Centre for Clinical Research in Emergency Medicine, Western Australian Institute for Medical Research, Perth, Australia; University of Western Australia, Crawley, Australia; Royal Perth Hospital, Perth, Australia; Fremantle Hospital, Fremantle, Australia.
J Allergy Clin Immunol. 2013 Nov;132(5):1141-1149.e5. doi: 10.1016/j.jaci.2013.06.015. Epub 2013 Aug 1.
Prospective human studies of anaphylaxis and its mechanisms have been limited, with few severe cases or examining only 1 or 2 mediators.
We wanted to define the clinical patterns of anaphylaxis and relationships between mediators and severity.
Data were collected during treatment and before discharge. Serial blood samples were taken for assays of mast cell tryptase, histamine, anaphylatoxins (C3a, C4a, C5a), cytokines (IL-2, IL-6, IL-10), soluble tumor necrosis factor receptor I, and platelet activating factor acetyl hydrolase. Principal component analysis defined mediator patterns, and logistic regression identified risk factors and mediator patterns associated with reaction severity and delayed reactions.
Of 412 reactions in 402 people, 315 met the definition for anaphylaxis by the National Institute of Allergy and Infectious Diseases/Food Allergy and Anaphylaxis Network. Of 97 severe reactions 45 (46%) were hypotensive, 23 (24%) were hypoxemic, and 29 (30%) were mixed. One patient died. Severe reactions were associated with older age, pre-existing lung disease, and drug causation. Delayed deteriorations treated with epinephrine occurred in 29 of 315 anaphylaxis cases (9.2%) and were more common after hypotensive reactions and with pre-existing lung disease. Twenty-two of the 29 delayed deteriorations (76%) occurred within 4 hours of initial epinephrine treatment. Of the remaining 7 cases, 2 were severe and occurred after initially severe reactions, within 10 hours. All mediators were associated with severity, and 1 group (mast cell tryptase, histamine, IL-6, IL-10, and tumor necrosis factor receptor I) was also associated with delayed deteriorations. Low platelet activating factor acetyl hydrolase activity was associated with severe reactions.
The results suggest that multiple inflammatory pathways drive reaction severity and support recommendations for safe observation periods after initial treatment.
过敏反应及其机制的前瞻性人体研究受到限制，只有少数严重病例或仅检查 1 或 2 种介质。
我们旨在确定过敏反应的临床模式以及介质与严重程度之间的关系。
在治疗和出院前收集数据。采集连续血样进行肥大细胞类胰蛋白酶、组胺、过敏毒素（C3a、C4a、C5a）、细胞因子（IL-2、IL-6、IL-10）、可溶性肿瘤坏死因子受体 I 和血小板激活因子乙酰水解酶检测。主成分分析确定介质模式，逻辑回归确定与反应严重程度和延迟反应相关的危险因素和介质模式。
在 402 人中的 412 次反应中，315 次符合美国国立过敏和传染病研究所/食物过敏和过敏反应网络的过敏反应定义。97 例严重反应中，45 例（46%）为低血压，23 例（24%）为低氧血症，29 例（30%）为混合性。有 1 例患者死亡。严重反应与年龄较大、既往肺部疾病和药物病因有关。接受肾上腺素治疗的 29 例 315 例过敏反应中的延迟恶化（9.2%）更常见于低血压反应和既往肺部疾病。29 例延迟恶化中的 22 例（76%）发生在初始肾上腺素治疗后 4 小时内。其余 7 例中，2 例为严重反应，且发生在初始严重反应后 10 小时内。所有介质均与严重程度相关，其中 1 组（肥大细胞类胰蛋白酶、组胺、IL-6、IL-10 和肿瘤坏死因子受体 I）也与延迟恶化相关。血小板激活因子乙酰水解酶活性低与严重反应有关。
结果表明，多种炎症途径可导致反应严重程度，并支持初始治疗后进行安全观察期的建议。
