Abstract
AIMS--To confirm the observation of extremely high concentrations of ferritin in postmortem serum samples in sudden infant death syndrome (SIDS); to examine the factors influencing blood ferritin concentrations postmortem; to determine whether or not these high blood ferritin concentrations are characteristic of SIDS. METHODS--Postmortem samples of cardiac blood were obtained from 58 full term infants who died of SIDS and 14 full-term infants who died of a variety of other causes. Whole blood and serum ferritin concentrations were determined and compared with age at death, liver iron concentration, serum iron concentration, and serum lactate dehydrogenase activity. RESULTS--The median postmortem blood ferritin concentration for all infants was 18,600 micrograms/l, which is about 200 times the concentration found in the serum of normal, live infants. Serum iron concentrations were high and there was a highly significant correlation between serum ferritin and iron concentrations suggesting that much of the serum iron was contributed by ferritin. There was no significant difference between serum and whole blood ferritin concentrations. H to L type ferritin ratios were higher in blood from the left than the right ventricle of the heart but the ferritin was always predominantly L type. Blood ferritin concentrations rose rapidly after death but in samples collected at postmortem examination there was a significant correlation with liver iron concentration and an inverse correlation with age. Median values for blood ferritin were higher in SIDS (22,500; n = 58) than in control cases (6900; n = 7) dying under one year of age; however, in both groups ferritin concentrations decreased with age. CONCLUSIONS--Release of ferritin into the blood postmortem seems to be characteristic of infants dying before the age of one year rather than characteristic of SIDS. Two factors may cause such ferritin release postmortem: tissue breakdown and the high level of storage iron in cells of the reticuloendothelial system (including endothelial cells lining vessel walls). SIDS occurs when tissue iron concentrations are higher than at any other time of life. It is possible that the ready availability of iron enhances free radical damage which might be implicated in SIDS.