Hirsutism in women is defined as the excess of terminal hair growth in a male pattern distribution [1]. Terminal hair is coarse and pigmented as opposed to the vellus hair which is fine, nonpigmented, and soft and covers the entire skin surface except the lips, palms, and soles [1]. The prevalence of hirsutism ranges from 4.3 to 10.8 % in African American and Caucasian women (variable due to some degree of examiner subjectivity), but is lower in Asian women [1]. About 5–15 % of hirsute women have no detectable androgen excess on blood testing [2]. The prevalence of hirsutism in postmenopausal women is not well studied [3], but mild degrees of hair excess are not uncommon in the years following the final menstrual period due to a profound decline in ovarian estrogens relative to the menopausal androgen milieu [4, 5]. The decline in ovarian estrogens and the associated decrease in hepatic sex hormone-binding globulin (SHBG) levels lead to an increase in the free androgen index (FAI), which may explain the common postmenopausal development of terminal hair on the face and chin, as well as the thinning of scalp hair as described in the index case [6].

There exists a regional variation in the degree of sensitivity of terminal hair to circulating androgens [7]. In addition to androgens, terminal hairs are affected by thyroid hormone, growth hormone, and local factors [7]. Areas such as the eyebrows, eyelashes, and lateral and occipital scalp are generally insensitive to androgens, whereas pubic (lower pubic triangle), axillary, and lower arm and leg hair are sensitive to low levels of androgens [7]. Terminal hair, typically in male pattern areas of growth including the sideburns, cheeks, chin, abdomen (male escutcheon/pelvic upper triangle), back, thighs, and upper arms, is sensitive to higher levels of androgens; presence of terminal hair in these locations, unless familial, is generally considered abnormal in women [7, 8].

A widely used classification scheme for hair excess in women is the Ferriman–Gallwey (FG) scoring system [8] that is based on pictorial representation of degrees of hair excess (ranging from 0 to 4 in increasing severity) at nine (originally eleven) androgen-sensitive areas (upper lip, chin, chest, upper and lower back, upper and lower abdomen, upper arms, and thighs). Using the modified FG scale, a score of less than 8 for all nine areas is considered normal [9]. There are considerable limitations to this scoring system, however, including observer subjectivity, omission of some important androgenic areas (sideburn, perianal area, buttocks), and a disregard of racial and ethnic differences in hair growth. Based on a total FG score of 11 at nine areas, the severity of hirsutism for the patient under discussion was deemed as “mild.”

Initial history in any woman with a chief complaint of hair excess should include location and rate of abnormal hair growth and occurrence of additional symptoms of androgen excess including acne, hair loss, and an inquiry about symptoms of virilization, which can include male pattern hair loss, deepening of voice, increased libido, worsening aggression, increased muscle mass, shrinkage in breast size, clitoral enlargement, and excessive perspiration. A complete history should also note any abdominal symptoms (such as increased girth, bloating, and constipation), nipple discharge, changes in skin coloration, and weight gain or loss. Personal history of medical disorders such as diabetes and hypertension, and family history of hirsutism and of scalp hair loss particularly in female members in the family should be enquired. A thorough review of medications including supplements should be undertaken, and use of topical androgenic agents by partner should be assessed, if appropriate.

Physical examination should include assessment of body mass index and blood pressure, quantitative and qualitative assessment of facial and bodily hair using FG scale, and assessment of scalp hair growth with particular attention to areas of hair loss. Female pattern hair loss primarily affects the crown with preservation of the frontal hair line which contrasts with the male pattern hair loss which involves recession of the frontal hair line and is associated with elevated circulating androgen levels [10]. Evaluation should take into consideration additional cutaneous stigmata such as acne (assess location and severity), facial plethora (Cushingoid feature), cutaneous striae (assessing location, width, and color of striae), fat deposition at the base of the neck (Cushingoid feature), and the presence of acanthosis nigricans or skin tags (markers of insulin resistance). Palpation should focus on detection of thyromegaly and abdominopelvic masses. External genital examination should assess for clitoromegaly.

