Worwood M, Raha-Chowdhury R, Fagan D G, Moore C A
Department of Haematology, University of Wales College of Medicine, Cardiff.
J Clin Pathol. 1995 Aug;48(8):763-7. doi: 10.1136/jcp.48.8.763.
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.
目的——证实婴儿猝死综合征(SIDS)尸检血清样本中铁蛋白浓度极高这一观察结果;研究影响死后血中铁蛋白浓度的因素;确定这些高血铁蛋白浓度是否为SIDS所特有。方法——从58例死于SIDS的足月婴儿和14例死于其他各种原因的足月婴儿身上获取心脏血的尸检样本。测定全血和血清铁蛋白浓度,并与死亡年龄、肝脏铁浓度、血清铁浓度和血清乳酸脱氢酶活性进行比较。结果——所有婴儿的尸检血铁蛋白浓度中位数为18,600微克/升,约为正常活婴血清中浓度的200倍。血清铁浓度较高,血清铁蛋白与铁浓度之间存在高度显著的相关性,表明大部分血清铁由铁蛋白提供。血清和全血铁蛋白浓度之间无显著差异。心脏左心室血中H型与L型铁蛋白比值高于右心室,但铁蛋白始终以L型为主。死后血铁蛋白浓度迅速上升,但在尸检时采集的样本中,与肝脏铁浓度存在显著相关性,与年龄呈负相关。SIDS组(22,500;n = 58)血铁蛋白中位数高于1岁以下死亡的对照组(6900;n = 7);然而,两组中铁蛋白浓度均随年龄下降。结论——死后铁蛋白释放入血似乎是1岁前死亡婴儿的特征,而非SIDS所特有。有两个因素可能导致死后铁蛋白释放:组织分解和网状内皮系统(包括血管壁内衬的内皮细胞)细胞中储存铁水平较高。当组织铁浓度高于生命中其他任何时期时,就会发生SIDS。铁的易获得性可能会增强自由基损伤,这可能与SIDS有关。