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Table 1 Observations, mechanism, typical imaging features and prevalence of iso- or hyperintensity signal characteristics on hepatobiliary phase

From: Spectrum of liver lesions hyperintense on hepatobiliary phase: an approach by clinical setting

Observations

Mechanisms

Typical imaging features

Prevalence of iso- or hyperintensity

Non-cirrhotic patients

Focal nodular hyperplasia

Overexpression of OATP1B3; suggested also an increase in well-differentiated bile ducts

Iso- or hyperintensity; hyperintense rim on HBP

97%

Hepatocellular adenomas

Overexpression of OATP1B3

Iso- or hyperintensity

83%, 19%, 0% and 0% of β-catenin, inflammatory, HNF1α inactivated, and unclassified HCAs, respectively

Fat sparing in steatotic liver

Preserved or even increased parenchymal function compared to the background steatotic liver

Homogeneous iso- or hyperintensity

Nearly always (no specific data available)

Primary or secondary vascular disorders

FNH-like nodule

Equal or overexpression of OATP1B3

Iso- or hyperintensity; hyperintense rim on HBP

100%

Oncologic patients

FNH-like nodule

Equal or overexpression of OATP1B3

Iso- or hyperintensity; hyperintense rim on HBP

100%

Metastases

Retention in fibrotic stroma; aberrant expression of OATP1B3

Targetoid appearance

No specific data available

Cholangiocarcinoma

Retention in fibrotic stroma

Targetoid enhancement

42–57%

Cirrhotic patients

Hepatocellular Carcinoma

Overexpression of OATP1B3

Homogeneous hyperintensity, mosaic pattern, nodule-in-nodule appearance or peritumoral hyperintensity

8.8–14%

Regenerative or low-grade dysplastic nodules

Overexpression of OATP1B3

Homogeneous iso- or hyperintensity

No specific data available

Multiacinar regenerative nodules

Overexpression of OATP1B3

Hyperintense rim on HBP

No specific data available

Periportal hyperintensity

Possible regenerative changes of periportal hepatocytes

Bandlike hyperintense areas along the portal tracts

3%