Hyperandrogenism is characterized by high levels of androgens in women. Two main natural androgens are testosterone and dihydrotestosterone (DHT). The most common signs of androgen excess are hirsutism, acne, and alopecia. It is important to recognize and treat androgen excess disorders as long-standing hyperandrogen­ism is associated with dyslipidemia, hypertension, and impaired glucose toler­ance [1].

Hyperandrogenism affects between 5% and 10% of women of reproductive age. The most common cause of hyperandrogenism is polycystic ovarian syndrome (PCOS). In patients with androgen excess, the prevalence is about 72–82% for PCOS, 7–16% for idiopathic hyperandrogenism, 5–8% for idiopathic hirsutism,

Androgen production occurs in the endocrine glands and peripheral tissues. The endocrine glands responsible for androgen production are the adrenal glands and ovaries. The peripheral tissues involved in androgen production are the liver, gut, fat, and, most importantly, skin.

Hyperandrogenism can lead to hirsutism, which is the excessive growth of terminal (coarse, thick) hair in a male-like pattern, including the upper lip, chin, sideburns, earlobes, tip of the nose, back, chest, areole, axillae, lower abdomen, pubic triangle, and anterior thighs. There are scoring systems available for quantifying hirsutism, such as the Ferriman and Gallwey scale shown in Fig.3.1 [5]. Not all patients with hirsutism have hyperandrogenism, and conversely, not all patients with androgen excess are found to have hirsutism. Familial, genetic, and ethnic differences can inuence the degree of hirsutism.

Acne, androgenic alopecia, and ovulatory dysfunction are also commonly found in women with androgen excess. Though acne is common in adolescents, resistant acne that persists into adulthood and is associated with hirsutism or ovulatory dys­function raises concern for hyperandrogenism. Androgenic alopecia is male-pattern temporal balding. Ovulatory dysfunction occurs to varying degrees in women with hyperandrogenism and can include oligomenorrhea, amenorrhea, menorrhagia, metrorrhagia, pelvic pain, premenstrual dysphoric syndrome, or infertility.

Virilization is a rare clinical nding of hyperandrogenism and occurs as a result of severe androgen excess. In addition to hirsutism, acne, and androgenic alopecia, virilization includes deepening of the voice, decreased breast size, increased muscle mass, clitoral enlargement, and amenorrhea. Virilization is usually caused by an

A thorough history and physical exam are essential for the diagnosis of hyperan­drogenism. In patients with suspected androgen excess, androgenic drugs should rst be excluded. Medications that are associated with hyperandrogenism include exogenous androgens, anabolic steroids, danazol, and valproic acid. Patients should specically be asked about topical androgen use by themselves and their partners. Medications that can cause hypertrichosis (excessive growth of androgen­independent hair) include phenytoin, penicillamine, diazoxide, minoxidil, and cyclosporine. The onset and progression of androgen excess symptoms should be identied, as severe, rapid, and progressive symptoms raise concern for an adrenal or ovarian androgen-secreting tumor. On physical exam, the provider should deter­mine if signs of hyperandrogenism are present. When evaluating for hirsutism, one should keep in mind that ethnic and genetic factors can contribute to idiopathic hirsutism.

Women with normal testosterone levels and cyclic menses likely have idiopathic hirsutism, and no further workup is needed. Idiopathic hirsutism is thought to be caused by increased activity of 5-alpha-reductase, which leads to increased conver­sion of testosterone to DHT. For women with conrmed or suspected androgen excess, the following tests should be added as clinically indicated: serum prolactin, TSH, FSH, LH, 17-hydroxyprogesterone, and DHEAS (Table3.1) [9]. In anovula­tory women with elevated testosterone levels, it is recommended to obtain serum TSH and prolactin. In PCOS, testosterone is mildly elevated or at the upper limit of normal. Some but not all patients with PCOS have an elevated LH/FSH ratio, and this is not required for the diagnosis. In PCOS, DHEAS can be mildly elevated, but it is not recommended to check a DHEAS level unless there is a concern for an androgen-producing tumor. Patients presenting with hyperandrogenism should be screened for NCCAH due to 21-hydroxylase deciency with a 17- hydroxyprogesterone level. It is recommended to check early morning 17-hydroxyprogesterone levels in the follicular phase or on a random day for those with amenorrhea or infrequent menses [10]. If the 17-hydroxyprogesterone level is over 2ng/mL, further evalua­tion should be conducted with a cosyntropin stimulation test. Androgen-producing tumors are suspected when the total testosterone level in a female is persistently