ATOPIC ALLERGIC DISEASES
Atopic dermatitis is a chronic itchy skin inflammatory disease based on IgE-dependent hypersensitivity, allergic inflammation controlled by Th2 and Th22, and mutations in the filaggrin gene on 1q21.3. In addition, Th1 and Th17 may be involved in the immunopathgenesis of atopic dermatitis.
Immunopathogenesis. In predisposed persons, or atopic individuals, house dust mite allergens and other allergens are inhaled (respiratory sensitization), ingested (oral sensitization) and enter the skin (so called epicutaneous sensitization), and trigger advanced B-cell-mediated immune response to the predominant formation of IgE antibodies, which are carried to the skin to be bound to FcεRI on mast cells. As a rule, the first symptoms of atopic dermatitis occur early in babies and toddlers and may appear as recurrences throughout life. In some cases, allergen tolerance to causative allergens is restored to lead to the long-term remission of the disease.
Repeated exposure to these allergens results in chronic skin inflammation with many types of skin lesions and severe itching. The epidermis is damaged by the skin lesions: macules, papules, vesicles, secondary lesions, crusts, fissures, excoriation, and lichenification. Meanwhile, specific lesions in atopic dermatitis are unavailable.
Skin itching is caused by histamine, thymic stromal lymphopoietin (TSLP), IL-31, IL-33, and nerve growth factor (NGF). If the skin lesions and itching are extensive the disease can significantly impact the quality of life for patients. Some patients may develop eczema, secondary bacterial, fungal, viral infections, and rough lichenification.
Treatment for the disease includes emollients, corticosteroid gels, creams and ointments, antihistamines, biologics like dupixent® (dupilumab), antimicrobial medications if required, and allergen-specific immunotherapy (AIT).