Many patients undergoing topical retinoid therapy experience erythema, scaling, dryness, burning and pruritus. These symptoms characterize the retinoid-specific irritant contact dermatitis commonly termed ‘retinoid dermatitis’. Other irritants and abrasives cause similar clinical symptoms and histological changes in the skin; however, there are differences in their timing of onset and duration. Unlike that of sodium lauryl sulfate, the transepidermal water loss increase after retinoic acid application is delayed and accompanied by an overall increase in stratum corneum hydration. Tretinoin also increases dermal collagen by stimulating synthesis and inhibiting degradation. This evidence suggests a unique pharmacological activity for retinoids, which is probably a receptor-mediated process. In mice with compromised receptor function, topical tretinoin fails to induce hyperplasia, desquamation and peeling. Many retinoid actions in the skin are probably receptor mediated, and the irritation, at least the scaling and peeling component, is partly related to these pharmacological effects. While there is convincing evidence that tretinoin may repair solar damage without irritation, there is less consistent evidence that less irritating retinoids can be comparably effective in acne treatment. Taken together, we lack a precise quantification and qualification of the difference between the clinical and irritant effects of these molecules.

Keywords:
Retinoid dermatitis, Retinoic acid, Tretinoin, Sodium lauryl sulfate
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© 2002 S. Karger AG, Basel
2002
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