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Sir, X-linked ichthyosis (XLI) appears in the immediate neonatal period as a generalized large, slightly adherent, lightly coloured desquamation commonly affecting the scalp, preauricular area and posterior neck (1). In time, large, often dark scales, preferentially located on the trunk and extensor aspect of the extremities, become prominent. The palms, soles and face are generally spared (1). Cutaneous histopathological findings of XLI are not diagnostic, being characterized by orthokeratotic hyperkeratosis and a normal or slightly thickened granular layer. In the dermis, oedema and a slight perivascular inflammatory infiltrate can be observed (1). The most common associated extracutaneous findings include corneal opacities, cryptorchidism, epilepsy and electro-encephalographic changes (1). XLI is caused by deficient activity of the steroid sulphatase (STS) enzyme due, in most patients, to complete or partial deletions of the STS gene mapped on Xp22.3 (2–5). Therapeutic approaches for the treatment of mild to moderate cutaneous manifestations of XLI include keratolytic agents, moisturizers and topical retinoids, while systemic retinoids have been successfully employed in severe forms (6, 7). We describe a 22-year-old man with XLI associated with epilepsy. A within-patient study comparing topical tazarotene 0.05% and glycolic acid 70% resulted in almost complete remission of cutaneous lesions, although a longer response durability was achieved with tazarotene.

Topical Tazarotene 0.05% versus Glycolic Acid 70% Treatment in X-linked Ichthyosis due to Extensive Deletion of the STS Gene