Contact Dermatitis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief:  Ogechukwu Hannah Nnabude, MD

## Pathophysiology[edit | edit source]

Irritant contact dermatitis

Irritant contact dermatitis arises from sufficient inflammation due to the release of proinflammatory cytokines from keratinocytes, in response to chemical stimuli. This causes skin barrier disruption, epidermal cellular changes, and cytokine release [1]

Irritants can be classified as [1]

* Cumulatively toxic (e.g., hand soap causing irritant dermatitis in a hospital employee)
* Subtoxic
* Degenerative
* Toxic (e.g., hydrofluoric acid exposure at a chemical plant).

Allergic contact dermatitis

Allergic contact dermatitis is T-cell mediated inflammation of the skin due to repeated skin exposure to haptens in a sensitized individual.[1]

Allergic contact dermatitis has two phases.[1]

* The sensitization phase; antigen-specific effector T cells are induced in the draining lymph nodes by antigen captured cutaneous dendritic cells that migrate from the skin.
* The elicitation phase; effector T cells that are activated in the skin by antigen captured cutaneous dendritic cells and produce various chemical mediators, which create antigen-specific inflammation.

Photo contact dermatitis occurs when an allergen becomes an irritant in the presence of light.[1]

Contact urticaria usually presents with as a 'wheal and flare' reaction after exposure to the offending topical agent. While most cases are mild, anaphylactic reactions can occur. Some common types of contact urticaria include [1]

* Exposure to cold
* Dermatographism
* Pressure
* Exercise
* Solar
* Heat
* Cholinergic.

Contact dermatitis can also occur after exposure to plants of the Urticaceae family.[1]

## References[edit | edit source]

1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Graham Litchman; Pragya A. Nair; Amber R. Atwater; Beenish S. Bhutta. Contact Dermatitis. StatPearls Publishing LLC. May 12, 2020.

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