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• W2150366942 startingPage "157" @default.
• W2150366942 abstract "Hereditary angio-oedema (HAE) is a rare but potentially life-threatening condition. Three types are now recognized. Types I and II HAE involve mutations in the C1NH (SERPING1) gene, encoding the C1 inhibitor protein, whereas type III HAE involves mutations in the F12 gene, encoding coagulation factor XII (Hageman factor). They share a common final pathway leading to increased bradykinin formation. HAE must be distinguished from acquired angio-oedema with C1 esterase inhibitor deficiency, angiotensin-converting enzyme inhibitor-induced angio-oedema and the much more common histaminergic angio-oedema, occurring with or without weals. Understanding the pathogenesis of HAE is leading to the introduction of new therapies that target the bradykinin receptor or inhibit kallikrein activity, innovations that will hopefully reduce morbidity and mortality in this group of severe genetic disease." @default.
• W2150366942 created "2016-06-24" @default.
• W2150366942 creator A5063930176 @default.
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• W2150366942 date "2010-04-29" @default.
• W2150366942 modified "2023-09-26" @default.
• W2150366942 title "New insights into hereditary angio-oedema: Molecular diagnosis and therapy" @default.
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• W2150366942 doi "https://doi.org/10.1111/j.1440-0960.2010.00649.x" @default.
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