Functional Analysis of the Stratum corneum of Patients with Atopic Dermatitis: Comparison with Psoriasis vulgaris

Background: The skin of patients with atopic dermatitis (AD) is known to have a defective barrier function of the stratum corneum (SC) that facilitates the induction of unique skin hypersensitivity to various environmental allergens and irritants. However, it has not been determined whether there are characteristics unique to AD, because an apparently similar dysfunction of the SC is also observable in other inflammatory dermatoses such as psoriasis. Objective: Our purpose was to analyze the SC functions of patients with AD in comparison with those with psoriasis, an endogenously induced immune-mediated dermatosis. Methods: We conducted functional analyses of the lesional and nonlesional skin of AD and psoriasis patients by using noninvasive biophysical methods. Results: When we classified their skin changes into several subtypes based on the clinical features, we found that a severity-dependent disruption in the barrier function as well as a decrease in the SC hydration occurred in both dermatoses and to a similar degree. The extent of their SC barrier damage on the skin of the trunk and limbs was almost comparable to that of normal facial skin of healthy individuals. We also found similarly small, immature corneocytes that are associated with epidermal hyperproliferation accompanied by poor differentiation in both dermatoses. Moreover, we found similar but much milder SC functional abnormalities in the nonlesional skin where the extent of the dysfunction was much closer to that of healthy skin than to that of lesional skin. Conclusion: From these data, we could not find any differences in the functional abnormalities of the SC of AD patients that would justify considering it to be a unique dermatosis at least in terms of barrier damage. Because the presence of smaller corneocytes reflects the active proliferation of the underlying epidermis, we think that the barrier impairment and deficient water-holding capacity of the SC develop as a result of the enhanced epidermal proliferation in both dermatoses that is caused by the underlying inflammation.