Expression of estrogen, androgen, and glucocorticoid receptors in recent striae distensae.

Int J Dermatol

Department of Clinical Medicine/Division of Dermatology, School of Medicine, State University of Campinas (UNICAMP), Campinas, São Paulo, Brazil.

Published: January 2010

Background: Stretch marks or striae distensae (SD) can be considered a common skin disorder, but their physiopathogenic mechanisms have not been totally clarified. Although it is considered an esthetic complaint, it may have serious psychosocial consequences besides the local and systemic alterations of the conjunctive tissue. This study aims at assessing and quantifying the estrogen, androgen and glucocorticoid receptors in skin samples with striae and comparing with normal skin.

Methods: Skin samples for biopsy were obtained from eight patients with SD and eight patients without lesions. The samples were frozen at -80 degrees C and underwent processing to obtain proteic extract to quantify the estrogen, androgen and glucocorticoid receptors with the Western Blot method.

Results: When the estrogen receptor in the skin with SD was compared with healthy skin, it was observed to have increased twice as much (P = 0.00001). The androgen and glucocorticoid receptors in the SD skin had also increased (P = 0.00015 and P = 0.00083, respectively).

Conclusions: These findings indicate that under certain conditions there is an increase in hormonal receptor expression, suggesting that regions that undergo greater mechanical stretching of the skin may express greater hormonal receptor activity. This activity may influence the metabolism of the extracellular matrix, causing the formation of SD. Alterations in hormone receptors occur within a well-defined time period during the formation of SD; however, there are differences in the functionality of hormone receptors during different stages in the development of the lesions. The preliminary results appear to be relevant and represent an initial step towards an understanding of the pathophysiology of SD.

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Source
http://dx.doi.org/10.1111/j.1365-4632.2008.04005.xDOI Listing

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