Evidence map›Paper›PMID 32834893›Full record

ReviewThe World Allergy Organization journal2020

Does hereditary angioedema make COVID-19 worse?

Yingyang Xu, Shuang Liu, Yan Zhang, Yuxiang Zhi

Open access · goldAbstract readReview
In one paragraph

Review in The World Allergy Organization journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. The Role of the Kinin System and the Effect of Des-ArginineInternational journal of molecular sciences · 2024
    Observational
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. COVID-19 triggers attacks in HAE patients without worsening disease outcome.The journal of allergy and clinical immunology. In practice · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Serine Protease Inhibitors to Treat Lung Inflammatory Diseases.Advances in experimental medicine and biology · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Yingyang XuDepartment of Allergy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China.
Shuang LiuSchool of Clinical Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100005, China.
Yan ZhangDepartment of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China.
Yuxiang ZhiDepartment of Allergy, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100730, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The coronavirus disease 2019 (COVID-19) pandemic has spread rapidly worldwide. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent for COVID-19, enters host cells via angiotensin-converting enzyme 2 (ACE2) and depletes ACE2, which is necessary for bradykinin metabolism. The depletion of ACE2 results in the accumulation of des-Arg (9)-bradykinin and possible bradykinin, both of which bind to bradykinin receptors and induce vasodilation, lung injury, and inflammation. It is well known that an overactivated contact system and excessive production of bradykinin comprise the key mechanisms that drive the pathogenesis of hereditary angioedema (HAE). It is reasonable to speculate that COVID-19 may increase disease activity in patients with HAE and vice versa. In this review, we explore the potential interactions between COVID-19 and HAE in terms of the contact system, the complement system, cytokine release, increased T helper 17 cells, and hematologic abnormalities. We conclude with the hypothesis that comorbidity with HAE might favor COVID-19 progression and may worsen its outcomes, while COVID-19 might in turn aggravate pre-existing HAE and prompt the onset of HAE in asymptomatic carriers of HAE-related mutations. Based on the pathophysiologic links, we suggest that long-term prophylaxis should be considered in patients with HAE at risk of SARS-CoV-2 infection, especially the prophylactic use of C1 inhibitor and lanadelumab and that HAE patients must have medications for acute attacks of angioedema. Additionally, therapeutic strategies employed in HAE should be considered for the treatment of COVID-19, and clinical trials should be performed.

Indexed as

ACE2acute respiratory distress syndrome, ARDSADAM metallopeptidase domain 17, ADAM17angiotensin-converting enzyme, ACEbradykinin, BKbradykinin receptor B1, B1Rbradykinin receptor B2, B2RC1 inhibitor, C1–INHComplement systemContact systemCoronavirus disease 2019, COVID-19COVID-19des-Arg(9)-bradykinin, DABKgranulocyte-colony stimulating factor, GCSFgranulocyte-macrophage colony stimulating factor, GM-CSFHereditary angioedemahereditary angioedema, HAEhigh-molecular-weight kininogen, HMWKinterleukin-1, IL-1macrophage inflammatory protein, MIPmannose-binding lectin associated serine protease, MASPmannose-binding lectin, MBLMiddle East respiratory syndrome coronavirus, MERS-CoVsevere acute respiratory syndrome coronavirus 2, SARS-CoV-2transforming growth factor-β, TGF-βtransmembrane serine protease, TMPRSS2tumor necrosis factor γ, TNF-γ

Identifiers

PMID32834893
PMCPMC7416729
OpenAlexW3048251847

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.