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Contact dermatitis 接触性皮炎

Contact dermatitis 接触性皮炎. Fang Hong 方 红 Dermatology Department, The 1st Affiliated Hospital, Medical School, Zhejiang University. Definition. Contact dermatitis is a generic term applied to acute or chronic inflammatory reactions to substances that come in contact with the skin.

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Contact dermatitis 接触性皮炎

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  1. Contact dermatitis接触性皮炎 Fang Hong 方 红 Dermatology Department, The 1st Affiliated Hospital, Medical School, Zhejiang University

  2. Definition • Contact dermatitis is a generic term applied to acute or chronic inflammatory reactions to substances that come in contact with the skin. • Irritant contact dermatitis (ICD) is caused by a chemical irritant; • Allergic contact dermatitis (ACD) by an antigen (allergen) that elicits a type IV (cell-mediated or delayed) hypersensitivity reaction.

  3. Definition • ICDis caused by exposure of the skin to chemical or other physical agents that are capable of irritating the skin, acutely or chronically. Severe irritants can cause toxic reactions even after a short exposure. Most cases, however, are caused by chronic cumulative exposure to one or more irritants. The hands are the most commonly affected area. • ACDis one of the more frequent, vexing, and costly dermatologic problems.

  4. Etiology • ACD is a manifestation of delayed hypersensitivity (type IV) and results from the exposure of sensitized individuals to contact allergens.

  5. Etiology Specific Ag recognition phase • Exposure of the antigen (Ag) to an antigen presenting cell (APC); • The LC internalizes the antigen and processes in the lysosomes; • The Ag binds noncovalently to an MHC II (HLA-DR) molecule intracellularly; • The Ag/MHC complex is transported to and expressed on the LC cell membrane; • The LC migrates the lymph nodes and presents this complex to MHC-restricted CD4 T cells with specific Ag recognition sites.

  6. Etiology Response phase • Ag-specific T cells are activated; • Stimulated T cells secrete IL-2 and interferon; • IL-2 nonspecifically stimulates other T cells to proliferate; • The released mediators attract an inflammatory infiltrate including macrophages, neutrophils, basophils, and eosinophils that are involved in the eczematous response.

  7. Etiology Resolution phase • CD4 cells decline and CD8 suppressor cells predominate; • Basophils and macrophages increase; • Macrophages produce prostaglandins that inhibit IL-2 and therefore downregulate inflammation.

  8. Allergens

  9. Clinical features Acute: • Symptoms: Intense pruritus; in severe reactions also stinging and pain; • Skin Lesions: Erythema, papules, vesicles, erosions, crusts, scaling; • Distribution: Confined to the site of exposure to the allergen. Margination is originally sharp; • Course: The duration varies among individuals, resolving in 1 to 2 weeks.

  10. ACD of lower leg, acute: Erythema, papules, vesicles, and erosions with oozing on the pretibial skin. This woman was allergic to neomycin and had used a neomycin-containing cream to treat an insect bite.

  11. Acute ACD in the face of a 32-year-old housewife who had used a neomycin-containing ointment for "itchiness" of the eyelids. Note massive edema and erythema of the eyelids and a papular eruption on the cheeks and forehead.

  12. Clinical features Subacute and chronic: • Symptoms: Mild; • Skin Lesions: Papules, scaling, lichenification, excoriations. Chronic inflammation with thickening, fissuring, scaling, and crusting results; • Distribution: Isolated, localized to one region (e.g., shoe dermatitis), or generalized (e.g., plant dermatitis); • Course: 2 weeks or longer.

  13. Chronic ACD in a construction worker who was hypersensitive to chromates. Note confluence of papules, edema, scaling, and oozing.

  14. Subacute ACD in the breast region. The distribution of the papular eruption suggested a causative role of the bra and indeed the patient proved to have a type IV hypersensitivity to latex.

  15. Subacute ACD consisting of multiple, confluent, and partly erosive papules on the hand in a health care worker.

  16. Diagnosis • History in contact; • Clinical findings: evaluation of site and distribution; • Patch Tests: Verification of offending agent (allergen).

  17. Differential Diagnosis • Atopic dermatitis • Seborrheic dermatitis (face) • Psoriasis (palms and soles) • Epidermal dermatophytosis (KOH) • Fixed drug eruption • Erysipelas phytophotodermatitis.

  18. Treatment • 1. Identify and remove the etiologic agent. Avoidance of the allergen is of paramount importance. • 2. Topical Therapy ▲Larger vesicles may be drained, but tops should not be removed. ▲ Wet dressings with cloths soaked in Burow's solution changed every 2 to 3 h. ▲ Topical glucocorticoid creams/gels are effective for early nonbullous lesions. ▲ The newer immunomodulating topicals pimecrolimus and tacrolimus are effective in ACD but are still being evaluated.

  19. Treatment Systemic Therapy －1. Glucocorticoids are indicated if severe: Prednisone beginning at 70 mg (adults), tapering by 5 to 10 mg/d over a 1- to 2-week period; －2. Antihistamines, particularly hydroxyzine (Atarax, Vistaril), will diminish itch and anxiety.

  20. Thanks！

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