{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T03:59:40Z","timestamp":1772164780435,"version":"3.50.1"},"reference-count":42,"publisher":"S. Karger AG","issue":"4","license":[{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Dermatology"],"published-print":{"date-parts":[[2015]]},"abstract":"<jats:p>&lt;b&gt;&lt;i&gt;Background:&lt;\/i&gt;&lt;\/b&gt; Angio-oedema (AO) can be attributable to bradykinin (BK) accumulation, as is the case for prototypical hereditary AO (HAO) due to C1 inhibitor (C1-INH) deficiency. However, our clinical experience in a reference centre has shown that some patients display a clinical history suggestive of HAO, but exhibit normal C1-INH function, have no mutation in the causative genes associated with HAO &lt;i&gt;(SERPING1, F12)&lt;\/i&gt;, and report no intake of drugs known to promote AO. &lt;b&gt;&lt;i&gt;Objective:&lt;\/i&gt;&lt;\/b&gt; We sought to determine the frequency and distribution of different AO subtypes suspected to be BK-mediated AO (BK-AO) and defined by clinical, history and biological criteria (enzyme activities implicated in BK formation and catabolism). &lt;b&gt;&lt;i&gt;Methods:&lt;\/i&gt;&lt;\/b&gt; The files of all patients referred to our centre for suspected BK-AO were retrospectively analysed. &lt;b&gt;&lt;i&gt;Results:&lt;\/i&gt;&lt;\/b&gt; The distribution of patients (n = 162) was 16 and 4% with a hereditary deficiency of C1-INH or a gain of factor XII function, respectively, 29% with iatrogenic BK-AO, 21% with non-iatrogenic defective kininase activity and 30% with idiopathic increased kinin formation. &lt;b&gt;&lt;i&gt;Conclusion:&lt;\/i&gt;&lt;\/b&gt; BK-AO may be caused by multiple inherited or acquired factors triggering BK accumulation. Therefore, we propose a novel typology for BK-AO based on the imbalance of production\/catabolism of BK.<\/jats:p>","DOI":"10.1159\/000371814","type":"journal-article","created":{"date-parts":[[2015,2,24]],"date-time":"2015-02-24T04:23:45Z","timestamp":1424751825000},"page":"324-331","source":"Crossref","is-referenced-by-count":13,"title":["Distinct Conditions Support a Novel Classification for Bradykinin-Mediated 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