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Although most <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>i\u2010induced angioedema (<jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>i\u2010A) cases are mild, severe cases requiring intensive care and even resulting in death have been reported in the literature. The mechanisms underlying <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>i\u2010A are not yet fully understood, but bradykinin and\/or substance P accumulation resulting from inhibition of <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content> is believed to play a crucial role. <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>i\u2010A occurs at variable frequencies across different racial groups, suggesting a genetic association with the development of <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>i\u2010A. To date, one genome\u2010wide association study and several candidate gene studies have been published on the association of genetic variation with <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>i\u2010A. Genetic associations reported have been attributed to several distinct mechanisms: (a) genes coding for alternative enzymes responsible for the degradation of bradykinin and\/or substance P in the diminution of <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content> activity (b) <jats:italic><jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content><\/jats:italic> gene function, (c) bradykinin receptor genes, (d) genes implicated in immune and inflammation regulation and (e) genes in the fibrinolytic and coagulation pathway. Despite several plausible genetic associations, there are currently no genetic variants with sufficient effect to be clinically useful. The low incidence of <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>i\u2010A suggests that a combination of genomic approaches with the capability to detect potentially important variants might be required to shed light on the mechanism of this adverse reaction. Additionally, many non\u2010genetic risk factors associated with <jats:styled-content style=\"fixed-case\">ACE<\/jats:styled-content>i\u2010A suggest the potential contribution of epigenetic dysregulation.<\/jats:p>","DOI":"10.1111\/cea.13326","type":"journal-article","created":{"date-parts":[[2018,12,8]],"date-time":"2018-12-08T12:54:32Z","timestamp":1544273672000},"page":"142-154","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Pharmacogenetics of angiotensin\u2010converting enzyme inhibitor\u2010induced angioedema"],"prefix":"10.1111","volume":"49","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2184-0538","authenticated-orcid":false,"given":"Yusmiati","family":"Liau","sequence":"first","affiliation":[{"name":"Department of Pathology and Biomedical Science University of Otago Christchurch New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ignatius","family":"Chua","sequence":"additional","affiliation":[{"name":"Canterbury Health Laboratories Canterbury District Health Board Christchurch New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin A.","family":"Kennedy","sequence":"additional","affiliation":[{"name":"Department of Pathology and Biomedical Science University of Otago Christchurch New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Simran","family":"Maggo","sequence":"additional","affiliation":[{"name":"Department of Pathology and Biomedical Science University of Otago Christchurch New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2019,1,8]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1093\/eurheartj\/ehs075"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijcard.2011.01.081"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1001\/jamainternmed.2014.348"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1592\/phco.23.7.909.32726"},{"key":"e_1_2_9_6_1","unstructured":"IMS Institute for Healthcare Informatics.The global use of medicines: Outlook through 2015. 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