Dermatologic Manifestations of Hirsutism 

Hirsutism is defined as the excessive growth of thick dark hair in locations where hair growth in women usually is minimal or absent (see the image below). Such male-pattern growth of terminal body hair usually occurs in androgen-stimulated locations, such as the face, chest, and areolae.

Although the terms hirsutism and hypertrichosis often are used interchangeably, hypertrichosis actually refers to excess hair (terminal or vellus) in areas that are not predominantly androgen dependent. Whether a patient is hirsute often is difficult to judge because hair growth varies among individual women and across ethnic groups. What is considered hirsutism in one culture may be considered typical in another. For example, women from the Mediterranean and the Indian subcontinent have more facial and body hair than do women from East Asia, sub-Saharan Africa, and northern Europe. Dark-haired, darkly pigmented individuals of either sex tend to be more hirsute than blond or fair-skinned persons.

In most cases, hirsutism is a benign condition and is primarily of cosmetic concern. However, when hirsutism is accompanied by masculinizing signs or symptoms, particularly when these arise well after puberty, hirsutism may be a manifestation of a more serious underlying disorder such as an ovarian or adrenal neoplasm. Fortunately, these disorders are rare.

Hirsutism can be caused by abnormally high androgen levels or by hair follicles that are more sensitive to normal androgen levels. Therefore, increased hair growth often is observed in patients with endocrine disorders characterized by hyperandrogenism, which may be caused by abnormalities of the ovaries or the adrenal glands.

The physiologic mechanism proposed for androgenic activity consists of the following 3 stages:

1. Production of androgens by the adrenals and ovaries
2. Androgen transport in the blood on carrier proteins (principally sex-hormone–binding globulin [SHBG])
3. Intracellular modification and binding to the androgen receptor

In short, central overproduction of androgen, increased peripheral conversion of androgen, decreased metabolism, and enhanced receptor binding are each potential causes of hirsutism. For circulating testosterone to exert its stimulatory effects on the hair follicle, it first must be converted into its more potent follicle-active metabolite, dihydrotestosterone. The enzyme, 5-alpha-reductase, which is found in the hair follicle, performs this conversion.

Overproduction of androgens results in an increased hair follicle size, hair fiber diameter, and duration of time hair follicles spend in the anagen (growth) phase. In addition to a change in hair quality and volume, oilier skin and hair may result from excess androgen secretion. The distribution of hair in women with high androgen levels is also altered. Excessive hair growth occurs in androgen-sensitive regions, but hair loss occurs on the scalp.^[1]

The severity of hirsutism does not correlate directly with the level of increased circulating androgens because of individual differences in conversion to 5-alpha-reductase and androgen sensitivity of hair follicles.

Testosterone stimulates hair growth, increasing the size and intensifying the pigmentation of hair. Estrogens act in opposition, slowing growth and producing finer, lighter hairs. Progesterone has minimal effect on hair growth.

The amount of free testosterone—the biologically active androgen that, after conversion to dihydrotestosterone, causes hair growth—is regulated by SHBG. Lower levels of SHBG increase the availability of free testosterone. SHBG levels decrease in response to the following:

• Exogenous androgens
• Certain disorders that affect androgen levels, such as polycystic ovarian syndrome (PCOS) (see the image below)The photograph depicts hirsutism in a young woman with polycystic ovarian syndrome. Note the acne lesions and excessive hair on her face and neck.
• Congenital or delayed-onset adrenal hyperplasia (see the image below)The patient has late-onset congenital adrenal hyperplasia. She has clinical features similar to those found in polycystic ovarian syndrome, including hirsutism, acne, obesity, diabetes, and menstrual irregularities.
• Cushing syndrome
• Obesity
• Hyperinsulinemia
• Hyperprolactinemia
• Excess growth hormone
• Hypothyroidism

Conversely, SHBG levels increase with higher estrogen levels, such as the levels that occur during oral contraceptive therapy. The resultant increased SHBG levels lower the activity of circulating testosterone.

Frequency

United States

Hirsutism is common and is estimated to occur in 1 in 20 women of reproductive age.

International

Familial hirsutism is found most commonly in southern European and South Asian countries, in which it is considered to be a normal trait. Hirsutism indicative of underlying endocrinopathy varies from culture to culture, depending on the incidence of the various endocrinopathies in a particular society.

Mortality/Morbidity

Hirsutism is a symptom, rather than a disease. Primarily, hirsutism is of cosmetic and psychological concern; however, it may indicate the presence of more serious associations, such as adrenal hyperplasia and ovarian tumors, particularly if it develops well after puberty.

Race

Familial hirsutism is noted most frequently in dark-skinned white persons. It is uncommon in sub-Saharan and African American blacks and is observed least commonly in East Asians and Native Americans.

Age

The onset of hirsutism depends on its cause. Familial or ethnic hirsutism typically begins during puberty. Hirsutism resulting from congenital adrenal hyperplasia (CAH) begins early in childhood, while late-onset CAH and PCOS often have onset after puberty. The growth of facial hair commonly observed in postmenopausal women may be caused by unopposed androgen.