In many cases of mild hirsutism (FG score 8–15), and particularly without other clinical features to suspect an underlying reversible cause, laboratory work-up may not be necessary [11], and empiric therapy may be initiated as discussed below. In cases of moderate to severe hirsutism (FG score over 15) and in cases exhibiting other stigmata of virilization, serum testosterone (total and free) and dehydroepiandrosterone sulfate (DHEAS) levels are the primary laboratory tests to assess for presence and source of androgen excess. Thyroid studies must be undertaken as coarsening of skin and hair loss can be seen in setting of uncontrolled thyroid disorders. Optimally, an early morning plasma-free testosterone level is a more sensitive test which can detect androgen excess states even when total testosterone levels are normal [12, 13]. Assays for free testosterone however are accurate only when measured by equilibrium dialysis, require strict quality controls to minimize operator-dependent variability, and are not therefore widely reliable [14, 15]. Total testosterone assays are more reproducible and widely available and may thus be the preferred test to obtain in general practice [14]. Depending on DHEAS and testosterone levels, imaging may be required to rule out a neoplastic hormone-producing process of the adrenals or ovaries, respectively. Pelvic ultrasound and MRI are most useful for ovarian imaging, and abdominal CT scans are most useful for adrenal imaging [3]. It should be noted that androgen-producing adrenal tumors are often very small in size, requiring high-resolution CT techniques that can detect lesions which may only be 0.5 cm in diameter [16]. Communication with the radiologist is therefore of paramount importance to optimize radiographic detection yield. Milder elevations of DHEAS levels in certain clinical settings should be further evaluated with a 24-h urinary-free cortisol and overnight dexamethasone suppression test to rule out Cushing’s syndrome, a differential diagnosis to consider especially when hypertension, diabetes, and low bone mass coexist with hair growth excess [14]. While late-onset congenital adrenal hyperplasia remains a differential diagnosis to consider in any adult female with hyperandrogenism, this condition will commonly present in early reproductive years; an initial presentation in postmenopausal women is rare.

Hirsutism in postmenopausal women with no biochemical evidence of androgen excess may be idiopathic or may be related to certain drugs, e.g., glucocorticoids, phenytoin, minoxidil, or cyclosporine [11, 17].

High testosterone levels with normal or mildly elevated DHEAS levels usually suggest an ovarian source of hyperandrogenism, although the possibility of exogenous exposure through topical contact with transdermal androgen products commonly used by men should be considered. The most common cause for androgen excess in women is polycystic ovarian syndrome (PCOS) [17, 18]. While PCOS is a well-recognized entity in the reproductive phase of life, the milieu of androgen excess persists well into menopause in this population [6]. Gynecological history spanning premenopausal period is thus particularly relevant when assessing hyperandrogenism in postmenopausal women, as women with PCOS often acknowledge a long history of irregular menstrual cycles and hyperandrogenic signs and symptoms since menarche, as did the patient under discussion.

Rising pituitary gonadotropin levels (particularly luteinizing hormone (LH)) after menopause can enhance androgen production from ovarian theca stromal cells, particularly for women with PCOS, which along with declining ovarian estrogen can contribute to worsening of hyperandrogenic symptoms. Assessment of gonadotropins can therefore provide useful insight into pathophysiology of postmenopausal hyperandrogenism and should be obtained during evaluation of symptoms of postmenopausal hair excess or scalp hair loss. An extreme form of ovarian androgen excess encountered in postmenopausal women is ovarian hyperthecosis, a syndrome where rapid virilization can occur and testosterone levels may even be in the tumor range (>200 ng/dL) [3]. Pelvic imaging often demonstrates enlarged solid-appearing echogenic ovaries without any focal mass [19].

Androgen-producing neoplastic processes of the ovaries and adrenals account for only 0.2 % percent of cases of androgen excess in women [18] and should be suspected when virilization is rapidly progressive and androgen levels exceed certain thresholds. Although some cross over can occur, DHEAS is an exclusively adrenal androgen, while testosterone can originate from both ovarian and adrenal tumors. Therefore, when serum DHEAS levels exceed 700 ng/ml, an adrenal tumor is most likely particularly when clinical and biochemical evidence of glucocorticoid and mineralocorticoid excess is also present [14]. On the other hand, testosterone levels exceeding 200 ng/dL may originate either from the adrenal or the ovaries, and both organs need to be imaged, particularly when DHEAS is also elevated [14]. Common androgen-producing ovarian tumors in postmenopausal women include Leydig cell tumors, Sertoli cell tumors, and steroid tumors, all of which are often small and unilateral. In the absence of adrenal or ovarian tumors, a tumor range serum androgen level is often due to ovarian hyperthecosis as discussed earlier.

