Nonallergic angioedema: role of bradykinin

@article{Ba2007NonallergicAR,
  title={Nonallergic angioedema: role of bradykinin},
  author={Murat Baş and V Adams and Tatsiana Suvorava and Tim Niehues and Thomas K. Hoffmann and Georg Kojda},
  journal={Allergy},
  year={2007},
  volume={62}
}
Angioedema is an underestimated clinical problem. Many cases are nonallergic reactions, e.g. bradykinin‐induced angioedema caused by genetic defects and angiotensin‐converting enzyme (ACE) inhibitors. This difference is crucial for successful therapy, in particular when complete emergency care is not available. Five important forms of nonallergic angioedema can be distinguished: hereditary (HAE), acquired (AAE), renin‐angiotensin‐aldosterone system (RAAS)‐blocker‐induced (RAE), pseudoallergic… Expand
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TLDR
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Angioedema Due to ACE Inhibitors
TLDR
The epidemiology, pathophysiology, genetics, clinical symptoms, diagnosis, and treatment of ACEI-AAE are reviewed. Expand
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TLDR
Typically, ACE inhibitor-associated AE can occur up to several years after initiating treatment, and may sporadically recur even after discontinuation, so a comprehensive investigation of AE must include analysis of complement factors, tryptase levels as well as specific allergy tests. Expand
Angioedema induced by cardiovascular drugs: new players join old friends
TLDR
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 DPP IV or neprilysin inhibitors. Expand
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