Skin atrophy caused by topical glucocorticoids is less common in patients with atopic dermatitis than in those with psoriasis

xlomafota13 shared this article with you from Inoreader Skin atrophy caused by topical glucocorticoids is less common in patients with atopic dermatitis than in those with psoriasis Via Experimental Dermatology SUMMARY Background Although the long-term use of topical glucocorticoids (TGC) may induce skin atrophy including striae distensae (SD), patients with atopic dermatitis (AD) appear to have lesser degree of skin atrophy than those with psoriasis (PSO). Periostin, encoded by POSTN, is involved in tissue remodeling processes of chronic AD lesions. Objectives This study was designed to investigate the difference in the occurrence of skin atrophy in patients with AD or PSO when treated with TGC and to elucidate the association between skin atrophy and periostin. Methods Big data analysis using Korean Health Claims Database was performed to determine the prevalence of SD in AD and PSO patients. Blood and skin eosinophils count and dermal fibrosis between AD and PSO patients were compared and immunohistochemistry for periostin and mRNA-sequencing in the dermis were performed. Animal experiments using AD and PSO murine model was conducted. Results Big data analysis revealed that patients with AD have significantly lesser degree of SD than patients with PSO. The ratio of the dermal fibrous tissues and eosinophil counts were significantly higher in AD patients. In AD skin, periostin was more widely distributed in the entire dermis and POSTN mRNAs were significantly upregulated. Dermal thickness and fibrosis were significantly higher in AD mice even after TGC treatment. A significant positive correlation was observed between dermal fibrosis and tissue eosinophil counts. Conclusion Lesser skin atrophy in AD patients even after long-term TGC application could be resulted from skin fibrosis caused by increased tissue eosinophils and periostin deposition. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.