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Jonathan Wilkin, MD
Houston

Arch Dermatol. 1981;117(1):4.

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

To the Editor.—

A 66-year-old woman who had had psoriasis of the arms and trunk in remission for the past three years began receiving 0.05 mg of clonidine hydrochloride every 12 hours for control of flushing. Three days after therapy was begun, erythematous, scaly plaques developed along the elbows and proximal part of the forearms. During the next week, the scales increased in thickness and the lesions evolved into characteristic psoriatic plaques.

Since I know of no other reports possibly incriminating clonidine in the recrudescence of psoriasis, this association may be purely fortuitous. Alternatively, a pharmacologic mechanism may obtain. Decreases in intracellular concentrations of cyclic adenosine monophosphate (AMP) have been found in the rapidly dividing cells of psoriatic epidermis.¹ Cutaneous hyperproliferative, psoriasiform eruptions from propranolol and practolol may be caused by epidermal β-adrenergic blockade, reducing epidermal intracellular cyclic AMP and leading to increased cell division.^2,3 Clonidine is a . . . [Full Text PDF of this Article]

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