Department of Medicine, Thomas Jefferson University, Philadelphia, Pa.
Department of Medicine, Thomas Jefferson University, Philadelphia, Pa.
J Allergy Clin Immunol Pract. 2013 Sep-Oct;1(5):442-5. doi: 10.1016/j.jaip.2013.07.005. Epub 2013 Aug 30.
Angiotensin-converting enzyme inhibitors (ACEI) are commonly prescribed for blood pressure control and renal protection. ACEI angioedema is a common problem in patients who are taking ACEI, although, in most cases, the disorder is self-limited, and spontaneous episodes of apparently unprovoked angioedema stop with the discontinuation of the medication. In a subset of patients, hospitalization and even intubation are required for airway protection. The diagnosis is made clinically. There are no laboratory studies that establish the diagnosis. However, such investigations help exclude alternative diagnoses as the cause for the patient's presentation. Conventional treatment with regimens used to control allergic angioedema is ineffective in this condition. The mechanism of ACEI-induced angioedema is thought to be related to its effect on the kallikrein-kinin system. Kallikrein is a protease that converts high-molecular-weight kininogens into kinins, primarily bradykinin. Medications recently developed, primarily icatibant and ecallantide, to control hereditary angioedema, a disorder also associated with kallikrein-kinin activation, have been used to treat ACEI angioedema with some success. The efficacy of these agents and their optimal use remains to be established by randomized and placebo controlled trials.
血管紧张素转换酶抑制剂(ACEI)常用于控制血压和保护肾脏。虽然 ACEI 血管性水肿在服用 ACEI 的患者中很常见,但在大多数情况下,这种疾病是自限性的,并且在停止药物治疗后,自发性、无明显诱因的血管性水肿发作会自行停止。在一部分患者中,需要住院治疗甚至插管以保护气道。该诊断主要通过临床来做出。目前还没有实验室研究来确定诊断。然而,这些检查有助于排除其他替代诊断,以确定患者的表现原因。控制过敏血管性水肿的常规治疗方案对这种情况无效。ACEI 引起的血管性水肿的机制被认为与其对激肽释放酶-激肽系统的影响有关。激肽释放酶是一种蛋白酶,可将高分子量激肽原转化为激肽,主要是缓激肽。最近开发的一些药物,主要是依卡替班和艾卡替班,用于控制遗传性血管性水肿,这也是一种与激肽释放酶-激肽激活相关的疾病,已被用于治疗 ACEI 血管性水肿,并取得了一定的成功。这些药物的疗效和最佳使用方法仍需通过随机和安慰剂对照试验来确定。