Update on the management of hirsutism

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ABSTRACTHirsutism is a source of significant anxiety in women. While polycystic ovary syndrome or other endocrine conditions are responsible for excess androgen in many patients, other patients have normal menses and normal androgen levels (“idiopathic” hirsutism). The goal of the evaluation is to rule out any underlying pathology. The goals of therapy are to treat any underlying condition and to remove the excess hair. Current options for hair removal are discussed. Educating patients so they have reasonable treatment expectations is essential, as significant improvement may take weeks or months, and treatment may need to be repeated on an ongoing basis.


  • The finding of polycystic ovaries is not required for the diagnosis of polycystic ovary syndrome, nor does their presence prove the diagnosis. Gonadotropin-dependent functional ovarian hyperandrogenism is believed to cause this syndrome; however, mild adrenocorticotropic-dependent functional adrenal hyperandrogenism also is a feature in many cases.
  • Even women with mild hirsutism with subtle symptoms and signs of hyperandrogenism can have elevated androgen levels, and thus, they deserve a laboratory evaluation.
  • Laser treatment does not result in complete, permanent hair reduction, but it is more effective than shaving, waxing, and electrolysis, producing partial hair reduction for up to 6 months.



Hirsutism causes significant anxiety and lack of self-esteem in women. Although it is itself a benign condition, it is often the sign of an underlying and possibly serious endocrine condition.

As we will discuss, the diagnosis begins with a detailed history and physical examination, with laboratory testing and imaging as needed to confirm or rule out underlying causes. Management begins with patient education and support and includes hair removal and drug treatment of any underlying metabolic derangement.


Hirsutism is a common disorder of excess growth of terminal hair in an androgen-dependent male distribution in women, including the chin, upper lip, breasts, upper back, and abdomen.1 It affects 5% to 10% of women of reproductive age.1,2

Hirsutism should be differentiated from hypertrichosis, which can be hereditary or acquired, and which is defined as increased general hair growth in androgen-independent areas.1

Excess hair is cosmetically concerning for women and can significantly affect self-esteem. 3 Normal or acceptable hair growth depends on a woman’s ethnicity and her perception of familial, cultural, and societal norms for the quantity and distribution of hair. Mediterranean women generally have a medium amount of body and facial hair, whereas Asian women have a minimal amount.1,4,5

Hirsutism can be clinically graded according to the Ferriman-Gallwey scale2,6 and is defined as a Ferriman-Gallwey score of 8 or higher.1


In androgen-dependent areas, circulating androgens influence hair follicle characteristics. Androgens increase the size and diameter of the hair fibers in certain androgen-dependent sites, as seen in puberty with the transformation of vellus hairs (small, nonpigmented hairs) into terminal hairs (large, pigmented hairs) in the pubic and axillary regions in women, as well as the beard area in men.2,7 Interestingly, the same circulating androgens cause miniaturization of the susceptible hair follicles of the central scalp.7 The susceptibility of the hair follicle to the effects of the androgens may be genetically determined.7,8

Hirsutism is a sign of hyperandrogenism and increased action of androgens on hair follicles. In women, about half of circulating testosterone arises from the ovaries and adrenal glands; the rest originates from peripheral conversion of weaker androgens (such as androstenedione produced by the adrenals and ovaries) into testosterone.9 Dehydroepiandrosterone sulfate (DHEAS) originates mainly in the adrenal glands.9,10 Testosterone is converted to the more potent dihydrotestosterone (DHT) by type II 5-alpha reductase in the skin, which can then act on susceptible hair follicles.7,11 Therefore, hirsutism can be a consequence of endogenous androgen over-production from the ovaries or the adrenal glands (or both), of exposure to an exogenous source of androgen such as a drug, or of heightened hair follicle sensitivity and metabolism of normal circulating androgen levels (target end-organ dysfunction).1


Many women with hirsutism are found to have polycystic ovary syndrome as the underlying cause, but hirsutism is also commonly labeled as idiopathic when it occurs without an obvious cause, eg, in women with regular menses and normal androgen levels and without features suspicious for other causes of hirsutism. 1,2,12,13 But while this term is commonly used,1,12 it may be misleading, especially if the diagnosis of idiopathic hirsutism is based on standard laboratory tests, which do not always detect androgen excess.2,13 Minor ovarian or adrenal functional hyperandrogenism,14 increased peripheral activity of 5-alpha reductase in the hair follicle, or abnormalities in the androgen receptor have been implicated in the pathogenesis of so-called idiopathic hirsutism. 2,15


Polycystic ovary syndrome, a metabolic syndrome, presents clinically with menstrual irregularities such as oligomenorrhea or amenorrhea, infertility, and signs of hyperandrogenism such as hirsutism, acne, or androgenetic alopecia.16,17 Metabolic disturbances including insulin resistance, impaired glucose tolerance, hyperlipidemia, and obesity (body mass index > 30 kg/m2) also can occur, thus increasing cardiovascular risk.16–18

The finding of polycystic ovaries is not required to make the diagnosis of polycystic ovary syndrome, and their presence does not prove the diagnosis.16,19 Gonadotropin-dependent functional ovarian hyperandrogenism is believed to cause this syndrome; however, mild adrenocorticotropic-dependent functional adrenal hyperandrogenism also is a feature in many cases. In rare cases, polycystic ovary syndrome presents with an isolated elevation of DHEAS.16,20


The syndrome of hyperandrogenism, insulin resistance, and acanthosis nigricans, abbreviated as HAIR-AN, is separate from polycystic ovary syndrome; it characterizes a group of inherited syndromes associated with severe metabolic abnormalities of insulin and glucose metabolism and with marked clinical signs of hyperandrogenism.12

The syndrome of seborrhea, acne, hirsutism, and acanthosis nigricans, abbreviated as SAHA, while not itself a diagnosis, is a clinical spectrum of dermatologic signs and symptoms also associated with hyperandrogenism. These are signs that may present with the HAIR-AN syndrome or with another cause of excess androgens, such as idiopathic, ovarian, adrenal, or hyperprolactinemic hyperandrogenism.21

Thyroid disease, hyperprolactinemia, acromegaly, Cushing syndrome, exogenous factors such as androgenic drugs, and nonclassical congenital adrenal hyperplasia can also produce hirsutism.12 In nonclassical congenital adrenal hyperplasia, which is typically caused by a deficiency of 21-hydroxylase, patients present with premature pubarche, hirsutism in the prepubertal years, and menstrual irregularities including primary amenorrhea.22,23

Important rare causes of hirsutism include benign and malignant androgen-secreting tumors of adrenal or ovarian origin. In such cases, hirsutism can have an acute onset or rapid progression and may be associated with features of virilization, such as deepened voice, increased muscle mass, androgenetic alopecia, clitoromegaly, and increased libido.12


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