Current Treatment of Angioedema Induced by ACE Inhibitors

Abstract

Purpose of Review: Angioedema is a well-known side effect of ACE inhibitors. Current knowledge shows that the underlying pathophysiological mechanism is an excess of bradykinin, most likely due to ineffective breakdown pathways. Since C1 inhibitor deficiency has the same pathophysiological background, it would be logical to assume that C1 inhibitor deficiency treatments could be of use in ACE inhibitor–induced angioedema. The objective of this review was to evaluate the evidence for treatment of ACE inhibitor–induced angioedema by means of drugs intervening in the bradykinin system. Recent Findings: We searched in the literature for double-blind placebo-controlled trials using either inhibitors of production of kallikrein, bradykinin receptor antagonists, C1 inhibitor concentrate, or fresh frozen plasma as treatment for ACE inhibitor–induced angioedema. The reference list of retrieved articles was checked for articles with the same subject (snowballing). The evidence for each treatment was evaluated by IT and DMC. Summary: Double-blind placebo-controlled trials were only found for ecallantide and icatibant. Both treatments did not show superiority over conventional treatment with histamine receptor antagonists and steroids. No double-blind placebo-controlled trials were found of fresh frozen plasma or C1 inhibitor concentrate. To date, there is insufficient evidence for the use of bradykinin receptor antagonists and kallikrein production inhibitors. Although case reports regarding the use of fresh frozen plasma and C1 inhibitor concentrate are positive, well-designed trials are lacking.