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Hypovascular hypointense nodules on hepatobiliary phase gadoxetic acid-enhanced MR images in patients with cirrhosis: potential of DW imaging in predicting progression to hypervascular HCC.

Radiology 2012 October
PURPOSE: To investigate the imaging features of hypovascular hypointense nodules on hepatobiliary phase gadoxetic acid-enhanced magnetic resonance (MR) images in patients with cirrhosis that may be associated with progression to hypervascular hepatocellular carcinoma (HCC).

MATERIALS AND METHODS: The institutional review board approved this retrospective study and waived informed patient consent. This study included 135 patients with a diagnosis of hepatitis B-induced liver cirrhosis and 214 hypovascular hypointense nodules on hepatobiliary phase gadoxetic acid-enhanced MR images. MR images were analyzed with respect to nodule size, degree of hypointensity at hepatobiliary phase (four grades), presence of fat, and signal intensity on T1- and T2-weighted and diffusion-weighted (DW) images. Univariate and multivariate Cox regression analyses were used to identify variables that are associated with developing hypervascular HCC.

RESULTS: On follow-up MR images, 139 nodules (65.0%) had no evidence of HCC (mean follow-up, 522 days) (group 1), but 75 (35.0%) became hypervascular HCC (mean follow-up, 388 days) (group 2). Univariable Cox analysis revealed that the degree of hypointensity on hepatobiliary phase images (P=.044 and .001) and hyperintensity on T2-weighted and DW images (P=.001 and .0001) was significantly related to the development of hypervascular HCC. According to the multivariable Cox analysis, no other variable significantly adjusted the model once hyperintensity at initial DW imaging was already included as an associated variable, (hazard ratio, 7.44; 95% confidence interval: 4.28, 12.94; P=.0001).

CONCLUSION: Hyperintensity on DW images in hypovascular hypointense nodules on hepatobiliary phase gadoxetic acid-enhanced MR images in patients with cirrhosis is strongly associated with progression to hypervascular HCC.

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