Abstract
To the Editor: Pityriasis rubra pilaris is a disease characterized by low serum levels of retinol-binding protein (RBP).1 The defect is probably transmitted genetically in an autosomal dominant manner.2 The clinical picture is characterized by an abnormality of the epidermal horny layer, associated with an accelerated turnover of follicular keratinocytes.It has recently been shown that genetically determined protein defects can be corrected by treatment with 17α-alkylated androgens. More specifically, in hereditary angioedema (C1-esterase-inhibitor protein deficiency), treatment with danazol3 or stanozolol4 induces clinical remission and corrects the biochemical defect; increases in α1-antitrypsin5 and antithrombin III6 have also been . . .

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