Abstract

ObjectivesTo evaluate the reproducibility of liver R2* measurements between a 2D cardiac ECG-gated and a 3D breath-hold liver CSE-MRI acquisition for liver iron quantification.MethodsA total of 54 1.5 T MRI exams from 51 subjects (18 women, 36 men, age 35.2 ± 21.8) were included. These included two sub-studies with 23 clinical MRI exams from 19 patients identified retrospectively, 24 participants with known or suspected iron overload, and 7 healthy volunteers acquired prospectively. The 2D cardiac and the 3D liver R2* maps were acquired in the same exam. Either acquisitions were reconstructed using a complex R2* algorithm that accounts for the presence of fat and residual phase errors due to eddy currents. Data were analyzed using colocalized ROIs in the liver.ResultsLinear regression analysis demonstrated high Pearson’s correlation and Lin’s concordance coefficient for the overall study and both sub-studies. Bland–Altman analysis also showed good agreement, except for a slight increase of the mean R2* value above ~ 400 s−1. The Kolmogorow–Smirnow test revealed a non-normal distribution for (R2* 3D–R2* 2D) values from 0 to 600 s−1 in contrast to the 0–200 s−1 and 0–400 s−1 subpopulations. Linear regression analysis showed no relevant differences other than the intercept, likely due to only 7 measurements above 400 s−1.ConclusionsThe results demonstrate that R2*-measurements in the liver are feasible using 2D cardiac R2* maps compared to 3D liver R2* maps as the reference. Liver R2* may be underestimated for R2* > 400 s−1 using the 2D cardiac R2* mapping method.

Highlights

  • Iron is a major component of essential proteins like hemoglobin and myoglobin

  • The second group was part of a prospective study performed in patients with known or suspected liver iron overload for the purposes of R2* quantification in the liver [25], in which cardiac R2* mapping was performed

  • 51 subjects with a total of 54 Magnetic resonance imaging (MRI) exams (18 women, 36 men, age 35.2 ± 21.8) were included in this study, using data combined from the retrospective clinical study and the prospective research study

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Summary

Introduction

The body iron is maintained in a narrow homeostatic range based primarily on the rate of absorption [1, 2]. Normal elimination occurs through sloughing of intestinal lining cells and skin cells, and by menstruation [2]. The most common cause for primary iron overload is hereditary hemochromatosis (HH), occurring in the Caucasian population with a prevalence between 0.2 and 0.45%. Iron overload from HH results from disruption in the hepcidin pathway, with subsequent excess absorption of iron from the gut [1, 4]. Increased intestinal uptake can lead to systemic iron overload after saturation of endogenous ferritin and transferrin [1], leading to free iron that is oxidative and can cause cellular injury [1].

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