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Angioedema induced by cardiovascular drugs: new players join old friends
Author(s) -
Bas M.,
Greve J.,
Strassen U.,
Khosravani F.,
Hoffmann T. K.,
Kojda G.
Publication year - 2015
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/all.12680
Subject(s) - angioedema , bradykinin , medicine , neprilysin , enalapril , hereditary angioedema , angiotensin converting enzyme , ace inhibitor , concomitant , intensive care medicine , immunology , receptor , blood pressure , enzyme , chemistry , biochemistry
During the last years, two new cardiovascular drug classes, namely inhibitors of DPP IV or neprilysin, have been developed. In both cases, there is clinical evidence for their potential to induce angioedema as known already from blockers of the renin–angiotensin–aldosterone system ( RAAS ). The majority of angioedema induced by DPP IV inhibitors occurs during concomitant treatment with ACE i and is therefore likely mediated by overactivation of bradykinin type 2 receptors (B2). In striking contrast, the molecular pathways causing angioedema induced by neprilysin inhibitors, that is, sacubitril, are unclear, although a contribution of bradykinin appears likely. Nevertheless, there is no clinical evidence suggesting that inhibition of B2 might relieve the symptoms and/or prevent invasive treatment including coniotomy or tracheotomy in angioedema caused by these drugs. Therefore, the risk of angioedema should always be considered, especially in ambulatory care situations where patients have no rapid access to intensive care.