Platt M S, Yunginger J W, Sekula-Perlman A, Irani A M, Smialek J, Mirchandani H G, Schwartz L B
Office of the Chief Medical Examiner of Maryland, Baltimore.
J Allergy Clin Immunol. 1994 Aug;94(2 Pt 1):250-6. doi: 10.1016/0091-6749(94)90047-7.
The pathogenesis of sudden infant death syndrome (SIDS) is elusive and probably multifactorial. The occurrence of mast cell activation in SIDS was assessed in this study by measuring concentrations of tryptase, a neutral protease produced mainly by mast cells, in postmortem sera from term infants with SIDS and from age-matched control infants who died unexpectedly at home from a known cause. Tryptase levels were significantly higher in the 50 infants with SIDS than in the 15 control infants (p = 0.0004). Forty percent of the infants with SIDS and none of the control infants had a tryptase level greater than 10 ng/ml, the threshold chosen to indicate premortem mast cell activation. An infant with SIDS had a 20-fold higher chance of having an elevated tryptase level compared with a control infant. The postmortem interval did not influence these results. Thus mast cell-mediated anaphylaxis is likely to be the pathogenetic mechanism involved in some but not all SIDS cases. Recognition of this pathway as operative in SIDS should facilitate a more precise identification of the allergens involved, the processes leading to mast cell activation, and procedures to identify those infants at risk for anaphylaxis, and should, in time, lead to better therapeutic interventions aimed at preventing this specific cause of SIDS.
婴儿猝死综合征（SIDS）的发病机制尚不明确，可能是多因素导致的。在本研究中，通过测量SIDS足月儿和年龄匹配的因已知原因在家中意外死亡的对照婴儿死后血清中类胰蛋白酶（一种主要由肥大细胞产生的中性蛋白酶）的浓度，来评估SIDS中肥大细胞活化的发生情况。50例SIDS婴儿的类胰蛋白酶水平显著高于15例对照婴儿（p = 0.0004）。40%的SIDS婴儿类胰蛋白酶水平高于10 ng/ml（选择该阈值来表明死前肥大细胞活化），而对照婴儿中无一例高于此值。与对照婴儿相比，SIDS婴儿类胰蛋白酶水平升高的几率高出20倍。死后间隔时间并未影响这些结果。因此，肥大细胞介导的过敏反应很可能是部分而非全部SIDS病例的发病机制。认识到这一途径在SIDS中起作用，应有助于更精确地识别所涉及的过敏原、导致肥大细胞活化的过程以及识别有过敏反应风险婴儿的程序，并最终应能带来旨在预防SIDS这一特定病因的更好治疗干预措施。
