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Chronic Inducible Urticaria (CIndU)/Physical Urticaria

Pathophysiology

• Not completely understood, though extensive evidence has confirmed that mast cell degranulation and liberation of histamine, eicosanoids, and other mediators are key molecular drivers of physical urticaria

• Underlying mechanisms converging on mast cell degranulation may be trigger-specific [3], and there may be subtypes within a given trigger

o Cholinergic: sweat antigen, transferable serum factor, cholinergic sympathetic

innervation of sweat glands (intradermal methacholine elicits symptoms that can

be reversed by atropine in some patients [4, 5])

o Solar: electromagnetic radiation altering chromophores

o Cold: anti-IgE IgG and/or IgM

o Aquagenic: osmotic pressure changes and water diffusion, water soluble antigens

o Vibratory: gain-of-function mutation in ADGRE2 on mast cells

• May have multiple triggers and/or need for multiple triggers to be present at the same time (ex. food-dependent exercise-induced phenomena [6-8]

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