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

Drug Toxicity: Allergic Reactions01:30

Drug Toxicity: Allergic Reactions

Drug-related allergies are immune-mediated responses triggered by the administration of pharmacological agents. These hypersensitivity reactions are classified based on the immune mechanisms involved. The four primary types—Type I, II, III, and IV—are mediated by different immunological pathways and exhibit distinct clinical manifestations.Type I Hypersensitivity/ IgE-Mediated Reactions: Immunoglobulin E (IgE) immediately mediates Type I hypersensitivity reactions. Upon initial exposure to a...
Staphylococcal Skin Infections01:29

Staphylococcal Skin Infections

Staphylococcus aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals. When the skin barrier is breached, it can shift from a commensal to an opportunistic pathogen. This transition is facilitated by surface adhesins, such as clumping factor B and S. aureus surface protein G (SasG), which bind to structural proteins, including loricrin and cytokeratin, in the damaged epidermis. Protein A, another key factor, binds the Fc region of...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...
Skin Diseases and Disorders01:23

Skin Diseases and Disorders

Skin is the first line of defense and encounters a variety of microbes. Some pathogenic strains are often the cause of a broad range of infections of the skin and other body systems. These conditions can affect people of all ages and may have different causes, including genetic factors, infections, autoimmune reactions, environmental factors, and lifestyle choices.
Gram-positive Staphylococcus spp. and Streptococcus spp. are responsible for many of the most common skin infections. However, many...
Allergic Reactions: Anaphylaxis01:30

Allergic Reactions: Anaphylaxis

Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin, heparin),...
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents01:24

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...

You might also read

Related Articles

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

Sort by
Same author

Concepts for the Development of Person-Centered, Digitally Enabled, Artificial Intelligence-Assisted ARIA Care Pathways (ARIA 2024).

The journal of allergy and clinical immunology. In practice·2024
Same author

World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow's Milk Allergy (DRACMA) guideline update - XII - Recommendations on milk formula supplements with and without probiotics for infants and toddlers with CMA.

The World Allergy Organization journal·2024
Same author

World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow's Milk Allergy (DRACMA) Guideline update - XIV - Recommendations on CMA immunotherapy.

The World Allergy Organization journal·2022
Same author

[Cutaneous manifestations in patients with COVID-19 with significant attention to urticaria].

Revista alergia Mexico (Tecamachalco, Puebla, Mexico : 1993)·2021
Same author

Update on latex allergy: New insights into an old problem.

The World Allergy Organization journal·2021
Same author

The challenges of chronic urticaria part 1: Epidemiology, immunopathogenesis, comorbidities, quality of life, and management.

The World Allergy Organization journal·2021

Related Experiment Video

Updated: May 11, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Aspirin-exacerbated cutaneous disease.

Mario Sánchez-Borges1, Fernan Caballero-Fonseca, Arnaldo Capriles-Hulett

  • 1Department of Allergy and Clinical Immunology, Centro Médico-Docente La Trinidad, Carretera La Trinidad-El Hatillo, Caracas, Venezuela. sanchezbmario@gmail.com

Immunology and Allergy Clinics of North America
|May 4, 2013
PubMed
Summary

Aspirin-exacerbated cutaneous disease involves chronic urticaria patients worsening with aspirin and NSAIDs. Management focuses on avoiding COX-1 inhibitors and treating the skin condition.

Related Experiment Videos

Last Updated: May 11, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Area of Science:

  • Dermatology
  • Pharmacology
  • Immunology

Background:

  • A significant number of chronic urticaria patients report symptom exacerbation upon exposure to aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs).
  • This condition is specifically termed Aspirin-exacerbated cutaneous disease (AECD).

Purpose of the Study:

  • To elucidate the pathogenesis of Aspirin-exacerbated cutaneous disease.
  • To outline current patient management strategies for AECD.

Main Methods:

  • Pathogenesis is linked to cyclooxygenase-1 (COX-1) inhibition.
  • This inhibition results in reduced prostaglandin E2 (PGE2) synthesis.
  • It also leads to increased cysteinyl leukotriene production in skin and subcutaneous tissues.

Main Results:

  • Cyclooxygenase-1 inhibition is the key mechanism in AECD.
  • Reduced PGE2 and increased cysteinyl leukotrienes contribute to symptom exacerbation.
  • Effective management involves a multi-faceted approach.

Conclusions:

  • Aspirin and NSAIDs can trigger significant skin reactions in susceptible chronic urticaria patients.
  • Understanding the COX-1 pathway is crucial for managing AECD.
  • Treatment includes medication, avoidance of triggers, and alternative pain relief options.