Strassen Ulrich, Bas Murat, Hoffmann Thomas K, Knopf Andreas, Greve Jens
Department of Otorhinolaryngology, Head and Neck Surgery, Technical University of Munich, Munich, Germany.
Department of Oto-Rhino-Laryngology, Head and Neck Surgery, Ulm University Medical Center, Ulm, Germany.
Laryngoscope. 2015 Jul;125(7):1619-23. doi: 10.1002/lary.25163. Epub 2015 Feb 3.
Angiotensin II receptor antagonists have been proposed as a replacement therapy after the occurrence of either an angiotensin converting enzyme (ACE) inhibitor-induced angioedema or cough. However, recent studies indicate that angioedema is associated with elevated bradykinin levels in a small fraction of patients treated with angiotensin-II-receptor blockers, suggesting a common pathophysiological mechanism. To date, a standard treatment for angiotensin II receptor blocker-induced angioedema does not exist.
We present a case series of patients admitted to our hospital due to angioedema induced by an angiotensin II receptor blocker. The patients were either treated with either icatibant (n = 3) or prednisolone-21-hydrogen succinate/clemastine (n = 5). Both patient groups were compared with an untreated patient cohort (n = 3). All patients were previously diagnosed with essential hypertonia.
Icatibant was an effective therapy for angiotensin II receptor blocker-induced angioedema. Full symptom recovery was achieved after 5 to 7 hours, whereas symptom remission occurred within 27 to 52 and 24 to 54 hours in patients treated with Solu-Decortin prednisolone/clemastine and untreated patients, respectively. The recovery time for icatibant was similar to that described in previous studies regarding the therapeutic efficacy of icatibant for the treatment of hereditary angioedema and patients suffering from angiotensin converting enzyme inhibitor-induced angioedema.
Icatibant is a safe and effective substance for the treatment of angiotensin II receptor blocker-induced angioedema. Although the pathophysiology of angiotensin II receptor blocker-induced angioedema remains unclear, it appears to be associated with the bradykinin pathway.
血管紧张素II受体拮抗剂已被提议作为血管紧张素转换酶（ACE）抑制剂引起血管性水肿或咳嗽后出现的替代疗法。然而，最近的研究表明，在一小部分接受血管紧张素II受体阻滞剂治疗的患者中，血管性水肿与缓激肽水平升高有关，提示存在共同的病理生理机制。迄今为止，尚无血管紧张素II受体阻滞剂引起的血管性水肿的标准治疗方法。
我们报告了一组因血管紧张素II受体阻滞剂引起血管性水肿而入住我院的患者病例系列。患者分别接受艾替班特治疗（n = 3）或琥珀酸氢化泼尼松/氯马斯汀治疗（n = 5）。将两组患者与未治疗的患者队列（n = 3）进行比较。所有患者既往均诊断为原发性高血压。
艾替班特是治疗血管紧张素II受体阻滞剂引起的血管性水肿的有效疗法。5至7小时后症状完全恢复，而接受氢化可的松琥珀酸钠泼尼松/氯马斯汀治疗的患者和未治疗的患者症状缓解分别发生在27至52小时和24至54小时内。艾替班特的恢复时间与先前关于艾替班特治疗遗传性血管性水肿和血管紧张素转换酶抑制剂引起的血管性水肿的疗效研究中描述的时间相似。
艾替班特是治疗血管紧张素II受体阻滞剂引起的血管性水肿的安全有效药物。虽然血管紧张素II受体阻滞剂引起的血管性水肿的病理生理学仍不清楚，但似乎与缓激肽途径有关。
