Background: MRI T2* and R2* mapping have gained clinical acceptance for noninvasive assessment of iron overload. Lower field MRI may offer increased measurement dynamic range in patients with high iron concentration and may potentially increase MRI accessibility, but it is compromised by lower signal-to-noise ratio that reduces measurement precision.
Purpose: To characterize a high-performance 0.55 T MRI system for evaluating patients with liver iron overload.
Study Type: Prospective.
Population: Forty patients with known or suspected iron overload (sickle cell anemia [n = 5], ß-thalassemia [n = 3], and hereditary spherocytosis [n = 2]) and a liver iron phantom.
Field Strength/sequence: A breath-held multiecho gradient echo sequence at 0.55 T and 1.5 T.
Assessment: Patients were imaged with T2*/R2* mapping 0.55 T and 1.5 T within 24 hours, and 16 patients returned for follow-up exams within 6-16 months, resulting in 56 paired studies. Liver T2* and R2* measurements and standard deviations were compared between 0.55 T and 1.5 T and used to validate a predictive model between field strengths. The model was then used to classify iron overload at 0.55 T.
Statistical Tests: Linear regression and Bland-Altman analysis were used for comparisons, and measurement precision was assessed using the coefficient of variation. A P-value < 0.05 was considered statistically significant.
Results: R2* was significantly lower at 0.55 T in our cohort (488 ± 449 s at 1.5 T vs. 178 ± 155 s at 0.55 T, n = 56 studies) and in the patients with severe iron overload (937 ± 369 s at 1.5 T vs. 339 ± 127 s at 0.55 T, n = 23 studies). The coefficient of variation indicated reduced precision at 0.55 T (3.5 ± 2.2% at 1.5 T vs 6.9 ± 3.9% at 0.55 T). The predictive model accurately predicted 1.5 T R2* from 0.55 T R2* (Bland Altman bias = -6.6 ± 20.5%). Using this model, iron overload at 0.55 T was classified as: severe R2* > 185 s , moderate 81 s < R2* < 185 s , and mild 45 s < R2* < 91 s .
Data Conclusion: We demonstrated that 0.55 T provides T2* and R2* maps that can be used for the assessment of liver iron overload in patients.
Evidence Level: 2 TECHNICAL EFFICACY: Stage 2.
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http://dx.doi.org/10.1002/jmri.27950 | DOI Listing |
Cureus
December 2024
Internal Medicine, National Hospital of Sri Lanka, Colombo, LKA.
Hereditary hemochromatosis occurs due to genetic mutations, namely, cysteine-to-tyrosine substitution at amino acid 282 (C282Y) and histidine-to-aspartic acid substitution at 63 (H63D) mutations. The role of H63D mutation in hemochromatosis is less clear, and its penetrance is low even in homozygotes. Therefore, iron overload in H63D heterozygotes is extremely rare and scarcely reported.
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January 2025
Key Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture and Rural Affairs, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.
Iron is a trace element that is indispensable for the growth and development of animals. Excessive iron supplementation may lead to iron overload and elevated reactive oxygen species (ROS) production in animals, causing cellular damage. Nevertheless, the precise mechanism by which iron overload causes cell injury remains to be fully elucidated.
View Article and Find Full Text PDFACS Appl Mater Interfaces
January 2025
Department of Neurosurgery, Guizhou Provincial People's Hospital, Guiyang 550000, China.
Spontaneous intracerebral hemorrhagic stroke (ICH) is a highly aggressive disease, with a high incidence and mortality rate. Iron deposition following ICH leads to oxidative damage and motor dysfunction, significantly impacting the overall quality of life for those affected. Here, a polyphenolic nanomedicine, catechin-based polyphenol nanoparticles surface-modified by thiol-terminated poly(ethylene glycol) (CNPs@PEG), was developed through the oxidative polymerization and self-assembly of catechin, a natural compound in tea.
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