By definition, regenerative nodules are present in all cirrhotic livers; however, these nodules are visualized in only 25% of unenhanced CT scans and approximately 50% of MR images. These nodules may present as high-attenuation lesions on unenhanced CT due to their iron and/or glycogen content, or simply because they are surrounded by lower-attenuation fibrosis. On portal venous phase contrast-enhanced scans, these nodules are rarely revealed. On MR images, these focal lesions can appear hypo-, iso-, or hyperintense on T1-weighted images, with isointense being the most usual and hyperintense the most unusual. On T2-weighted images, they typically appear as hypointense nodules (iron causes local magnetic field inhomogeneities, with decrease of liver signal intensity due to shortening of the T2 relaxation time). Following the administration of a gadolinium-containing extracellular contrast agent (GBCA), regenerative nodules usually appear hypointense during arterial and portal venous phases and become more isointense during the equilibrium and delayed phases. Using a combined gadolinium-containing contrast agent, such as gadoxetate, regenerative nodules generally demonstrate contrast uptake and excretion during the hepatocyte phase due to preserved hepatocellular function and intact organic ion transporters; therefore, regenerative nodules demonstrate signal intensity similar to that of background liver during the hepatocyte phase.

Dysplastic nodules develop from regenerative nodules and contain atypical hepatocytes but do not have definite features of malignancy on histology. They are present in 15–25% of cirrhotic livers and are histologically classified as low or high grade, depending on the degree of dedifferentiation. High-grade dysplastic nodules are considered premalignant and can undergo malignant transformation in a period as short as 4 months and are rarely detected by CT. If detected, they may appear slightly hyper- or isodense on unenhanced scans. On MR imaging, they appear iso- or hyperintense on T1-weighted images and iso- to hypointense on T2-weighted images. Following administration of an extracellular contrast agent, dysplastic nodules usually are hypodense/hypointense during the arterial, portal venous, and delayed phases. However, these lesions occasionally demonstrate hyperenhancement during the arterial phase, thus mimicking HCC. Using a combined MR contrast agent such as gadoxetate, their appearance during the hepatocyte phase varies [2, 5, 6]. As with regenerative nodules, dysplastic nodules receive their blood supply mainly from the portal vein, although high-grade nodules may develop arterial hypervascularity. With progression of atypia, the number of expressed organic ion transporters decreases, reducing their ability to take up gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd- EOB-DTPA). In the hepatocyte phase of gadoxetate, nodules that retain their ability to take up the agent but not excrete it appear homogenously or heterogeneously hyperintense due to intracellular cholestasis, whereas nodules that have lost their ability to take up the agent appear hypointense. Such hypointense nodules can be mistaken for HCCs in the hepatocyte phase. On the other hand, MR imaging with hepatobiliary contrast agents is the only modality that can detect these premalignant lesions [7] and open the window for the treatment of early HCC.