Retrospective Evaluation of Patients with Angioedema Treated with C1 Inhibitors in an Emergency Department
Makaleler > Tam Makale · 2022
Yazarlar: Sercan YALÇINLI, Güçlü Selahattin KIYAN, Funda KARBEK AKARCA
Eurasian Journal of Emergency Medicine, Diğer Kurumların Hakemli Dergileri, Uluslararası, Scopus, 2022, cilt 21, ss 183-187
DOI: 10.4274/eajem.galenos.2020.82787
Özet
Acquired, hereditary and idiopathic causes lead to angioedema.Acquired causes of angioedema occur as allergic (histaminergic), non-allergic (non-histaminergic), drug-related [particularly for angiotensin-converting enzyme inhibitor (ACEI) and nonsteroidal anti-inflammatory drugs] or complement-mediated (acquired C1 inhibitor deficiency).Hereditary angioedema (HAE) is often caused by a C1 inhibitor deficiency (type 1) due to a C1 inhibitor gene mutation or functional inhibition despite normal C1 inhibitor levels (type 2).In rare cases, HAE is related to a factor 12 mutations or estrogen effects (type 3) (2-4).Angioedema develops through the mechanisms of histamines and bradykinin.Since the treatment approach is different, it is important to know which mediator caused the angioedema.Histamine-induced angioedema, also known as allergic angioedema, releases histamines through immunoglobulin E-mediated mast cell degranulation after allergen (food, drug, insect etc.) contact, after which rapid onset angioedema develops as a result.This type of angioedema responds to anti-histaminic, glucocorticoid and adrenaline treatments.Bradykinin-induced angioedema is the most common cause of non-allergic Retrospective Evaluation of Patients with Angioedema Treated with C1 Inhibitors in an Emergency Department