Hormonal Acne: A Paradigm Shift in the Management of Acne
Hormonal Acne: A Paradigm Shift in the Management of Acne
The androgens mainly influence sebum production to play a vital role in acne formation. The adrenal gland and the testes or ovaries produce a significant portion of circulating androgens. In addition, inactive adrenal precursors such as dehydroepiandrosterone (DHEA), DHEA-sulfate (DHEA-S) and androstenedione are also converted into a large quantity of androgens in the skin. Other androgen-responsive structures of the skin, apart from the sebaceous glands, namely the hair follicles, sweat glands, epidermis and dermis, also play a role in the enzymatic conversion of DHEA, DHEA-S and androstenedione into the more potent androgens dihydrotestosterone (DHT) and testosterone. DHT and testosterone interact with the androgen receptors on sebaceous glands. Of the two, DHT is five- to ten-times more potent than testosterone. The sebaceous glands are the site for the conversion of inactive adrenal precursors to potent androgen. The key steroidogenic enzymes that facilitate this conversion are 3β-hydroxysteroid dehydrogenates, 17β-hydroxysteroid dehydrogenates and 5α-reductase.
There are studies showing that elevated levels of serum IGF-I correlate with overproduction of sebum and acne. It is likely that adult acne patients might frequently have autoimmune thyroid disease and this should be kept in mind when screening women with postadolescent acne.
Yet another noteworthy aspect is that corticotrophin-releasing hormone levels change during stress, and corticotropin-releasing hormone regulates sebaceous gland function, thus explaining the relationship between stress and acne.
Hormonal Pathogenesis of Acne
The androgens mainly influence sebum production to play a vital role in acne formation. The adrenal gland and the testes or ovaries produce a significant portion of circulating androgens. In addition, inactive adrenal precursors such as dehydroepiandrosterone (DHEA), DHEA-sulfate (DHEA-S) and androstenedione are also converted into a large quantity of androgens in the skin. Other androgen-responsive structures of the skin, apart from the sebaceous glands, namely the hair follicles, sweat glands, epidermis and dermis, also play a role in the enzymatic conversion of DHEA, DHEA-S and androstenedione into the more potent androgens dihydrotestosterone (DHT) and testosterone. DHT and testosterone interact with the androgen receptors on sebaceous glands. Of the two, DHT is five- to ten-times more potent than testosterone. The sebaceous glands are the site for the conversion of inactive adrenal precursors to potent androgen. The key steroidogenic enzymes that facilitate this conversion are 3β-hydroxysteroid dehydrogenates, 17β-hydroxysteroid dehydrogenates and 5α-reductase.
There are studies showing that elevated levels of serum IGF-I correlate with overproduction of sebum and acne. It is likely that adult acne patients might frequently have autoimmune thyroid disease and this should be kept in mind when screening women with postadolescent acne.
Yet another noteworthy aspect is that corticotrophin-releasing hormone levels change during stress, and corticotropin-releasing hormone regulates sebaceous gland function, thus explaining the relationship between stress and acne.