. Image obtained before mangafodipir administration (a) demonstrates an ill-defined hepatic mass (arrow). Image obtained after mangafodipir administration (b) shows enhancement of contrast between normal liver tissue and the mass (arrow), which was known to represent focal nodular hyperplasia. Note the absence of uptake in the central region of scar tissue, which lacks hepatocytes. (c, d) Axial 2D T1-weighted spoiled GRE images obtained in a 38-year-old woman. Image obtained before mangafodipir administration (c) demonstrates a low-signal-intensity hepatic mass (arrow). Image obtained after mangafodipir administration (d) depicts enhancement of the liver parenchyma and an absence of manganese uptake in the mass (arrow), a nonspecific feature that could be indicative of either a metastasis or a hemangioma. Dynamic gadolinium-enhanced images (not shown) helped confirm the diagnosis of a hemangioma.

 

Figure 13
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  		Figure 13d.  Negative enhancement characteristics of focal nodular hyperplasia and hemangioma after mangafodipir administration. (a, b) Axial 2D T1-weighted spoiled GRE images obtained in a 45-year old woman. Image obtained before mangafodipir administration (a) demonstrates an ill-defined hepatic mass (arrow). Image obtained after mangafodipir administration (b) shows enhancement of contrast between normal liver tissue and the mass (arrow), which was known to represent focal nodular hyperplasia. Note the absence of uptake in the central region of scar tissue, which lacks hepatocytes. (c, d) Axial 2D T1-weighted spoiled GRE images obtained in a 38-year-old woman. Image obtained before mangafodipir administration (c) demonstrates a low-signal-intensity hepatic mass (arrow). Image obtained after mangafodipir administration (d) depicts enhancement of the liver parenchyma and an absence of manganese uptake in the mass (arrow), a nonspecific feature that could be indicative of either a metastasis or a hemangioma. Dynamic gadolinium-enhanced images (not shown) helped confirm the diagnosis of a hemangioma.

 




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