Ceramides and the Defective Barrier in Atopic Dermatitis.

BACKGROUND

Atopic dermatitis (AD) is a common remitting-relapsing inflammatory skin disease characterized by eczematous lesions, xerosis, and pruritus. It is associated with a defective permeability barrier and increased susceptibility to Staphylococcus aureus colonization. It has been demonstrated that the abrogated epidermal barrier is related to a decreased mass of ceramides and long-chain fatty acids in the stratum corneum (SC). The inherent pH of healthy SC is below 5, and a low pH is required for proper assembly of the barrier lipids. In AD, the pH is elevated.

SUMMARY: A defective permeability barrier of the SC is the primary defect in AD. This defect reflects a reduction of ceramide and fatty acid mass in the SC due to reduced glucocerebrosidase and acid sphingomyelinase activity and a shift in fatty acid synthesis from long-chain to short-chain fatty acids and the incorporation of these shorter fatty acids into ceramides. Topically applied ceramides can restore epidermal function to a damaged barrier. Ceramide-containing moisturizers have produced partial restoration of the barrier function in AD by influencing lipid organization. Other topical and systemic therapies are also discussed.

KEY MESSAGE: Correcting the barrier defect by topically supplied ceramides and long-chain fatty acids in sufficient amounts could contribute to restoration of the microbiome and decreasing irritation and pruritus.