Abstract
ACE-inhibitor induced angioedema is a non-allergic drug-related side effect. Inhibited bradykinin degradation leads to an unphysiological enhanced bradykinin plasma level with vascular leakage and, consequently, to angioedema. ACE-inhibitor induced angioedema develop rapidly in the head and neck region. Typical sites of manifestation are lips, tongue, and larynx. Novel pharmacotherapies may allow a causal treatment of the ACE-inhibitor induced angioedema in the future.
MeSH terms
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Adrenal Cortex Hormones / therapeutic use
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Algorithms
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Angioedema / blood
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Angioedema / chemically induced*
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Angioedema / diagnosis
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Angioedema / diagnostic imaging
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Angioedema / drug therapy
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Angioedema / physiopathology
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Angioedema / therapy
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Angioedemas, Hereditary / diagnosis
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Angiotensin-Converting Enzyme Inhibitors / adverse effects*
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Angiotensin-Converting Enzyme Inhibitors / pharmacology
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Bradykinin / analogs & derivatives
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Bradykinin / blood
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Bradykinin / physiology
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Bradykinin / therapeutic use
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Bradykinin Receptor Antagonists
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Forecasting
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Histamine Antagonists / therapeutic use
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Humans
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Laryngeal Edema / chemically induced*
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Laryngeal Edema / diagnosis
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Laryngoscopy
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Magnetic Resonance Imaging
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Time Factors
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Tomography, X-Ray Computed
Substances
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Adrenal Cortex Hormones
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Angiotensin-Converting Enzyme Inhibitors
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Bradykinin Receptor Antagonists
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Histamine Antagonists
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icatibant
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Bradykinin