Ghebrehiwet Berhane, Joseph Kusumam, Kaplan Allen P
Division of Rheumatology, Allergy, and Clinical Immunology, SUNY-Stony Brook, Stony Brook, NY, United States.
Division of Pulmonary and Critical Care Medicine, The Medical University of South Carolina, Charleston, SC, United States.
Front Allergy. 2024 Jan 25;5:1302605. doi: 10.3389/falgy.2024.1302605. eCollection 2024.
Anaphylaxis is a potentially life-threatening multi-system allergic reaction to a biological trigger resulting in the release of potent inflammatory mediators from mast cells and basophils and causing symptoms in at least two organ systems that generally include skin, lungs, heart, or gastrointestinal tract in any combination. One exception is profound hypotension as an isolated symptom. There are two types of triggers of anaphylaxis: immunologic and non-Immunologic. Immunologic anaphylaxis is initiated when a foreign antigen directly binds to IgE expressed on mast cells or basophils and induces the release of histamine and other inflammatory substances resulting in vasodilation, vascular leakage, decreased peripheral vascular resistance, and heart muscle depression. If left untreated, death by shock (profound hypotension) or asphyxiation (airway obstruction) can occur. The non-immunologic pathway, on the other hand, can be initiated in many ways. A foreign substance can directly bind to receptors of mast cells and basophils leading to degranulation. There can be immune complex activation of the classical complement cascade with the release of anaphylatoxins C3a and C5a with subsequent recruitment of mast cells and basophils. Finally, hyperosmolar contrast agents can cause blood cell lysis, enzyme release, and complement activation, resulting in anaphylactoid (anaphylactic-like) symptoms. In this report we emphasize the recruitment of the bradykinin-forming cascade in mast cell dependent anaphylactic reactions as a potential mediator of severe hypotension, or airway compromise (asthma, laryngeal edema). We also consider airway obstruction due to inhibition of angiotensin converting enzyme with a diminished rate of endogenous bradykinin metabolism, leading not only to laryngeal edema, but massive tongue swelling with aspiration of secretions.
过敏反应是一种对生物触发因素产生的潜在危及生命的多系统过敏反应，导致肥大细胞和嗜碱性粒细胞释放强效炎症介质，并在至少两个器官系统中引发症状，这些器官系统通常包括皮肤、肺部、心脏或胃肠道，可任意组合。一个例外是仅表现为严重低血压的情况。过敏反应有两种触发因素：免疫性和非免疫性。当外来抗原直接与肥大细胞或嗜碱性粒细胞上表达的IgE结合，并诱导组胺和其他炎症物质释放，导致血管扩张、血管渗漏、外周血管阻力降低和心肌抑制时，就会引发免疫性过敏反应。如果不进行治疗，可能会因休克（严重低血压）或窒息（气道阻塞）而死亡。另一方面，非免疫性途径可以通过多种方式启动。外来物质可以直接与肥大细胞和嗜碱性粒细胞的受体结合，导致脱颗粒。经典补体级联反应可通过免疫复合物激活，释放过敏毒素C3a和C5a，随后募集肥大细胞和嗜碱性粒细胞。最后，高渗性造影剂可导致血细胞溶解、酶释放和补体激活，从而引发类过敏反应（类似过敏反应的症状）。在本报告中，我们强调在肥大细胞依赖性过敏反应中激肽形成级联反应的募集，它是严重低血压或气道损害（哮喘、喉水肿）的潜在介质。我们还考虑了由于血管紧张素转换酶抑制导致内源性缓激肽代谢速率降低而引起的气道阻塞，这不仅会导致喉水肿，还会导致大量舌肿胀并伴有分泌物误吸。
