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Role of the Barrier in the Pathogenesis of Inflammatory Dermatoses and Therapeutic Implications

Arch Dermatol. 2001;137:1079-1081.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

WE HAVE BEEN in the era of immunology in skin disease. Since the classic experiment of Schellander and Marks¹ describing epidermal hyperplasia following dermal implantations of carrageenan, the epidermal changes that accompany inflammatory dermatoses have been considered downstream participants in disease pathogenesis (inside-outside concept). Accordingly, the current paradigm calls for either nonspecific treatment of inflammation or therapy aimed at specific T-cell components.² Since the epidermal changes are considered mere downstream participants, therapies aimed at normalizing epidermal function are considered secondary and inconsequential. Despite the acknowledged importance of xerosis and epidermal injury in these diseases, recent consensus reports barely mention the use of emollients in the therapy of atopic dermatitis and psoriasis.^3-5

But the concept of the epidermis as a primary or essential participant in disease pathogenesis, like gossip in a darkened corridor, keeps reasserting itself!^6-7 Dermatologists increasingly sense that the epidermal abnormality is not just a secondary phenomenon, but a . . . [Full Text of this Article]

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