Hirsutism is defined as the presence of excessive growth of hair in locations where hair growth in women is normally minimal or absent. The most common areas affected are the face, chest, areola, lower abdomen, lower back, buttocks and inner thighs. Hirsutism is rarely caused by a serious underlying disorder. Nevertheless, in our society, too much facial or body hair is considered abnormal. Excess hair growth can cause great psychological distress and social embarrassment. Fortunately, this is a treatable problem, but many women do not realize that there are numerous treatment options available.
For most women, the tendency towards hirsutism is inherited. The number of hair follicles is fixed before birth, and is dependent on genetic factors. For example, women and men of Mediterranean background have more hair follicles than people of Asian descent. Hirsutism usually begins at puberty, but mild hirsutism can start at any age. Because it is not considered a suitable topic of conversation, many affected women do not realize how prevalent a problem this is for many women. At least 25% of normal middle-aged women remove unwanted facial hair.
Usually, hair is vellus or fine and light, as opposed to terminal hair, which is coarse and darker like the hair of the eyebrows. Vellus hair is transformed into terminal hairs when subjected to androgens (male-type hormones). Low levels of androgen produce pubic and axillary hairs and the few strands around the areola, the brown circles of the nipple. When there is a higher circulating level of androgen, terminal hair appears under the chin, above the lip, on the sideburn area and on the upper abdomen (a diamond-shaped extension of the normal public hair triangle). Terminal hairs on the arms and legs vary in their response to androgens so they are not a reliable indicator of hirsutism. The amount of terminal hair increases with age due to the duration of exposure to androgens.
The primary mechanism leading to the development of hirsutism is increased secretion of androgens by the ovary or adrenal glands. Normally, circulating testosterone in women is derived from direct secretion of the ovary and by conversion of androstenedione (a weak androgen) produced by the ovary into testosterone by fat and muscle tissue. The adrenal gland, which lies on top of the kidney, also produces androstenedione and another androgen known as DHEAS (dehydroepiandrosterone sulfate), also converted into testosterone. Testosterone, in turn, enters cells of the skin where it is changed into a very potent hormone, dihydrotestosterone by the enzyme
5, alpha – reductase. Hirsute women can convert testosterone to dihydrotestosterone at the same rate a man does, up to four times that of a nonhirsute woman.
A very common cause of hirsutism is Polycystic Ovarian Syndrome (PCOS) affecting approximately 5% of the younger female population. PCOS is characterized by anovulation (sparse irregular periods), hyperandrogenism (hirsutism and acne) and the presence of many small cysts in the ovaries identified by ultrasound. Laboratory tests show an elevated or normal total testosterone, an elevated active free testosterone and a high LH/FSH (luteinizing hormone/follicle stimulating hormone) ratio. FSH causes several small follicles (cysts), to grow and mature in preparation for ovulation with usually one large follicle releasing an oocyte (egg). LH is responsible for causing ovulation of the follicle and stimulates certain cells of the ovary to produce androgens. Polycystic ovarian disease is usually diagnosed in adulthood, but the symptoms date back to the onset of puberty. Hirsutism begins with the onset of menses with a slow progression during adolescence.
In women with mild hirsutism who have ovulatory menstrual cycles and normal levels of testosterone, androstenedione and adrenal androgens, excess body hair is due to increased sensitivity of the hair follicle unit (pilosebaceous and oil glands) to normal levels of androgens. Other more serious conditions associated with an abrupt onset of hirsutism are rare androgen-secreting ovarian or adrenal tumors. A small number of hirsute women have an enzyme defect in the pathway leading to the manufacture of cortisol, the major product of the adrenals. In an attempt to make more cortisol, a gland in the brain called the pituitary, secretes more ACTH (a hormone which stimulates the adrenal gland), forcing the adrenals to increase all of its hormones, so the adrenal androgens also rise to high levels. This picture is seen in late-onset congenital adrenal hyperplasia, a hereditary disorder. If the defect is only partial, symptoms are not seen until the teen-age years or later. Part II will discuss the evaluation and treatment of hirsutism.

Debra A. Minjarez, M.D.
Rose Medical Center

Source: http://www.9news.com/health/rose_arc/hirsutism1.htm

Kat note: I couldn’t find part II of this article

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