Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Aneurysm II: Clinical Manifestations and Diagnostic Studies01:21

Aneurysm II: Clinical Manifestations and Diagnostic Studies

Thoracic, aortic arch and abdominal aneurysms are significant vascular conditions that can present with various clinical manifestations and lead to serious complications. Understanding these manifestations and the appropriate diagnostic studies is essential for effective management and treatment.Thoracic Aortic AneurysmsThoracic aortic aneurysms often remain asymptomatic until they reach a size that impinges on adjacent structures. They typically cause deep, diffuse chest pain that radiates to...
Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies01:22

Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies

The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
Angina III: Clinical Manifestations and Assessment01:29

Angina III: Clinical Manifestations and Assessment

Angina manifests as chest pain, tightness, or squeezing discomfort typically located behind the breastbone. It can radiate to the neck, jaw, shoulders, and inner aspects of the upper arms, most commonly the left arm. Patients may experience shortness of breath, fatigue, profuse sweating, dizziness, indigestion, heartburn, palpitations, anxiety, and vomiting as accompanying symptoms. This pain often lasts a few minutes and is triggered by physical exertion, emotional stress, heavy meals, or cold...
Pulmonary Edema II: Pathophysiology01:18

Pulmonary Edema II: Pathophysiology

Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Classification of angioedema types using decision tree modeling.

Frontiers in immunology·2026
Same author

Ugeskrift for laeger·2026
Same author

Garadacimab-gxii-A Novel Prophylactic Treatment for Hereditary Angioedema: A Drug Review.

The Annals of pharmacotherapy·2026
Same author

Unsuspected Adverse Drug Reactions to Dermatologic Medications: An Epidemiological Hypothesis-Free Screening Study of Real-World Data in Denmark.

Drug safety·2025
Same author

[Autoimmune progesterone dermatitis].

Ugeskrift for laeger·2025
Same author

Ugeskrift for laeger·2025

Related Experiment Video

Updated: Jun 26, 2026

Testing Acetylcholine Followed by Adenosine for Invasive Diagnosis of Coronary Vasomotor Disorders
05:58

Testing Acetylcholine Followed by Adenosine for Invasive Diagnosis of Coronary Vasomotor Disorders

Published on: February 3, 2021

[Hereditary angioedema--diagnostic problems].

Rasmus Overgaard Bach1, Anette Bygum

  • 1Dermato-venerologisk Afdeling I, Odense Universitetshospital, DK-5000 Odense C. Sarastro11@yahoo.com

Ugeskrift for Laeger
|January 30, 2009
PubMed
Summary

Hereditary angioedema (HAE) is a rare condition causing swelling due to C1-INH deficiency. Early diagnosis and effective treatment are crucial to prevent fatal laryngeal edema, as seen in two Danish cases.

Area of Science:

  • Immunology
  • Genetics
  • Emergency Medicine

Background:

  • Hereditary angioedema (HAE) is a rare genetic disorder characterized by recurrent swelling episodes.
  • It results from a deficiency in complement-C1-inhibitor (C1-INH), impacting the complement system.
  • Laryngeal edema, a severe complication, can be life-threatening, with two documented fatalities in Denmark within the last decade.

Observation:

  • This report details two cases of HAE presenting with complex symptoms.
  • The cases highlight diagnostic challenges associated with HAE.
  • Recurrent swelling episodes affected the skin, gastrointestinal tract, and upper airways.

Findings:

  • The underlying cause of HAE is a lack of functional C1-INH.
  • The presented cases underscore the critical need for timely diagnosis.

More Related Videos

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
10:28

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Published on: March 15, 2022

A Novel Method: Super-selective Adrenal Venous Sampling
06:08

A Novel Method: Super-selective Adrenal Venous Sampling

Published on: September 15, 2017

Related Experiment Videos

Last Updated: Jun 26, 2026

Testing Acetylcholine Followed by Adenosine for Invasive Diagnosis of Coronary Vasomotor Disorders
05:58

Testing Acetylcholine Followed by Adenosine for Invasive Diagnosis of Coronary Vasomotor Disorders

Published on: February 3, 2021

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
10:28

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Published on: March 15, 2022

A Novel Method: Super-selective Adrenal Venous Sampling
06:08

A Novel Method: Super-selective Adrenal Venous Sampling

Published on: September 15, 2017

  • Effective treatment strategies are essential for managing HAE and preventing severe outcomes.

    • Implications:

    • Accurate and prompt diagnosis of HAE is vital for patient survival.
    • Implementing effective treatment plans can mitigate the risk of fatal laryngeal edema.
    • Understanding HAE's clinical presentation aids in differential diagnosis and patient management.