Edouard Reizine1,2, Maxime Ronot3,4,5, Frederic Pigneur1, Yvonne Purcell2, Sebastien Mulé1, Marco Dioguardi Burgio2, Julien Calderaro6,7,8, Giuliana Amaddeo7,8,9, Alexis Laurent7,10, Valérie Vilgrain2,11,12, Alain Luciani1,7,8. 1. Department of Radiology, APHP, HU Henri Mondor, Creteil, Val-de-Marne, France. 2. Department of Radiology, APHP, University Hospitals Paris Nord Val de Seine, Beaujon, 100 Boulevard du Général Leclerc, 92118, Clichy, Hauts-de-Seine, France. 3. Department of Radiology, APHP, University Hospitals Paris Nord Val de Seine, Beaujon, 100 Boulevard du Général Leclerc, 92118, Clichy, Hauts-de-Seine, France. maxime.ronot@aphp.fr. 4. University Paris Diderot, Sorbonne Paris Cité, Paris, France. maxime.ronot@aphp.fr. 5. INSERM U1149, centre de recherche biomédicale Bichat-Beaujon, CRB3, Paris, France. maxime.ronot@aphp.fr. 6. Department of Pathology, APHP, HU Henri Mondor, Creteil, Val-de-Marne, France. 7. Faculté de Médecine, Universite Paris Est Creteil, 94010, Creteil, France. 8. INSERM Unit U 955, Equipe 18, 94010, Creteil, France. 9. Department of Hepatology, APHP, HU Henri Mondor, Creteil, Val-de-Marne, France. 10. Department of Liver Surgery, APHP, HU Henri Mondor, Creteil, Val-de-Marne, France. 11. University Paris Diderot, Sorbonne Paris Cité, Paris, France. 12. INSERM U1149, centre de recherche biomédicale Bichat-Beaujon, CRB3, Paris, France.
Abstract
PURPOSE: This study was conducted in order to evaluate if iso- or hyperintensity of HCAs on HBP is systematically related to a high uptake of hepatospecific contrast agent, using a quantitative approach. METHODS: This bicentric retrospective study included all patients with histologically confirmed and subtyped HCA from 2009 to 2017 who underwent MRI with HBP after Gd-BOPTA injection and who showed iso- or hyperintensity on HBP. The signal intensity of tumors on pre- and postcontrast images and the presence of hepatic steatosis were noted. Contrast uptake on HBP was quantified using the liver-to-lesion contrast enhancement ratio (LLCER) and compared between HCA subtypes (Wilcoxon signed-rank test). Categorical variables were compared using chi-square tests. RESULTS: Twenty-four HCAs showed iso- or hyperintensity on HBP, specifically 17 inflammatory (IHCAs) and 7 β-catenin HCAs (BHCAs). Eighteen HCAs (75%) (17 IHCAs and 1 BHCAs) had a LLCER < 0% (median - 13.6%, group 1), of which 94% were hyperintense on precontrast T1-W images, with background hepatic steatosis. Six HCAs (25%) had LLCER ≥ 0% (median 2.9%, group 2), and all were BHCAs. A LLCER ≥ 1.6% was associated with the diagnosis of BHCA with a sensitivity of 86% and a specificity of 100%. CONCLUSION: In conclusion, iso- or hyperintensity of hepatocellular adenomas on HBP does not necessarily correspond to an increased hepatospecific contrast-agent uptake. In IHCA, tumor hyperintensity on precontrast images and the underlying steatosis likely explain such iso- or hyperintensity, which do show reduced HBP contrast-agent uptake. On the other hand, marked contrast uptake can be observed, especially in BHCA. KEY POINTS: • Iso- or hyperintensity on HBP does not necessarily reflect a high uptake of hepatospecific contrast agent. • Discrepancies between qualitative signal intensity and quantitative hepatospecific contrast uptake can be explained in IHCA by a combination of tumor hyperintensity on precontrast images and underlying hepatic steatosis. • In BHCA, iso- or hyperintensity on HBP does actually correspond to a greater contrast uptake than that of the liver, demonstrated by an increased lesion-to-liver contrast enhancement ratio (LLCER).
PURPOSE: This study was conducted in order to evaluate if iso- or hyperintensity of HCAs on HBP is systematically related to a high uptake of hepatospecific contrast agent, using a quantitative approach. METHODS: This bicentric retrospective study included all patients with histologically confirmed and subtyped HCA from 2009 to 2017 who underwent MRI with HBP after Gd-BOPTA injection and who showed iso- or hyperintensity on HBP. The signal intensity of tumors on pre- and postcontrast images and the presence of hepatic steatosis were noted. Contrast uptake on HBP was quantified using the liver-to-lesion contrast enhancement ratio (LLCER) and compared between HCA subtypes (Wilcoxon signed-rank test). Categorical variables were compared using chi-square tests. RESULTS: Twenty-four HCAs showed iso- or hyperintensity on HBP, specifically 17 inflammatory (IHCAs) and 7 β-catenin HCAs (BHCAs). Eighteen HCAs (75%) (17 IHCAs and 1 BHCAs) had a LLCER < 0% (median - 13.6%, group 1), of which 94% were hyperintense on precontrast T1-W images, with background hepatic steatosis. Six HCAs (25%) had LLCER ≥ 0% (median 2.9%, group 2), and all were BHCAs. A LLCER ≥ 1.6% was associated with the diagnosis of BHCA with a sensitivity of 86% and a specificity of 100%. CONCLUSION: In conclusion, iso- or hyperintensity of hepatocellular adenomas on HBP does not necessarily correspond to an increased hepatospecific contrast-agent uptake. In IHCA, tumor hyperintensity on precontrast images and the underlying steatosis likely explain such iso- or hyperintensity, which do show reduced HBP contrast-agent uptake. On the other hand, marked contrast uptake can be observed, especially in BHCA. KEY POINTS: • Iso- or hyperintensity on HBP does not necessarily reflect a high uptake of hepatospecific contrast agent. • Discrepancies between qualitative signal intensity and quantitative hepatospecific contrast uptake can be explained in IHCA by a combination of tumor hyperintensity on precontrast images and underlying hepatic steatosis. • In BHCA, iso- or hyperintensity on HBP does actually correspond to a greater contrast uptake than that of the liver, demonstrated by an increased lesion-to-liver contrast enhancement ratio (LLCER).
Entities:
Keywords:
Adenoma; Contrast media; Liver neoplasms; Magnetic resonance imaging
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