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[Hormonal factors in etiology of common acne].

Authors :
Bergler-Czop B
Brzezińska-Wcisło L
Source :
Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego [Pol Merkur Lekarski] 2004 May; Vol. 16 (95), pp. 490-2.
Publication Year :
2004

Abstract

Common acne is steatorrhoeic chronic disease, to which specific is, among others, the presence of blackheads, papulopustular eruptions, purulent cysts and cicatrices. Such hormonal factors belong to elements inherent in etiology of the affection. Sebaceous glands have cell receptors on their surface for androgens. In etiopathogenesis of common/simple acne, a decisive role is played by a derivative of testosterone, i.e. 5-alpha-dihydrotestosterone (DHT). However, some experts are of opinion that there is no correlation between the increased intensity of common acne and other symptoms of hyperandrogenism. Numerous authors assume, however, that common acne-affected patients may be sometimes subjected to intense reactions caused by sebaceous glands against physiological androgens concentrations. Naturally, estrogens can inhibit release of such androgens. Under physiological conditions, natural progesterone does not conduct to intensification of the seborrhea, but the activity of sebum secretion may be triggered off by its synthetic counterparts. Hormonal etiology can be very distinctly visible in the steroid, androgenic, premenstrual, menopausal acne, as well as in juvenile acne and acne neonatorum. In case of females affected by acne, hormonal therapy should be persistently supported and consulted with dermatologists, endocrinologists and gynecologists. Antiandrogenic preparations are applied, such as: cyproterone acetate concurrently administered with estrogens and, as well as not so frequently with chlormadinone acetate (independently or during estrogenic therapy).

Details

Language :
Polish
ISSN :
1426-9686
Volume :
16
Issue :
95
Database :
MEDLINE
Journal :
Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
Publication Type :
Academic Journal
Accession number :
15518435