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Angioedema
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===Hereditary angioedema=== [[Hereditary angioedema]] (HAE) exists in three forms, all of which are caused by a genetic mutation inherited in an [[Dominance (genetics)|autosomal dominant]] form. They are distinguished by the underlying genetic abnormality. Types I and II are caused by mutations in the ''SERPING1'' gene, which result in either diminished levels of the [[C1-inhibitor]] protein (type I HAE) or dysfunctional forms of the same protein (type II HAE). Type III HAE has been linked with mutations in the ''F12'' gene, which encodes the coagulation protein [[factor XII]]. All forms of HAE lead to abnormal activation of the [[complement system]], and all forms can cause swelling elsewhere in the body, such as the [[digestive tract]]. If HAE involves the [[larynx]], it can cause life-threatening [[asphyxiation]].<ref>{{cite journal |author=Zuraw B.L. |title=Clinical practice. Hereditary angioedema |journal=N. Engl. J. Med. |volume=359 |issue=10 |pages=1027β36 |date=September 2008 |pmid=18768946 |doi=10.1056/NEJMcp0803977}}</ref> The pathogenesis of this disorder is suspected to be related to unopposed activation of the contact pathway by the initial generation of kallikrein and/or clotting factor XII by damaged endothelial cells. The end product of this cascade, bradykinin, is produced in large amounts and is believed to be the predominant mediator leading to increased vascular permeability and vasodilation that induces typical angioedema "attacks".<ref>{{cite web|last=Loew|first=Burr|title=A 68-Year-Old Woman With Recurrent Abdominal Pain, Nausea, and Vomiting|url=http://www.medscape.org/viewarticle/743937_2|publisher=MedScape|access-date=19 October 2012|url-status=live|archive-url=https://web.archive.org/web/20121022004946/http://www.medscape.org/viewarticle/743937_2|archive-date=22 October 2012}}</ref>
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