Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder. Even after visible inflammation subsides, patients exhibit non-lesional ‘atopic dry skin’ with impaired stratum corneum (SC) barrier and water-retention functions.
These deficiencies heighten vulnerability to pruritus, irritants, and allergens, leading to frequent relapse. AD is thus regarded as a treatment-resistant, relapsing skin disease.1-3
SC dysfunction primarily results from a marked reduction in total ceramide content,3-8 and altered ceramide profiles.9 However, similar changes in psoriatic skin suggest these shifts may reflect general inflammatory responses rather than AD-specific defects.10
In AD, up-regulated transepidermal water loss (TEWL) and reduced capacitance values in non-lesional skin correlate with disease severity.11,12 These abnormalities likely arise from past inflammation, making these metrics useful for estimating disease state and treatment efficacy. A clinical trial showed that CER (pseudo-ceramide) cream normalized both parameters to levels seen in healthy skin, while HIRU (Hirudoido) cream achieved only mild improvements.11,12
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