Table 1 Comparative overview of Angioedema and Contact Dermatitis hypersensitivity reactions

Type of Hypersensitivity

Type I Hypersensitivity: associated with IgE-mediated mast cell activation

HAE (due to C1INH deficiency): includes HAE-type 1 (deficiency) or type 2 (malfunction) of C1 INH. It causes the uncontrolled release of BK.

Drug-Induced AE: Some drugs (e.g. ACE inhibitors) can cause AE by reducing the levels of degraded BK.

Specific Mutations: HAE-FXII XII, HAE-Plasminogen, HAE-Angiopoietin-1, HAE-Kininogen, HAE-1 Myoferlin, HAE-HS3ST, and unknown (idiopathic) HAE.

Type IV Hypersensitivity: delayed hypersensitivity reaction. When an allergen (such as nickel) comes into contact with the skin, it is processed by antigen-presenting cells and presented to T cells that mediate the immune response.

Main Mediators

Histamine, BK

T lymphocytes, Cytokines (e.g. IL-2, IL-4, IL-5, IFN-γ, TNF-α and IL-17)

Localization

Deeper tissues (subcutaneous and submucosal)

Epidermal layers of the skin

Timing

Immediate for Type I, Delayed for HAE

Delayed (hours or day)

Symptoms

Deep swelling, often without itchiness

Itching, redness, blisters/desquamation