Another hyperandrogenic condition associated with elevated DHEAS levels is nonclassical congenital adrenal hyperplasia (CAH) which accounts for 1.5–2.5 % of causes of hirsutism in women. The commonest variant of nonclassical CAH is due to a 21-hydroxylase deficiency and is commonly associated with elevated serum levels of 17-hydroxyprogesterone (17-OHP), often in excess of 200 ng/dL [14, 17, 18].

The first step in management of a postmenopausal patient with complaints of hair excess and/or scalp hair loss is a thorough evaluation to rule out identifiable and potentially reversible causes of androgen excess, as discussed earlier. In those iatrogenic cases due to certain drugs, significant improvement in hair growth can be expected following discontinuation of the offending agent, which is preferably done in collaboration with the prescribing provider, lest undesirable effects emerge from this alteration in medical regimen. Similarly, hirsutism in women who are hyperandrogenic due to nonclassical CAH will improve after initiation of steroid therapy and consequent decline in adrenal androgen production. Women with evidence of Cushing’s necessitate evaluation for the source of cortisol excess (medication, adrenal tumor, pituitary adenoma, and inherited disorders such as multiple endocrine neoplasia). Definitive management would depend on the underlying mechanism for cortisol excess and should mitigate symptoms. For women with thyroid dysfunction, a gradual improvement in hair growth can be expected with attainment of euthyroid status. Due to the prolonged duration of hair growth and differentiation cycle (discussed elsewhere in this textbook), any improvement after intervention for hirsutism may not become clinically evident for several months or even up to a year [11]. Additional cosmetic measures may be required for faster relief, as discussed below.

The combination oral contraceptive pill (COCP) is the mainstay of pharmacotherapy for hirsutism in reproductive age women, and its use for such can be extended to healthy perimenopausal and early postmenopausal women [14]. The progestin component of COCP suppresses pituitary LH secretion, the main stimulant of ovarian androgen, and, to a lesser extent, adrenal androgen production [20]. Estrogenic component of COCP reduces free androgen levels by increasing hepatic production of SHBG [14]. While effective as first-line strategy in the younger perimenopausal and early menopausal women, COCP use is not risk-free and formulations containing the lowest estrogen doses should be used to minimize this risk. COCP use is contraindicated for women with a history of breast cancer and other hormone-sensitive tumors, for those deemed at risk for cardiovascular disease (CVD) and venous thromboembolism (VTE), for those with liver disease and uncontrolled hypertension, and for smokers. The choice of formulation should take into account the type of progestin and the dose of estrogenic component of the formulation. Progestins of low androgenic potency, such as norgestimate, norethindrone, and desogestrel, or antiandrogenic effects, such as drospirenone and cyproterone, should be preferentially considered when choosing a formulation to address symptoms of hyperandrogenism [21]. For the older symptomatic menopausal woman experiencing symptoms of hair excess and/or acne, lower dose menopausal hormone therapy (MHT) regimen is preferred to COCP; in addition to providing relief from vasomotor symptoms, estrogen component of MHT, particularly when administered orally, can bring about some decrease in the free androgen index (FAI) through direct effects on hepatic SHBG production and thereby offer cutaneous benefit for some [22, 23]. Decision to initiate MHT for cosmetic benefit alone must take into consideration the overall clinical picture including presence of menopausal symptoms, personalized risk for CVD, thromboembolism, and for fragility fractures. For women similar to our case under discussion, i.e., an older and asymptomatic menopausal woman with comorbidities who is remote from the final menstrual period, potential for harm associated with use of systemic MHT is deemed to outweigh any possible benefit that MHT may offer against hyperandrogenism; MHT should not be a consideration for the case under discussion [24].