4.5 Article

Effects of a multilamellar emulsion on glucocorticoid-induced epidermal atrophy and barrier impairment

Journal

JOURNAL OF DERMATOLOGY
Volume 33, Issue 2, Pages 80-90

Publisher

WILEY
DOI: 10.1111/j.1346-8138.2006.00018.x

Keywords

epidermal atrophy; glucocorticoid; lamellar; multilamellar emulsion (MLE); skin barrier

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Skin atrophy is one of the most frequent side-effects of the topical glucocorticoid. Skin barrier impairment has also been reported as a steroid-induced side effect. Although there have been various studies on preventing or minimizing this atrophogenic effect, little has been reported about preventing barrier impairment. This study was performed to determine the effects of a multilamellar emulsion (MLE) that had a well-ordered lamellar structure on the steroid-induced barrier impairment and epidermal atrophy. To confirm these effects of MLE, 0.05% clobetasol-17-propionate (CP) and 0.05% clobetasol-17-propionate in MLE (MLE/CP) were topically applied to both flanks of hairless mice for 9 days. The topically applied CP induced a significant impairment of the epidermal permeability barrier, and MLE/CP also did not have a preventive effect on this change. However, skinfold thickness studies and histological studies showed that MLE/CP significantly reduced the steroid-induced atrophy. The topical application of MLE/CP was also shown to have a preventive effect on the steroid-induced increase of the stratum corneum (SC) surface pH. In addition, the electron microscopic findings showed relatively well-conserved lamellar bilayers in the skin treated with MILE, as compared to CP only. The results showed that the topical application of MILE immediately after CP treatment prevented the glucocorticoid-induced transepidermal water loss values increase. Light microscopy measurements showed that the skin treated with MILE immediately after CP treatment for 1 week had a slightly lower decline of skin thickness than did the CP-treated skin. These results suggest that MILE should be effective for preventing glucocorticoid-induced epidermal atrophy and for repairing the barrier impairment.

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