Glucocorticoid Receptor Beta And Its Prognostic Value On Treatment Response In Chronic Vulvar Dermatitis

Background: Chronic vulvar dermatitis (CVD) is the most prevalent disease in gynecologic dermatology. The treatment mainly depends on topical glucocorticoids (TGC) but is challenged by insufficient treatment response. On a histological level, the upregulation of the glucocorticoid receptor beta (GR beta), an inhibitor of the active glucocorticoid receptor alpha (GR alpha), is discussed as mechanism of glucocorticoid insensitivity. Objectives: To analyze whether the expression of GR beta protein at baseline in keratinocytes may predict responsiveness to TGC in patients with CVD. Methods: In this retrospective cohort study, clinical and biological data of 25 women with a histological diagnosis of chronic vulvar eczema were analyzed. Randomization was done according to the responsiveness to TGC treatment (responsive vs. nonresponsive). Clinical data and the expression of GR beta in the immunohistochemical stained biopsies were examined. Results: Fifty-two percent of women with CVD were nonresponsive to TGC. GR beta was abundantly expressed in the cytoplasma of keratinocytes of the vulvar epithelium, but no difference in the level of expression was found among GC responsive and nonresponsive patients in the semiquantitative (p = 0.376) and quantitative analysis (p = 0.894). Conclusion: GR beta is highly expressed in keratinocytes of the vulvar epidermis affected by CVD, but GR beta expression was not increased in patients nonresponsive to TGC compared to responsive patients. Thus, the failure mechanism in nonresponders still remains to be elucidated.