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An important and serious side effect of <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>Is is angioedema caused by a reduction in bradykinin degradation. In a national medical chart abstraction study conducted at the <jats:styled-content style=\"fixed-case\">US<\/jats:styled-content> Veterans Affairs Health Care System in 2008, 0.20% of <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>I initiators developed angioedema while on the medication. The angiotensin\u2010converting enzyme is a part of the renin\u2010angiotensin system that converts angiotensin I to angiotensin <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>. It is additionally responsible for the degradation of bradykinin, which is generated from high molecular weight kininogen by kallikrein. Via bradykinin 2 receptors, bradykinin affects vascular permeability and stimulates the release of substance P, which is a peptide that causes vasodilation and fluid extravasation into tissues. Inhibition of <jats:styled-content style=\"fixed-case\">the angiotensin\u2010converting enzyme<\/jats:styled-content> and subsequent blockade of bradykinin degradation is thought to be a likely explanation for <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>I\u2010induced angioedema. Studies have shown that blacks, women, and smokers are at an increased risk for <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>I\u2010induced angioedema. A 2005 study identified black race, history of drug rash, age older than 65\u00a0years, and seasonal allergies as independent risk factors for angioedema related to enalapril. Angioedema may occur at any time during treatment with <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>Is and may continue after the medication is discontinued. The degree of <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>I\u2010angiotensin receptor blocker angioedema cross\u2010reactivity is difficult to determine from the literature. However, multiple studies have reported relatively low rates of native angioedema with <jats:styled-content style=\"fixed-case\">angiotensin receptor blockers<\/jats:styled-content> (approximately half that of <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>Is, or 0.1%) and a low incidence of cross\u2010reactivity (&lt;10%). Common treatments for angioedema, such as antihistamines and glucocorticoids, have not been shown to be effective in <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>I\u2010induced angioedema. However, medications that have been used for acute treatment of hereditary angioedema and target the factors that cause <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>I\u2010mediated angioedema are being explored.<\/jats:p>","DOI":"10.1111\/jch.13097","type":"journal-article","created":{"date-parts":[[2017,10,10]],"date-time":"2017-10-10T05:22:44Z","timestamp":1507612964000},"page":"1377-1382","source":"Crossref","is-referenced-by-count":110,"title":["Angiotensin\u2010converting enzyme inhibitor\u2013induced angioedema: A review of the literature"],"prefix":"10.1111","volume":"19","author":[{"given":"Teresa","family":"Brown","sequence":"first","affiliation":[{"name":"Department of Medicine Rutgers Robert Wood Johnson Medical School  New Brunswick NJ USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jimmy","family":"Gonzalez","sequence":"additional","affiliation":[{"name":"Department of Pharmacy Practice Western New England University School of 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