Weiss M E, Adkinson N F
University of Washington Hospital, Seattle.
Clin Rev Allergy. 1991 Fall-Winter;9(3-4):339-55. doi: 10.1007/BF02802312.
Recent advances in medicine, such as cardiac catheterization, phoresis, dialysis, and cardiopulmonary bypass technology, have increased the need for heparin anticoagulation. To antagonize heparin's effect and prevent hemorrhagic complications after the procedure, protamine has likewise been used more frequently. With its increased use have come increased reports of adverse protamine reactions consisting of rash, urticaria, elevation of pulmonary artery pressure, systemic hypotension, and, at times, death. The elevation of pulmonary artery pressure, which appears to be a rather common occurrence in animals, may be an isolated finding without clinical consequences in humans. However, this pulmonary vasoconstriction may, when severe, lead to acute right-sided heart failure and systemic hypotension. Other protamine reactions involve a decrease in systemic vascular resistance and systemic hypotension without changes in pulmonary artery pressure. Causes of acute protamine reactions may involve the generation of anaphyatoxins and prostanoids either from protamine-heparin complexes or complement-fixing antiprotamine IgG antibodies, from inhibition of plasma Carboxypeptidase N, from crosslinking of cell-surface antiprotamine IgE on mast cells and basophils with subsequent mediator release, or from potentiation of IgE-mediated release of histamine through a polycationin-recognition site. Although we have come a long way in understanding the mechanisms by which protamine can cause its ill effects in humans, more work is clearly needed to define, in prospective studies, the incidence of and risk factors for protamine reactions in various patient groups, and to delineate more clearly which mechanisms are involved in each clinical type of acute protamine reaction. Hopefully, this will lead to strategies and protamine alternatives that will prevent or diminish, in frequency or severity, adverse protamine reactions. Alternatively, a clearer picture of the risk factors important for protamine reactions and the predictive value of diagnostic tests (e.g., protamine IgE antibody) can also minimize the clinical impact of this increasingly common adverse event.
医学领域的最新进展，如心脏导管插入术、电泳法、透析和体外循环技术，增加了肝素抗凝的需求。为了对抗肝素的作用并预防术后出血并发症，鱼精蛋白的使用也同样更加频繁。随着其使用的增加，关于鱼精蛋白不良反应的报告也增多了，这些不良反应包括皮疹、荨麻疹、肺动脉压升高、全身性低血压，有时甚至导致死亡。肺动脉压升高在动物中似乎相当常见，在人类中可能是一个孤立的发现而无临床后果。然而，这种肺血管收缩严重时可能导致急性右侧心力衰竭和全身性低血压。其他鱼精蛋白反应包括全身血管阻力降低和全身性低血压，而肺动脉压无变化。急性鱼精蛋白反应的原因可能涉及从鱼精蛋白 - 肝素复合物或补体固定抗鱼精蛋白IgG抗体产生过敏毒素和类前列腺素，抑制血浆羧肽酶N，肥大细胞和嗜碱性粒细胞上细胞表面抗鱼精蛋白IgE交联并随后释放介质，或通过聚阳离子识别位点增强IgE介导的组胺释放。尽管我们在理解鱼精蛋白在人类中产生不良影响的机制方面已经取得了很大进展，但显然还需要更多工作，以前瞻性研究确定不同患者群体中鱼精蛋白反应的发生率和危险因素，并更清楚地描绘每种临床类型的急性鱼精蛋白反应涉及哪些机制。希望这将带来预防或减少鱼精蛋白不良反应的频率或严重程度的策略和鱼精蛋白替代物。或者，更清楚地了解对鱼精蛋白反应重要的危险因素以及诊断测试（如鱼精蛋白IgE抗体）的预测价值，也可以将这种日益常见的不良事件的临床影响降至最低。
