Abstract

Atopic dermatitis is a multifactorial, chronic relapsing, inflammatory disease, characterized by xerosis, eczematous lesions, and pruritus. The latter usually leads to an “itch-scratch” cycle that may compromise the epidermal barrier. Skin barrier abnormalities in atopic dermatitis may result from mutations in the gene encoding for filaggrin, which plays an important role in the formation of cornified cytosol. Barrier abnormalities render the skin more permeable to irritants, allergens, and microorganisms. Treatment of atopic dermatitis must be directed to control the itching, suppress the inflammation, and restore the skin barrier. Emollients, both creams and ointments, improve the barrier function of stratum corneum by providing it with water and lipids. Studies on atopic dermatitis and barrier repair treatment show that adequate lipid replacement therapy reduces the inflammation and restores epidermal function. Efforts directed to develop immunomodulators that interfere with cytokine-induced skin barrier dysfunction, provide a promising strategy for treatment of atopic dermatitis. Moreover, an impressive proliferation of more than 80 clinical studies focusing on topical treatments in atopic dermatitis led to growing expectations for better therapies.

Highlights

  • Atopic dermatitis (AD) is a multifactorial, chronic relapsing, inflammatory disease, characterized by xerosis, eczematous lesions, and pruritus

  • It is important to notice that pruritus usually leads to an “itch-scratch” cycle that may compromise the epidermal barrier, resulting in transepidermal water loss (TEWL), xerosis, or secondary infection, especially with Staphylococcus aureus [3]

  • Even clinically uninvolved sites of skin show abnormal skin barrier function and greater TEWL compared to healthy individuals [6,7,8,9]

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Summary

Introduction

Atopic dermatitis (AD) is a multifactorial, chronic relapsing, inflammatory disease, characterized by xerosis, eczematous lesions, and pruritus. It is important to notice that pruritus usually leads to an “itch-scratch” cycle that may compromise the epidermal barrier, resulting in transepidermal water loss (TEWL), xerosis, or secondary infection, especially with Staphylococcus aureus [3]. The pathogenesis of AD involves skin barrier dysfunction, environmental and infectious agents, and immune abnormalities. Subsequent studies demonstrated epidermal barrier abnormalities in AD dysfunction that correlate with the disease severity. TEWL is greater in areas with clinical disease. Even clinically uninvolved sites of skin show abnormal skin barrier function and greater TEWL compared to healthy individuals [6,7,8,9]. It must be noted that TEWL is only relevant when regarding the penetration of molecules less than 500 daltons, such as water, irritants, and haptens

Skin Barrier Dysfunction in AD
Therapeutic Aspects
Emollients
Barrier Repair Therapy
Topical Corticosteroids and Immunomodulators
Treatment of Skin Infections
Findings
Future Perspectives
Full Text
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