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]