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Whole-body R2∗ mapping to quantify tissue iron in iron storage organs: reference values and a genotype.

M L Kromrey1, A Röhnert2, S Blum2

  • 1Institute of Diagnostic Radiology and Neuroradiology, University Medicine Greifswald, Greifswald, Germany.

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This study established reference values for transverse relaxation rate (R2∗) in iron storage organs using MRI. The human haemochromatosis protein (HFE) genotype did not significantly influence tissue iron levels, suggesting non-specific HFE mutations do not alter iron accumulation.

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Area of Science:

  • Radiology and Imaging
  • Genetics and Genomics
  • Biomedical Engineering

Background:

  • Iron storage diseases are a group of disorders characterized by excessive iron accumulation.
  • Accurate assessment of tissue iron levels is crucial for diagnosing and managing these conditions.
  • The human haemochromatosis protein (HFE) gene plays a role in iron metabolism, but its impact on iron storage phenotypes requires further clarification.

Purpose of the Study:

  • To establish reference values for transverse relaxation rate (R2∗) in key iron storage organs using whole-body MRI.
  • To investigate the influence of HFE gene single nucleotide polymorphisms (SNPs) on R2∗ values and consequently on iron storage.
  • To determine if non-specific HFE mutations are associated with altered tissue iron accumulation.

Main Methods:

  • Whole-body MRI with a five-echo gradient-echo sequence was performed on 483 healthy volunteers.
  • R2∗ values were quantified in the liver, spleen, pancreas, heart, bones, and brain parenchyma.
  • HFE genotype was analyzed for specific SNPs, and R2∗ values were compared between individuals with and without HFE mutations.

Main Results:

  • Reference R2∗ values were successfully defined for liver, spleen, pancreas, heart, bone, and brain parenchyma in volunteers without HFE mutations.
  • No statistically significant differences in R2∗ values were observed in any of the examined organs between participants with and without HFE gene mutations.
  • HFE gene mutations, including rs1799945, rs1800562, and rs1800730, did not correlate with altered tissue iron accumulation as measured by R2∗.

Conclusions:

  • Established R2∗ reference values provide a basis for diagnosing iron storage diseases using MRI.
  • Non-specific mutations within the HFE gene SNPs studied do not appear to significantly impact the phenotype of tissue iron accumulation.
  • Further research may be needed to explore the role of other genetic factors or specific HFE mutations in iron storage disorders.