WP 2.4 - Non-histaminergic angioedema: Identification, characterization and treatment.

Background:

Angioedema(AE) manifests as potential life-threatening episodes of localized swelling in the dermis and submucosa. In a population sample from Denmark (DK) the lifetime prevalence of AE was 7.4%.  In the US, AE has become the most frequent cause of hospital admission of all acute allergy-like non-asthmatic diseases. Epidemiological data on AE is however sparse. Two kinds of angioedema are recognized: histaminergic and non-histaminergic (mediated by bradykinin). Traditionally patients and physicians relate all AE to type I allergy (IgE-mediated) and treat it with corticosteroids, antihistamines and adrenaline. These drugs are not effective on non-histaminergic AE, which means that patients need to be monitored until the swelling spontaneously resolves or there is a risk of asphyxiation, if angioedema involves the upper aerodigestive tract.

 

Treatment 

Histaminergic Angioedema

Non- histaminergic Angioedema

Antihistamines

++++

-

Corticosteroids

++++

-

Adrenaline

++++

(+)

Icatibant

Not Known

++

 

Hypothesis:

  1. The number of patients with drug-induced AE (especially from ACE-inhibitors) is increasing in DK.
  2. Non-histaminergic AE is overlooked in the acute setting, and therefore not treated correctly, posing a risk of death by asphyxiation.
  3. Diagnosis and treatment of AE in the acute setting can be improved by developing an algorithm.

Methods:

#1 Literature review and register-based National study of AE and its association with drugs in Denmark since 1995.

#2 One year prospective study with follow-up of patients seen in emergency rooms with a diagnosis of acute angioedema in the Region of Southern Denmark. Subsequent investigations in our Department with an extended diagnostic work-up.

#3. Develop a diagnostic and therapeutic algorithm based on literature review, register studies and clinical data.

prospective observational study is the cornerstone of the clinical part. Descriptive statistics will be used to present demographic data, suspected drugs, clinical characteristics, course of disease, treatments and outcomes. A systematic review of the literature will be performed and if possible a meta-analysis will be made. We will analyse data from register studies and use logistic regression to estimate the odds ratios for drug-induced AE.  A systematic compilation of data will help develop clinical diagnostic guidelines and therapeutic algorithms in emergency care settings.


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