Magnetic resonance elastography of liver: clinical applications

Abstract

Magnetic resonance elastography (MRE) has been successfully implemented in the assessment of diffuse liver diseases. Currently, MRE is the most accurate noninvasive technique for detection and staging of liver fibrosis with a potential to replace liver biopsy. Magnetic resonance elastography is able to differentiate isolated fatty liver disease from steatohepatitis with or without fibrosis. Potential clinical applications include the differentiation of benign and malignant focal liver masses and the assessment of treatment response in diffuse liver diseases.

FIGURE 1

Setup for clinical liver MRE examination. The active driver is placed outside the scanner room. The active driver is connected via a long plastic tube to the passive driver placed over the liver.

FIGURE 2

Schematic diagram showing the placement of the passive driver for liver MRE. The driver is positioned at the level of xiphisternum.

FIGURE 3

Magnetic resonance elastography of the liver in a patient with NASH. Images from a single MRE slice show the magnitude (A) and phase (B) images from the MRE sequence. Processed images from the inversion algorithm includes a gray-scale stiffness map (C), color stiffness map with a 0- to 8-kPa scale (D), confidence map (E) with hatched out areas representing less valid areas for measurement, and a color wave image (F). The mean stiffness of the liver was 4.1 kPa.

FIGURE 4

Axial T2-weighted (A, D) and postcontrast T1-weighted MR images (B, E) and stiffness maps (C, F) obtained with MRE in a patient with chronic hepatitis C (top row) and another patient with alpha-1-antitrypsin deficiency (bottom row). The physical examination and liver function tests were normal in both patients. T2-weighted and postcontrast MRI images do not show any significant abnormalities to suggest chronic liver disease. Magnetic resonance elastography revealed a normal liver stiffness of 2.3 kPa in the patient with chronic hepatitis C and an elevated stiffness of 3.3 kPa in the patient with alpha-1-antitrypsin deficiency, consistent with mild fibrosis.

FIGURE 5

Representative MRE images from different patients with chronic hepatitis C and biopsy-proven fibrosis stages F0 through F4. Each column represents different patients. The top row images are magnitude images, with corresponding wave images (middle row) and color stiffness maps (bottom row). The color scale for shear stiffness in kilopascals is on the right. Mean ± SD values of liver stiffness are at the bottom of the column.

FIGURE 6

Examples of steatosis only, steatohepatitis, and steatohepatitis with fibrosis. Magnetic resonance elastography magnitude images (top row) and stiffness maps (bottom row) in patients with biopsy-proven steatosis only (first column), steatohepatitis (second column), and steatohepatitis with grade 1 fibrosis (third column). The mean liver stiffness was 2.1, 3.6, and 4.3 kPa, respectively.

FIGURE 7

Contrast-enhanced T1-weighted image (B) and stiffness map (B) in chronic hepatitis C. The mean liver stiffness was 6.5 kPa, and the spleen stiffness was 15.7 kPa. The liver is nodular with an enlarged left lobe. Nodular liver, splenomegaly (*), and esophageal varices (arrow) are consistent with cirrhosis with portal hypertension.

FIGURE 8

Magnetic resonance elastography of focal liver lesions. Non–contrast-enhanced (top row) and contrast-enhanced (middle row) T1-weighted images and stiffness maps (bottom row) of hepatic adenoma (first column), focal nodular hyperplasia (second column), hepatocellular carcinoma (third column), and intrahepatic cholangiocarcinoma (fourth column). The tumors are outlined by dotted lines in the stiffness maps. Benign tumors are softer than malignant tumors. The stiffness of hepatic adenoma is 2.8 kPa and that of focal nodular hyperplasia is 3.1 kPa. The mean stiffness of hepatocellular carcinoma is 7 kPa (K). Note the surrounding stiff cirrhotic liver parenchyma. Cholangiocarcinomas are much stiffer and have a stiffness of 12 kPa (L) in the example illustrated.

FIGURE 9

A 60-year-old man with chronic hepatitis C. Contrast-enhanced T1-weighted images (top row) and stiffness maps (bottom row) at baseline (A, C) and 3 years after antiviral treatment (B, D). The baseline liver stiffness was 4.2 kPa, which was reduced to 2.8 kPa at follow-up, suggestive of response to treatment. The serum liver enzyme levels were normal both at baseline and at follow-up.

FIGURE 10

Biopsy-proven NASH. Baseline MRI with in- (A) and opposed-phase (B) images showed an estimated hepatic fat signal fraction of 30% and a mean liver stiffness of 3.2 kPa with MRE (C). Three years later and with about 7-lb weight loss, MRI (D, E) shows that the estimated hepatic fat signal fraction was reduced to 4% and a mean liver stiffness of 2.5 kPa.

FIGURE 11

Progression of chronic liver disease. A 60-year-old man with chronic hepatitis C at presentation showed a mean liver stiffness of 4.1 kPa. After initiation of antiviral treatment, a year later, the liver stiffness increased to 6.3 kPa (B, E), and 3 years later (C, F), there was progression of chronic liver disease with increased stiffness to 8.5 kPa. Note that there are no gross morphologic changes of liver fibrosis in the liver at 1 year, but the left lobe is enlarged and there is mild spleen enlargement at 3 years, suggesting progression of disease.