After carefully reading the comprehensive review article by Velasco1 on the diagnosis and treatment of leg ulcers, we write to comment further on a new therapeutic option referred to by that author. Several studies have reported the positive effect on skin and mucosal healing of the activation of β-adrenergic receptors,2–5 as the author of the above-mentioned review points out with a reference to the work of Margolis et al.2 However, research in the field of wound healing is now focusing on the significant impact on the healing process of glucocorticoid (GC) activity.

The presence of high GC levels is associated with delayed cutaneous wound healing and barrier recovery after mechanical disruption.6,7 The present group has shown the negative effect of GCs on epidermal differentiation and proliferation.7 Using models based on exogenous GC administration or endogenous release secondary to psychological stress, several authors have demonstrated the inhibitory action of GCs on fibroblast proliferation.6 In both models, systemic GC blockade improved wound healing and barrier recovery.

Because of the potential complications of systemic blockade of GC activity, current research on new treatments is focusing on both the blockade of GC receptors and on the activity of 11β-hydroxysteroid dehydrogenase-1 (11β-HSD1), the enzyme responsible for the peripheral conversion of cortisone to its active form cortisol.6,8,9

Given the high levels of GC observed in diabetic patients and the recent suggestion of a possible association between GC activity and systemic complications in diabetes mellitus,6 topical treatments that block such activity would appear to be a promising therapeutic tool in wound healing. The dermatological application of such topical treatments could therefore be very useful in the treatment of leg ulcers. This is a field in which, as Velasco has pointed out1, dermatologists should play a greater role.