Edston E, Gidlund E, Wickman M, Ribbing H, Van Hage-Hamsten M
Department of Forensic Medicine, Linköping, Sweden.
Clin Exp Allergy. 1999 Dec;29(12):1648-54. doi: 10.1046/j.1365-2222.1999.00679.x.
Increased concentrations of mast cell tryptase in post mortem blood have frequently been observed in sudden infant deaths but the cause of this has not yet been clarified.
The aim was to evaluate factors (immunological, morphological and anamnestic data) behind the observed increase in mast cell tryptase in sudden infant deaths with elevated tryptase.
Mast cell tryptase and total immunoglobulin (Ig) E were measured in post mortem sera from 44 infants younger than 1.5 years. Radioallergosorbent tests were performed for possible allergens (mixture for relevant food allergens, Phadiatop and latex). IgG subclasses, IgM, and complement factors (C3, C4 and factor B) were measured with radial immunodiffusion. Mast cells, labelled with antibodies against mast cell tryptase, were counted in the lungs and heart. The circumstances of death and medical history of the deceased infant and family were obtained through police and hospital records.
In 40% of the SIDS cases tryptase was elevated (>10 microg/L). Total IgE in serum was increased in 33% compared with clinical reference values but showed no association with mast cell tryptase. RAST tests were positive in three cases. In one of these cases both tryptase and total IgE were elevated. The only variable that was associated with high tryptase values was prone position at death (P < or = 0.05 ). Allergy or asthma in the family were alleged in 50% of the cases, but was not associated with elevated tryptase or IgE. Children with elevated total IgE also displayed high concentrations of IgG1 and IgG2. Infants who died in the spring had significantly higher IgE than the others (P < or = 0.05).
The results do not support the hypothesis that the elevated tryptase concentrations in sudden infant death are caused by allergy. The association between prone position at death and elevated tryptase could hypothetically be explained by mast cell degranulation due to, for example, a hypoxic stimulus in these infants.
在婴儿猝死的尸检血液中，经常观察到肥大细胞类胰蛋白酶浓度升高，但其原因尚未阐明。
评估婴儿猝死时肥大细胞类胰蛋白酶升高背后的因素（免疫学、形态学和既往史数据）。
检测了44名1.5岁以下婴儿尸检血清中的肥大细胞类胰蛋白酶和总免疫球蛋白（Ig）E。针对可能的过敏原（相关食物过敏原混合物、Phadiatop和乳胶）进行了放射变应原吸附试验。用放射免疫扩散法检测IgG亚类、IgM和补体因子（C3、C4和B因子）。用抗肥大细胞类胰蛋白酶抗体标记的肥大细胞在肺和心脏中进行计数。通过警方和医院记录获取死亡婴儿及其家庭的死亡情况和病史。
在40%的婴儿猝死综合征（SIDS）病例中，类胰蛋白酶升高（>10μg/L）。与临床参考值相比，33%的血清总IgE升高，但与肥大细胞类胰蛋白酶无关联。放射变应原吸附试验在3例中呈阳性。其中1例中类胰蛋白酶和总IgE均升高。与高类胰蛋白酶值相关的唯一变量是死亡时的俯卧位（P≤0.05）。50%的病例中称家族中有过敏或哮喘，但与类胰蛋白酶或IgE升高无关。总IgE升高的儿童也表现出高浓度的IgG1和IgG2。春季死亡的婴儿IgE明显高于其他婴儿（P≤0.05）。
结果不支持婴儿猝死时类胰蛋白酶浓度升高是由过敏引起的这一假设。死亡时的俯卧位与类胰蛋白酶升高之间的关联，据推测可能是由于这些婴儿例如缺氧刺激导致肥大细胞脱颗粒所致。
