Kuperstock Jacob E, Pritchard Nicholas, Horný Michal, Xiao Christopher C, Brook Christopher D, Platt Michael P
Department of Otolaryngology - Head and Neck Surgery, Boston University School of Medicine, Boston, MA 02118, United States.
Boston University School of Medicine, Boston, MA 02118, United States; Department of Otolaryngology - Head and Neck Surgery, University of South Florida, Tampa, FL 33612, United States.
Am J Otolaryngol. 2018 Mar-Apr;39(2):111-115. doi: 10.1016/j.amjoto.2017.12.013. Epub 2017 Dec 27.
BACKGROUND/OBJECTIVE: The etiology and risk factors for angioedema remain poorly understood with causative triggers often going undiagnosed despite repeated reactions. The purpose of this study was to determine the relationship between inhalant allergen sensitization and angioedema.
A retrospective review of patients who had in vitro inhalant allergy testing from 2006 to 2010 was performed. Patients with a diagnosis of angioedema who underwent inhalant allergy testing were identified. Analyses for co-morbidities, class of sensitization, seasonal timing of angioedema, and concurrent use of known hypertensive medications that can cause angioedema were performed.
There were 1000 patients who underwent inhalant allergy testing and qualified for the study. 37/1000 had at least one episode of angioedema and of these patients, 34 had positive inhalant sensitization testing results. Multivariate regression models showed overall sensitization status, seasonal allergen and epidermal/mite sensitization as independent risk factors (p<0.001, p=0.005, p=0.025 respectively) when controlling for ACE inhibitor use and other covariates. Tree, and epidermal/mite sensitizations were independent risk factors for angioedema in mono-sensitized subject analysis (p=0.028, p=0.029, respectively).
Both seasonal and perennial allergen sensitizations are independent risk factors for the development of angioedema. In patients with angioedema and an unknown trigger, inhalant allergen sensitization should be considered as a potential contributing factor to the development of angioedema.
背景/目的:尽管血管性水肿反复发生,但病因和危险因素仍未得到充分了解,致病诱因常常无法确诊。本研究旨在确定吸入性过敏原致敏与血管性水肿之间的关系。
对2006年至2010年进行体外吸入性过敏检测的患者进行回顾性研究。确定接受吸入性过敏检测且诊断为血管性水肿的患者。对合并症、致敏类别、血管性水肿的季节性发作时间以及同时使用可能导致血管性水肿的已知高血压药物进行分析。
共有1000例患者接受了吸入性过敏检测并符合研究条件。其中37/1000至少有一次血管性水肿发作,在这些患者中,34例吸入性致敏检测结果呈阳性。在控制使用血管紧张素转换酶抑制剂和其他协变量时,多变量回归模型显示总体致敏状态、季节性过敏原以及表皮/螨虫致敏是独立危险因素(分别为p<0.001、p=0.005、p=0.025)。在单致敏受试者分析中,树木和表皮/螨虫致敏是血管性水肿的独立危险因素(分别为p=0.028、p=0.0z9)。
季节性和常年性过敏原致敏都是血管性水肿发生的独立危险因素。对于血管性水肿且诱因不明的患者,应考虑吸入性过敏原致敏是血管性水肿发生的潜在促成因素。