Hypertrichosis and hirsutism are the excessive growth of hair on the female body, specifically a thick and usually dark type of hair. Though the differences between hypertrichosis and hirsutism concern mostly the degree and extension of the excessive hairiness, I would like to make some important points regarding these concepts. The designation hypertrichosis is more appropriate for the excessive growth of hair on the parts of the female body in which all women normally have thick hair, as the genitals and their surrounding and/or near areas. On the other hand, the term hirsutism, besides including all severe forms of hypertrichosis, concerns mostly the significant growth of thick hair on those parts of women's bodies in which the presence of hair is quite unusual and abnormal.

Frequently associated to acne, hypertrichosis and hirsutism are part of the well-known androgenic manifestations in women. In cases of actual hyperandrogenic disorders ( that is, the presence of considerably high androgen levels ), these manifestations may also include, in their more severe forms, other signs and symptoms like hypertrophy of the clitoris, male-like changes in the voice, severe menstrual alterations including amenorrhea, hair loss and several other problems ( see Note 1 below ).

Nevertheless, most of the cases of hypertrichosis and hirsutism that we see in clinical practice - associated or not to disorders of the ovarian cycle -, are slight or mild ones and only rarely are due to major disorders in the androgenic metabolism. Usually they comprehend two basic groups with several in-between situations : 1) slightly heightened androgen levels and/or other slight alterations in the metabolism of these hormones; 2) increased sensitivity and responsivity of the androgen-receptors to the aforementioned hormones.

Before continuing, I have to call everybody's attention to the existence of iatrogenic cases of hypertrichosis and/or hirsutism - and even menstrual disorders - due to the ill-advised use of androgens and other steroids possessing androgenic properties, like some medicines for "gaining weight" and "developing musculature" ( "anabolizing" steroids ). Women should never use such products, and this must be quite clear.

Most cases of slightly or moderately heightened androgen levels are usually due to ovarian pathologies like those of the polycystic ovaries group and also a condition named hyperthecosis ( also present in polycystic ovaries ). In these pathologies the ovaries not only produce an increased amount of the androgens androstenedione and/or testosterone but also there is a deficiency in their respective transformation into the estrogens estrone and estradiol. As it is widely known, the androgens are the biochemical precursors of the estrogens in the biosynthesis of the sexual hormones. Androstenedione is turned into estrone both in the ovaries and the adipose tissue. Testosterone is turned into estradiol in the ovaries.

Typical polycystic ovaries are characterized by: 1) interruption of the follicular growth in its earlier stages, resulting in the presence of a great number of small follicles that do not continue their development; 2) hyperplasia of the follicular theca and the ovarian stroma ( hyperthecosis ), responsible mostly for the production of androgens; 3) bilateral ovarian enlargement; 4) thickening of the tunica albuginea, the ovarian external coating; 5) chronic anovulation; 6) deficient conversion of androgens into estrogens, with the consequent androgenic accumulation in the follicles; 7) excessive ovarian production of androgens; 8) the resulting increased blood levels of androgens; 9) menstrual disorders like oligomenorrhea ( long-lasting cycles ) and amenorrhea. For more details on this subject, see my articles "Polycystic Ovaries Syndrome" and "The Curious Relation Between Androgens and Estrogens in Women".

Some cases of moderately heightened androgen levels may also be due to very slight forms of virilizing adrenal hyperplasias that may become manifest only later in life ( during adolescence and adulthood ). Nevertheless, we must emphasize that, in this pathology, the androgenic levels are usually higher - even in its slightest forms. Virilizing adrenal hyperplasias are genetically inherited pathologies of the adrenal glands mostly due to variable degrees of 21-hydroxylase deficiency ( 21-hydroxylase is an enzyme whose activity is fundamental in the synthesis of cortisol, one of the most important hormones produced by the adrenal cortex. Cortisol plays a crucial role in human endocrine physiology ) ( See Notes 2 and 3 below ). If the adrenal glands fail in producing the necessary levels of cortisol due to 21-hydroxylase deficiency, the pituitary greatly increases its production of ACTH ( adrenocorticotropic hormone ) in order to better stimulate the adrenal glands and try to improve the cortisol levels. Nevertheless, this adrenal over-stimulation by continuous high levels of ACTH ends up by generating the adrenal hyperplasia and the consequent heightened production of androgens.

As already mentioned, another factor of great importance in many cases of hypertrichosis and hirsutism concerns the peripheral androgenic metabolism and the responsiveness of the androgen-receptors to these hormones. In clinical practice we frequently verify that many cases of slight hypertrichosis and/or hirsutism do not exhibit any significant alteration in the ovarian and/or adrenal production of androgens. These cases are considered constitutional, since the main origin of the problem seems to be an increased responsiveness of the hair follicles to normal levels of androgens.

