Urticaria and Angioedema
Pathophysiology and Immunological Mechanisms
Urticaria and angioedema involve immune-mediated and non-immune mechanisms leading to transient swelling and redness. Effective treatments range from antihistamines to monoclonal antibody therapies.
Urticaria and Angioedema: Pathophysiology and Immunological Mechanisms
Urticaria and angioedema are common dermatological conditions characterized by transient swelling and redness due to vascular leakage triggered by immunological and non-immunological mechanisms.
Introduction
Urticaria, commonly known as hives, is an inflammatory skin condition marked by erythematous, itchy wheals. Angioedema involves deeper dermal and subcutaneous tissue swelling. Both conditions can be acute or chronic.
Pathophysiology
Immunological Mechanisms
- Type I Hypersensitivity: Mediated by IgE antibodies responding to allergens, leading to mast cell degranulation.
- Complement Activation: Some forms involve complement-mediated histamine release.
- Autoimmune Factors: Presence of autoantibodies against IgE receptors.
Non-Immunological Triggers
Physical stimuli such as pressure, heat, cold, exercise, and drugs (e.g., NSAIDs) can induce urticaria and angioedema.
Clinical Presentation
Symptoms vary from localized wheals to systemic anaphylaxis in severe cases. Chronic urticaria lasts longer than six weeks and often has an unidentified trigger.
Treatment Approaches
First-Line Therapy
- Non-sedating H1-antihistamines
- Avoidance of known triggers
Second-Line and Advanced Therapies
- Increased antihistamine dosage
- Systemic corticosteroids (short-term)
- Omalizumab (anti-IgE therapy)
Conclusion
Understanding the underlying pathophysiology of urticaria and angioedema aids in effective treatment strategies and patient management. Emerging therapies targeting immune pathways are promising.
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