ArticleThe World Allergy Organization journal2010
The pathophysiology of hereditary angioedema.
Article in The World Allergy Organization journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Indirect treatment comparison of lanadelumab and a C1-esterase inhibitor in pediatric patients with hereditary angioedema.Journal of comparative effectiveness research · 2025Pooled it
- Lanadelumab demonstrates rapid and sustained prevention of hereditary angioedema attacks.Allergy · 2020Trial
- Hereditary angioedema and the gastrointestinal tract.The World Allergy Organization journal · 2026Article
- Clinical features of hereditary angioedema involving the gastrointestinal tract: A retrospective analysis.The World Allergy Organization journal · 2026Article
- Identification of an elusiveFrontiers in allergy · 2025Article
- Gene Therapy for Immunoglobulin E, Complement-Mediated, and Eosinophilic Disorders.Human gene therapy · 2023Review
- Pediatric Angioedema without Wheals: How to Guide the Diagnosis.Life (Basel, Switzerland) · 2023Article
- C1 esterase inhibitor-mediated immunosuppression in COVID-19: Friend or foe?Clinical immunology communications · 2022Review
- Attenuated androgen discontinuation in patients with hereditary angioedema: a commented case series.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2022Article
- Safety Aspects and Rational Use of Lanadelumab Injections in the Treatment of Hereditary Angioedema (HAE): Clinical Insights.Drug, healthcare and patient safety · 2022Review
- A novel murine in vivo model for acute hereditary angioedema attacks.Scientific reports · 2021Article
- Impact of lanadelumab in hereditary angioedema: a case series of 12 patients in Canada.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2021Article
- Gene therapy for C1 esterase inhibitor deficiency in a Murine Model of Hereditary angioedema.Allergy · 2019Article
- Lanadelumab for the Prophylactic Treatment of Hereditary Angioedema with C1 Inhibitor Deficiency: A Review of Preclinical and Phase I Studies.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2019Review
- Subcutaneous C1 inhibitor for prevention of attacks of hereditary angioedema: additional outcomes and subgroup analysis of a placebo-controlled randomized study.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019Article
- THE JEREMIAH METZGER LECTURE NOVEL THERAPEUTIC STRATEGIES OF ALLERGIC AND IMMUNOLOGIC DISORDERS.Transactions of the American Clinical and Climatological Association · 2018Review
- Pediatric Angioedema.Current allergy and asthma reports · 2017Review
- Outcomes of long term treatments of type I hereditary angioedema in a Turkish family.Anais brasileiros de dermatologiaArticle
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary angioedema (HAE) causes recurrent episodes of angioedema that may be very severe and are frequently associated with significant morbidity and even mortality. Understanding the pathophysiology of this disease is crucial for proper diagnosis and management of these patients. HAE is caused by mutations in the SERPING1 gene that result in decreased plasma levels of functional C1 inhibitor. A large number of different mutations have been described that result in HAE. About 15% of patients have a mutation at or near the active site of the reactive mobile loop, resulting in a protein that lacks functional activity (type II HAE). Type I HAE is caused by a diverse range of mutations, some of which cause the nascent protein to misfold and thus to be unable to enter the secretory pathway. The primary mediator of swelling in HAE is bradykinin, a product of the plasma contact system. Bradykinin induces increased vascular permeability by activating the bradykinin B2 receptor, which results in phosphorylation of vascular endothelial cadherin. The regulation of both the bradykinin B2 receptor and peptidases that degrade bradykinin may influence HAE disease severity. HAE results from mutations in the SERPING1 gene that lead to a loss of functional C1 inhibitor. Attacks of angioedema result from generation of bradykinin, which acts on bradykinin B2 receptors to enhance vascular permeability.
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Registered trials
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.