key: cord-0695557-76uduqb6
authors: Belbézier, Aude; Arnaud, Mélanie; Boccon‐Gibod, Isabelle; Pelletier, Fabien; McAvoy, Chloé; Gobert, Delphine; Fain, Olivier; Du‐Thanh, Aurélie; Launay, David; Lupo, Julien; Bouillet, Laurence
title: COVID‐19 as a trigger of acute attacks in people with hereditary angioedema
date: 2021-04-04
journal: Clin Exp Allergy
DOI: 10.1111/cea.13870
sha: 6324ffc423b65d4cf2c1c406463c20a782e6af27
doc_id: 695557
cord_uid: 76uduqb6

Acute attacks could occur during the convalescent phase of COVID‐19 illness, more commonly in patients with a history of frequent attacks. However it is unclear whether the acute attacks during the convalescent phase are specifically triggered by COVID‐19 or not.[Image: see text]

terfering with bradykinin degradation and bradykinin concentration in extracellular space. 3, 4 Therefore, we have concerns about showing the possibility of down-regulated ACE2 activity during COVID-19 resulting in bradykinin-mediated angioedema attacks in patient with hereditary angioedema (HAE). HAE is a rare, life-threatening, genetic disease 5 characterized by transitory recurrent subcutaneous and/or submucosal swelling episodes which mainly affect skin, gastrointestinal tract, and upper airways. 6 It should be divided in three forms according to the level of C1 inhibitor: HAE type I (HAE I) or II (HAE II) with C1-inhibitor deficiency (HAE C1-INH), 6 and HAE with normal C1 inhibitor (HAE nC1-INH) level. 7 In all forms, the swelling episodes are explained by a sudden, localized, and bradykininmediated increase of vascular permeability. Some triggers have been identified such as infection. 8 Thanks to this registry, we could analyse prospectively data from 13 HAE patients including in 4 different centres between April 2020 and January 2021. Oral consent from all patient was collected. 

All authors report no disclosures. We certify that the submission is not under review at any other publication. The principal author, Laurence Bouillet, takes full responsibility for the data, the analyses and interpretation, and conduct of the research. Bouillet has full access to all data and has the right to publish any and/or all data, separately from or with any sponsor. No financial or other relationships exist that might lead to a perceived conflict of interest.

Aude Belbezier contributed to acquisition of data, analysis, interpretation of the data, drafting the manuscript for intellectual contents, 

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions. Olivier Fain 2,4

Nonallergic angioedema: role of bradykinin

SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor

Angiotensinconverting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target

Kallikreinkinin blockade in patients with COVID-19 to prevent acute respiratory distress syndrome. eLife. 2020;9

Hereditary and acquired angioedema: problems and progress: Proceedings of the third C1 esterase inhibitor deficiency workshop and beyond

Hereditary angioedema: classification, pathogenesis, and diagnosis

Hereditary angioedema type III: an additional French pedigree with autosomal dominant transmission

Triggers and prodromal symptoms of angioedema attacks in patients with hereditary angioedema

Real-time tracking of self-reported symptoms to predict potential COVID-19

COVID-19 affecting hereditary angioedema patients with and without C1 inhibitor deficiency