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Liver iron concentrations in sudden infant death syndrome
C A Moore1, R Raha-Chowdhury, D G Fagan
1First Community Health Trust, Stafford Central Clinic.
Insights
Sudden Infant Death Syndrome (SIDS) infants had significantly higher liver iron concentrations than controls. High iron levels may increase infection risk and free radical damage in infants.
Area of Science:
- Pediatric Pathology
- Biochemistry
- Immunology
Background:
- Sudden Infant Death Syndrome (SIDS) is a leading cause of post-neonatal mortality.
- Elevated non-haem iron levels in infant livers have been observed, but their significance is unclear.
Purpose of the Study:
- To investigate the biological significance of high non-haem iron concentrations in the livers of infants who died from SIDS.
Main Methods:
- Liver tissue samples were collected post-mortem from 66 SIDS infants and 28 control infants.
- Iron concentrations were measured and compared between groups, with analysis adjusted for age.
Main Results:
- Median liver iron concentration in SIDS infants (396 µg/g) was significantly higher than in controls (105 µg/g) between 1 month and 1 year of age.
- No association was found between high liver iron and the HLA-A3 gene, ruling out hemochromatosis as a cause.
Conclusions:
- Peak SIDS incidence coincides with the highest mean liver iron concentrations.
- While not a direct cause, elevated iron may compromise infant immunity and increase oxidative stress, potentially contributing to SIDS pathophysiology.
Abstract:
To determine the biological significance of high concentrations of non-haem iron in the livers of infants dying from sudden infant death syndrome (SIDS), liver samples were obtained at necropsy from 66 infants who died from SIDS and 28 control infants who died before 2.5 years of age. All were full term deliveries. Liver iron concentrations decreased rapidly with age in the two groups. Liver iron concentrations in the SIDS infants and controls were compared for those infants who died between 1 month and 1 year of age. The median liver iron concentration in the SIDS infants was 296 micrograms/g wet weight; significantly higher than the median of 105 micrograms/g in controls. There was an inverse relation between iron concentration and age in the two groups, but an analysis of covariance confirmed the significantly lower values in controls. The frequency (22%) of HLA-A3 in SIDS infants was similar to that expected for the United Kingdom population (25%) and does not implicate the gene for haemochromatosis as a cause of high liver iron concentrations. These findings show that the peak incidence of SIDS occurs when mean concentrations of iron in liver tissue are higher than at any other time of life. Although a primary causal connection seems unlikely, high tissue iron concentrations may lower resistance to infection and enhance free radical formation, leading to tissue damage.