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CONTACT DERMATITIS

  • Inflammatory response of the skin to an antigen (allergen) or irritant

  • Allergic contact dermatitis (ACD)

    • Delayed type hypersensitivity reaction (type IV)

    • Dermal Dendritic cells play a central role in processing and presenting antigen complexes in the sensitization phase

    • Individuals previously sensitized to the allergen can develop a cutaneous response with subsequent exposure to the allergen. These responses can be incrementally more severe with each exposure.

    • Common allergens include plants from the Toxicodendron genus (e.g., poison ivy), nickel sulfate, fragrances, preservatives, and rubber additives

    • Acute ACD: lesions appear within 24 to 96 hours of exposure to the allergen in sensitized individuals

  • Irritant contact dermatitis (ICD)

    • Irritants are cytotoxic to the keratinocyte, disrupt the lipid architecture, and promote the release of inflammatory mediators

    • ICD will only occur in areas of the skin that has been in direct contact with the offending chemical agent

    • Subsequent inflammatory response in the dermis

    • Two types:

      • – Mild irritants: require prolonged or repeated exposure before inflammation is noted (e.g., soap)

      • – Strong irritants: strong acids, alkalis, can produce immediate reactions similar to thermal burns

  • Clinical Presentation

    • Acute contact dermatitis: clear fluid–filled vesicles or bullae that appear on bright red edematous skin, pruritic. ICD generally occurs within the area of contact with the chemical, whereas ACD can extend beyond the borders of the contact area

    • Subacute contact dermatitis: less edema and formation of papules, pruritic

    • Chronic contact dermatitis: minimal edema, scaling, skin fissuring, and lichenification

    • Histology

    • Dermis with perivascular lymphocytes and other mononuclear cells and epidermal spongiosis are seen in ACD. Cytotoxicity more commonly seen in ICD

    • Chronic ACD: acanthosis with hyperkeratosis and parakeratosis. Difficult to distinguish, clinically and histologically, allergic contact from irritant contact dermatitis in the chronic phase

CONTACT URTICARIA

  • An immunoglobulin E (IgE)—mediated immediate hypersensitivity reaction (type I)

  • Immediate release of inflammatory mediators, resulting in a wheal-and-flare reaction

  • Rubber latex currently is the most important source of allergic contact urticaria

PHOTOSENSITIVITY INDUCED BY EXOGENOUS AGENTS

  • Photodermatitis

    • Diagnosed by the presence of lesions limited to sun-exposed body areas (sparing of the submental chin, posterior auricular area, and inner arms can be clues). Certain substances transform into allergens (photoallergic) or irritants (phototoxic) by ultraviolet light

  • Photoallergic reaction

    • Delayed-type hypersensitivity reaction (type IV); a form of allergic contact dermatitis whose distribution is limited to sun-exposed areas of the body

    • Onset delayed as long as 24 to 96 hours after exposure to the drug and light

    • Amount of inciting substance (chemical allergen, drug, etc.) required to elicit photoallergic reactions is considerably smaller than that required for phototoxic reaction

    • Irradiation of certain substances by ultraviolet light results in the transformation of the substance into allergens

    • Examples of agents that can cause a photoallergic reaction (Tables 6-1 and 6-2)

  • Phototoxic reaction

    • Chemically induced nonimmunologic acute skin irritation with damage to to cell membranes from the effects of light-activated compounds

    • Active chemical may enter the skin via topical administration ...

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