Benson Michael D
Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, 101 Bentley Court, Deerfield, IL 60015, USA.
Med Hypotheses. 2007;68(5):1019-25. doi: 10.1016/j.mehy.2006.09.052. Epub 2006 Nov 16.
Amniotic fluid embolism, a rare, sudden and often fatal illness of pregnancy may not be a true embolic event resulting from the physical obstruction of the pulmonary vasculature. The high degree of variability in symptoms, the lack of characteristic findings on radiological exam, the absence of a dose-response effect on symptoms, and the occasional occurrence of coagulopathies are not entirely consistent with a physical block to the circulation as the main mechanism of disease. Alternatively, it might be the result of complement activation initiated by fetal antigen leaking into the maternal circulation. This rare immune response may be initiated by a rare pathological antigen, or by common antigens presented uncommonly--in amount, timing, or frequency of entry into the maternal circulation. Some very early evidence in AFE patients supports this hypothesis but is not conclusive. Complement levels remain well within the normal range during uncomplicated parturition. A prior theory that AFE might be a result of maternal anaphylaxis to fetal antigen has much less evidence to support it. The disseminated intravascular coagulation often seen in this and other serious obstetrical illnesses may be a secondary result of complement activation rather than the direct introduction of pro-coagulants into the maternal circulation although the link between the complement and coagulation pathways, if any, remains poorly defined. Through currently available laboratory testing, both the complement hypothesis and the anaphylaxis mechanism are able to be assessed. Direct measurement of serum complement as well as serum tryptase and urinary histamine are readily obtained tests in community hospitals as well as tertiary care hospitals. If the hypothesis proves true, this investigation may be of profound importance to understanding immune tolerance. Rather, than asking why one pregnant woman in 20,000 develops a violent immune reaction to the fetus, a better question is why do not all pregnant women reject the fetus which is a large collection of foreign antigens?
羊水栓塞是一种罕见、突发且往往致命的妊娠疾病，它可能并非由肺血管系统的物理阻塞导致的真正栓塞事件。症状的高度变异性、放射学检查缺乏特征性表现、症状不存在剂量反应效应以及偶尔出现的凝血病，并不完全符合以循环系统的物理阻塞作为主要疾病机制的情况。相反，它可能是胎儿抗原漏入母体循环引发补体激活的结果。这种罕见的免疫反应可能由罕见的病理性抗原引发，或者由常见抗原以不常见的方式引发——在进入母体循环的量、时间或频率方面。羊水栓塞患者的一些非常早期的证据支持这一假说，但并不确凿。在无并发症的分娩过程中，补体水平仍保持在正常范围内。先前认为羊水栓塞可能是母体对胎儿抗原过敏反应的结果这一理论，支持它的证据要少得多。在这种疾病以及其他严重产科疾病中经常见到的弥散性血管内凝血，可能是补体激活的次要结果，而非促凝剂直接进入母体循环所致，尽管补体与凝血途径之间的联系（如果存在的话）仍不清楚。通过目前可用的实验室检测，补体假说和过敏反应机制都能够得到评估。在社区医院以及三级护理医院，血清补体、血清类胰蛋白酶和尿组胺的直接测量都是容易获得的检测项目。如果该假说被证明是正确的，这项研究对于理解免疫耐受可能具有深远的重要性。与其问为什么两万分之一的孕妇会对胎儿产生强烈的免疫反应，一个更好的问题是为什么并非所有孕妇都排斥胎儿，而胎儿是大量外来抗原的集合？
