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Does hereditary angioedema make COVID-19 worse?
Yingyang Xu1,2,3,4, Shuang Liu5, Yan Zhang6
1Department of Allergy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China.
The World Allergy Organization Journal
|August 25, 2020
Summary
The coronavirus disease 2019 (COVID-19) pandemic may worsen hereditary angioedema (HAE) due to bradykinin system activation. Treatments for HAE, like C1 inhibitor and lanadelumab, may help manage COVID-19 symptoms.
Area of Science:
- Immunology
- Pathophysiology
Background:
- COVID-19, caused by SARS-CoV-2, involves ACE2 depletion, leading to bradykinin accumulation and inflammation.
- Hereditary angioedema (HAE) pathogenesis is driven by an overactivated contact system and excessive bradykinin production.
Purpose of the Study:
- To explore potential interactions between COVID-19 and HAE.
- To hypothesize the impact of comorbidity on disease progression and outcomes.
Main Methods:
- Review of pathophysiologic links between COVID-19 and HAE.
- Analysis of the contact system, complement system, cytokine release, T helper 17 cells, and hematologic abnormalities.
Main Results:
- COVID-19 may increase HAE activity and severity.
- COVID-19 might aggravate existing HAE or trigger onset in carriers.
- Shared mechanisms include bradykinin system activation and inflammation.
Conclusions:
- Comorbidity with HAE may worsen COVID-19 outcomes.
- COVID-19 may exacerbate HAE, necessitating prophylaxis (e.g., C1 inhibitor, lanadelumab) and acute attack medications.
- HAE therapeutic strategies may benefit COVID-19 treatment; clinical trials are recommended.
Keywords:
ACE2ADAM metallopeptidase domain 17, ADAM17C1 inhibitor, C1–INHCOVID-19Complement systemContact systemCoronavirus disease 2019, COVID-19Hereditary angioedemaMiddle East respiratory syndrome coronavirus, MERS-CoVacute respiratory distress syndrome, ARDSangiotensin-converting enzyme, ACEbradykinin receptor B1, B1Rbradykinin receptor B2, B2Rbradykinin, BKdes-Arg(9)-bradykinin, DABKgranulocyte-colony stimulating factor, GCSFgranulocyte-macrophage colony stimulating factor, GM-CSFhereditary angioedema, HAEhigh-molecular-weight kininogen, HMWKinterleukin-1, IL-1macrophage inflammatory protein, MIPmannose-binding lectin associated serine protease, MASPmannose-binding lectin, MBLsevere acute respiratory syndrome coronavirus 2, SARS-CoV-2transforming growth factor-β, TGF-βtransmembrane serine protease, TMPRSS2tumor necrosis factor γ, TNF-γMore Related Videos
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