The androgen that really stimulates most of the androgen-receptors is not testosterone, but dihydrotestosterone. Dihydrotestosterone results exclusively from the peripheral conversion of androstenedione and testosterone and depends on the activity of an enzyme named 5-alpha-reductase. Under the action of 5-alpha-reductase, androstenedione and testosterone are turned into dihydrotestosterone at the level of the tissues sensitive to the androgens ( see Note 4 below ). In this way, the origin of many cases of slight hypertrichosis and hirsutism may be an increased activity of this enzyme, resulting on a higher rate of conversion of androstenedione and testosterone into dihydrotestosterone and a consequent major stimulation of the hair-follicles' androgen-receptors. As dihydrotestosterone is an exclusive result of peripheral transformation, it is not produced by the ovaries and adrenals, and this must be quite clear.

In the genesis of several cases of androgenic manifestations in women, several authors also attribute considerable importance to the rate of testosterone's liaison to the SHBG ( sexual hormone binding globulin ), a plasmatic protein that carries the sexual hormones in the bloodstream. In this way, the amount of testosterone linked to the SHBG would not be promptly available in terms of biological action, while the not-linked testosterone ( free-testosterone ) is immediately ready for biological use. It is said that the estrogens, by stimulating the production of SHBG, indirectly increase the liaison of testosterone to this globulin, reducing the amount of free-testosterone.

All cases of hypertrichosis, hirsutism and other androgenic manifestations in women require careful investigation of the ovarian and adrenal function. Nevertheless, most of the cases of slight hypertrichosis and/or hirsutism are mostly due to ovarian dysfunctions and/or constitutional factors. In cases like these, the adrenal dysfunctions do not seem to be so frequent ( or are much harder to detect ). Among the ovarian dysfunctions, the most frequent ones are, as already said, those related to the polycystic ovaries and hyperthecosis. The most frequent adrenal dysfunction is the 21-hydroxylase deficiency. In some cases, ovarian and adrenal dysfunctions may be associated. It is also important to emphasize that we only consider a case as constitutional when the result of all hormonal investigations is normal.

Before finishing, given the complexity of the subject, I would like to make it clear that this is only a very, very introductory article on hypertrichosis, hirsutism and other androgenic manifestations in women. A detailed approach to this subject would obviously require a series of articles. I also would like to remark that I did not mention the several existing treatments for the problem in order to avoid self-medication on the part of some readers.

Note 1: Though they are not the subject of this article, some words must be said about the serious hyperandrogenic disorders. These ones are usually due to severe virilizing adrenal hyperplasias and ovarian and adrenal tumors that produce androgens. A remarkable point here is that the clinical manifestations of these conditions vary according to the phase of life in which they become manifest. If the excessively heightened androgen levels appear during intrauterine life, mostly in the period of sexual differentiation, female fetuses will suffer total or partial masculinization of the external genitals. If they appear in childhood, the result in the female sex will be heterosexual precocious pseudo-puberty ( appearance of some male puberty signs in little girls ). If the very heightened androgen levels appear later in life, women will present severe hirsutism, clitoral hypertrophy, serious menstrual disorders including amenorrhea, male-like changes in the voice, hair loss, etc.

Note 2: The adrenal glands comprehend two regions, the cortical and the medular ones. The cortical region, known as adrenal cortex, produces basically three groups of hormones: 1) the glucocorticoids, of which cortisol is the most important one; 2) the mineralocorticoids, of which aldosterone is the main one; 3) sexual steroids, mostly androgens. The adrenals are an important source of androgens, both in women and men, and this is what matters the most for our subject. The function of the adrenal cortex is mostly controlled by the pituitary through the production of ACTH ( adrenocorticotropic hormone ). As for the adrenal medular region, it produces adrenalin under nervous stimulation.

Note 3: 11-beta-hydroxylase is another adrenal enzyme whose activity is fundamental for the synthesis of aldosterone. By regulating the balance of sodium in the organism, aldosterone is another very important adrenal hormone. There are also cases of virilizing adrenal hyperplasias due to a deficiency of 11-beta-hydroxylase, but they are very rare.

Note 4: In men, a congenital deficiency of 5-alpha-reductase causes the androgen insensitivity syndrome, formerly known as testicular feminization.

Nelson Soucasaux is a gynecologist dedicated to Clinical, Preventive and Psychosomatic Gynecology. Graduated in 1974 by Faculdade de Medicina da Universidade Federal do Rio de Janeiro, he is the author of several articles published in medical journals and of the books "Novas Perspectivas em Ginecologia" ("New Perspectives in Gynecology") and "Os Órgãos Sexuais Femininos: Forma, Função, Símbolo e Arquétipo" ("The Female Sexual Organs: Shape, Function, Symbol and Archetype"), published by Imago Editora, Rio de Janeiro, 1990, 1993.

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