Liver-specific agents for contrast-enhanced MRI: role in oncological imaging

Abstract

Liver-specific magnetic resonance (MR) contrast agents are increasingly used in evaluation of the liver. They are effective in detection and morphological characterization of lesions, and can be useful for evaluation of biliary tree anatomy and liver function. The typical appearances and imaging pitfalls of various tumours at MR imaging performed with these agents can be understood by the interplay of pharmacokinetics of these contrast agents and transporter expression of the tumour. This review focuses on the applications of these agents in oncological imaging.

Figure 1

Axial fat-suppressed T₁-weighted three-dimensional (3D) gradient recalled echo (GRE) images of a healthy liver with gadoxetic acid administration obtained at (A) precontrast, (B) 30 s, (C) 60 s, (D) 2 min, (E) 5 min, and (F) 20 min. There is progressive enhancement of the liver parenchyma while the portal venous vasculature shows progressive decrease in signal intensity. At 20 min, excreted contrast into the bile ducts (arrow) causes strong enhancement of the biliary tree that is visualized even in the segmental ducts.

Figure 2

Schematic diagram of gadoxetic acid/gadobenate dimeglumine transport through hepatocytes. Gadoxetic acid and gadobenate dimeglumine (represented by black circles) are actively transported from the sinusoids via organic anion transporting polypeptide (OATP) 1B1 and 1B3 into the hepatocytes. They are excreted into the biliary canaliculi via multidrug resistance protein 2 (MRP2) on the canalicular membrane. MRP3 is also involved in efflux of gadoxetic acid back to the sinusoids at the basolateral membrane.

Figure 3

Axial fat-suppressed T₁-weighted 3D GRE images of Edmondson grade 3–4 hepatocellular carcinoma in a 72-year-old man. Images obtained during (A) unenhanced phase, (B) arterial phase, and (C) portal venous phase after gadoxetic acid administration show characteristic left-lobe hepatocellular carcinoma (HCC) arterial hypervascularity and portal venous washout with a mosaic pattern and pseudocapsule formation. (D) At the 20-min hepatocellular phase, there is strong enhancement of the background liver parenchyma, but no uptake in the HCC.

Figure 4

Ductal type cholangiocarcinoma at the common bile duct in a 58-year-old man. (A, B) Axial and coronal fat-suppressed T₁-weighted 3D GRE images performed 20 min after gadoxetic acid administration show excreted contrast within the biliary radicles adjacent to the hypointense vascular structures of the portal triads. There is a filling defect (arrow) and abrupt truncation of the common bile duct at the site of the obstructing tumour. (C) Maximum-intensity projection of the coronal images produce a T₁-weighted magnetic resonance cholangiopancreatography (MRCP)-like picture demonstrating the anatomy of the biliary tree. Note that the pancreatic duct and stomach are not hyperintense, unlike on a conventional T₂-weighted MRCP. (D) T₂-weighted MRCP performed 2 weeks later after biliary stent insertion.

Figure 5

Axial fat-suppressed T₁-weighted 3D GRE images of focal nodular hyperplasia (FNH). Images obtained during (A) unenhanced phase, (B) late arterial phase, and (C) portal venous phase with gadoxetic acid show avid homogeneous arterial enhancement persisting on the portal venous phase. (D) At 3 min after contrast injection, the liver shows increasing parenchymal enhancement whereas the vessels are isointense to hypointense. (E) At the 20-min hepatocellular phase, there is strong enhancement of the background liver but equivalently strong gadoxetic acid uptake in the FNH, which thus appears isointense to the liver. As contrast is no longer circulating within the intravascular compartment, the vessels appear as branching hypointense reticular structures. (F) Axial T₂-weighted image showing the hyperintense scar (arrow) and almost isointense appearance of FNH.

Figure 6

Axial fat-suppressed T₁-weighted 3D GRE images of a small haemangioma. Images obtained during (A) unenhanced phase, (B) arterial phase, and (C) portal venous phase after gadoxetic acid administration show the arterially enhancing lesion (arrowhead) with persistent hyperintensity on the portal venous phase. However, at 90 s (D), increasing uptake of gadoxetic acid in the liver results in diminished relative hyperintensity of the blood pool within the haemangioma. (E) At the 20-min hepatocellular phase, the haemangioma appears as a hypointense lesion (arrowhead) against the enhanced liver background. (F) Axial T₂-weighted image showing the classical light-bulb sign of the haemangioma.

Figure 7

Sinusoidal obstruction syndrome in a 68-year-old man with colorectal metastases on oxaliplatin. (A, B) Axial and coronal fat-suppressed T₁-weighted 3D GRE images obtained 20 min after gadoxetic acid administration show characteristic reticular hypointensities in non-tumoural portions of the liver. A small focal hypointense lesion (arrow) adjacent to the right hepatic vein is a metastatic deposit. (C) Axial fat-suppressed T₂-weighted image shows patchy areas of hyperintensity that may be related to oedema. (D) Oxaliplatin was discontinued, and the follow-up scan performed with gadoxetic acid 5 months later shows resolution of the findings. Unfortunately, there is progression of hepatic metastases (arrow).