ArticleIndian journal of dermatology
Cortisol Homeostasis in the Epidermis is Influenced by Topical Corticosteroids in Patients with Atopic Dermatitis.
Article in Indian journal of dermatology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Topical steroid withdrawal: dissecting the controversy.Frontiers in medicine · 2026Review
- Steroid Phobia: Is There a Basis? A Review of Topical Steroid Safety, Addiction and Withdrawal.Clinical drug investigation · 2021Review
- Molecular skin changes in Cushing syndrome and the effects of treatment.Journal of endocrinological investigation · 2021Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe skin produces cortisol by itself and regulates its own proliferation and differentiation. There is a possibility that topical corticosteroids (TCSs) influence the cortisol homeostasis in the skin. AIMS AND
objectivesThe author described the density and distribution of cortisol and its parties in the epidermis after application of topical steroids immunohistologically. MATERIALS AND
methodsThe forearm skin was biopsied before and after 2 weeks' application of clobetasol propionate 0.05% two times a day in one healthy volunteer. The biopsied skin was stained immunohistologically by ant-MLN64, StAR, CPY11A1, cortisol, HSD11B1, HSD11B2, glucocorticoid receptor alpha, glucocorticoid receptor beta (GRB), and mineralocorticoid receptor (MCR) antibodies. The skin biopsy was performed similarly in 19 adult patients with atopic dermatitis who had used TCS for a considerable period. They were 4 TCS present users (TCS+), 12 TCS nonusers with skin manifestation on the biopsied site (TCS-E+) and 3 TCS nonusers without skin manifestation on the biopsied site (TCS-E-).
resultsThe staining density increased during TCS application in MLN64, cortisol and HSD11B2 in a healthy volunteer. The staining density was stronger in HSD11B2 of the basal layer and MCR of the spinous layer in the TCS-E+ patients than in the TCS+ and TCS-E- patients. The staining density was weaker in MLN64 of the basal and granular layers, HSD11B1 of the basal layer and GRB of the whole layer in the TCS-E+ patients than in the TCS+ and TCS-E- patients.
conclusionThe hypertrophy of the epidermis and insufficient keratinization recognized in the TCS-E+ patients might be caused by the decreased cortisol synthesis regulated by MLN64 and the increased cortisol inactivation by HSD11B2. Decreased GRB and increased MCR might enhance the reactivity of cortisol in the keratinocytes.
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