Polycystic Ovary Syndrome and Acne

Sandy S. Chuan, MD; R. Jeffrey Chang, MD

Disclosures

Skin Therapy Letter. 2010;15(10):1-4. 

In This Article

Pathophysiology and Prevalence

Polycystic ovary syndrome (PCOS) is typically characterized by excessive ovarian androgen production, failure of ovulation, and slightly enlarged ovaries with numerous peripheral small follicles that appear as cysts. Individuals with this phenotype comprise 5–10% of reproductive aged women.[1–3] The disorder is commonly accompanied by insulin resistance and infertility. Clinical manifestations include irregular menstrual bleeding due to anovulation and dermatologic sequelae of hyperandrogenemia, including hirsutism, acne vulgaris, and androgenic alopecia. The prevalence of acne in women with PCOS has been estimated to be 10–34%.[4–7] However, in post-pubertal and adolescent PCOS women it is unclear whether acne arises secondary to androgen excess or occurs as a result of normal puberty. During puberty, acne is common and attributable to the surge of adrenal androgens with adrenarche. In adolescent girls, moderate to severe acne has been reported to be greater than 50%.[1]

Acne is the most common skin disorder, affecting approximately 40–50 million people in the United States.[8] This condition results from the formation of comedones, due to sebum accumulation, along with desquamated follicular epithelial cells, which allows colonization by the bacterium, Propionibacterium acnes (P. acnes).[9] Androgens may worsen acne formation by increasing sebum production within the pilosebaceous unit. Many PCOS women with acne exhibit facial lesions and up to 50% of individuals demonstrate lesions on the neck, chest, and upper back.[10]

Past studies have shown that androgen levels are elevated in women with acne, although the severity of acne has not been positively correlated with any particular hormone, with the exception of the adrenal androgen, dehydroepiandrosterone sulfate (DHEA-S).[11–13] Notably, several studies have demon-strated an inverse relationship with sex-hormone binding globulin (SHBG).[11,14]

About 50% of normal women with acne do not have clinical or biochemical evidence of hyperandrogenism.[15] Conversely, in many PCOS women hirsutism is not associated with acne. These discrepancies may be due to variable local androgen bioactivity. It has been postulated that androgen levels within the skin are more important mediators of acne than circulating levels.[13,16]

In the hair follicle, androgen bioactivity is regulated, in part, by 5-α-reductase, which acts to convert free testosterone to the more potent dihydrotestosterone (DHT). This enzyme has two isoforms: type 1 is found in the sebaceous glands and pubic skin and type 2 is located primarily in the hair follicle, genital skin, and adult scalp. The relative activities of these isoenzymes within the hair follicle could account for the variable clinical presentation seen in hyperandrogenic women when the degree of hirsutism is not compatible with the severity of the acne.10 In addition, 5-α-reductase expression is also stimulated by excess androgen, insulin, and insulin-like growth factor, which likely contributes to increased local androgen bioactivity, resulting in the hirsutism and acne seen in PCOS women.[10,17]

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