Ace inhibitor-induced angioedema T73.3

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Acquired bradykinin-mediated angioedema without C1-INH deficiency; angioedema acquired, ACE-induced; RAE; RAE Angioedema

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Occurrence of angioedema after taking ACE inhibitors or angiotensin II receptor blockers (AT2RB). The latency period between drug intake and initial manifestation of the edema is highly variable (on average 2-3 years; about 2/3 of angioedema occurs within the first 3 months). In some cases, angioedema only develops in connection with a relevant infection or in combination with other drugs (e.g. diuretics, antidiabetics or even antibiotics). Due to the large number of medications taken, it is not always possible to clearly assign the ACE inhibitor etiologically and/or chronologically. Angioedema has also been reported in connection with dipeptidyl peptidase IV inhibitors (saxagliptin) and neprilysin inhibitors (sacubitrile).

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incidence 400-700/100,000 (0.4-0.7%); purely arithmetically, around 20,000-35,000 cases/year would be expected in Germany. In about 20% of these patients, the angioedema is severe, making an inpatient stay necessary.

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ACE inhibitors inhibit the breakdown of bradykinin, which leads to increased production of bradykinin in plasma and tissue. In rare cases, angioedema can also occur under AT-1 blockers.

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In contrast to HAE ( hereditary angioedema), RAE almost always manifests in the head and neck region.

Clinical features
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  • Edema occurs several months after the start of therapy, but also after years of problem-free use (on average 2-3 years). The bradykinin level is elevated during a seizure. The cough induced by ACE inhibitors is not a precursor of angioedema.
  • The clinic of RAE angioedema is treacherous because it often starts as harmless mucosal edema, but after hours it develops into severe edema. The larynx and pharynx area is often affected. Swelling subsides after 24-72 hours, but can last up to 5 days. Infestation of hands, feet and the gastrointestinal tract is also possible.

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Clinical picture and anamnesis is diagnostic. Other forms of angioedema must be excluded (see below)

Differential diagnosis
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Angioedema of a different etiology (see below angioedema).

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  • Stop the ACE inhibitor!
  • The angioneurotic edema usually subsides within 1-5 days after discontinuation of the ACE inhibitor or the AT-II receptor blocker.
  • In case of a vital threatening laryngeal edema, immediate securing of the respiratory tract (initiation of immediate intensive care measures - sedation, analgesia, if necessary intubation, tracheotomy; stabilization of circulation; see below shock, anaphylactic).
  • Immediate administration ofC1 inactivator concentrate: 20IE/kg KG Berinert P.
  • Alternatively: Icatibant (Firazyr), a synthetically produced decapeptide (protein fragment) is the most effective antagonist of the bradykinin B2 receptor to date. To date, Icatibant has only been approved by the EMA for the symptomatic treatment of acute attacks of hereditary angioedema in adults with C1 esterase inhibitor deficiency. Off-label use is currently only available for applications outside this indication. In a smaller study (n=12), the use of Icatibant (30mg s.c.) leads to a prompt improvement of angioedema.

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Note: Antiallergic therapy is not effective in this form of angioedema.

Angioedema is also induced by renin inhibitors.

In ACEI-induced angioedema, switching to an AT1 receptor blocker is not a solution to the problem, as these can also cause angioedema (although less frequently than ACEI).

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  5. Sachs B et al (2018) Drug-associated angioedema. Dermatologist 69: 298-305
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Last updated on: 29.10.2020