Approach To Hirsutism

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Hirsutism should be viewed as both an endocrine and a cosmetic problem. It is most commonly associated with anovulation; however, other causes of increased androgen levels must be ruled out, such as adrenal and ovarian diseases. The most sensitive marker of excess androgen production is hirsutism.

followed by acne, oily skin, increased libido, and virilization. Virilization consists of clitoromegaly. deepening of the voice, balding, increased muscle mass, and male body habitus. Adrenal hyperplasia and androgen-secreting tumors of the adrenal gland or ovary are causes of virilization. Treatment depends on the underlying etiology.

The pattern of hair growth is genetically predetermined. Differences in hair growth between ethnic groups are secondary to variations in hair follicle concentration and 5-a-reductase activity. Hair growth can be divided into three phases: anagen (growing phase), catagen (involution phase), and telogen (quiescent phase). Hair length is determined by the length of the anagen phase, and the stability of hair is determined by the length of the telogen phase. Hair found on the face, axilla, chest, breast, pubic area, and anterior thighs are termed "sex hair" because they respond to sex hormones. Androgens (especially testosterone) initiate growth of, and increase the diameter and pigmentation of, "sex hair." Androgens may be produced by the ovary or adrenal gland or by peripheral conversion. Dehydroepiandrosterone sulfate (DHEA-S) is derived almost exclusively from the adrenal gland. Dihydrotestosterone (DHT) is metabolized from testosterone by 5-a-reductase; increased activity of 5-a-reductase leads to an increase in DHT and stimulation of hair growth. The majority of testosterone is bound to sex hormone-binding globulin (SHBG), and it is the unbound portion that is primarily responsible for androgenicity. Hyperandrogenism decreases SHBG and thus exacerbates hirsutism.

The appearance and cosmetic changes associated with hirsutism depend on the number of follicles present, ratio of growth to resting phases, asynchrony of growth cycles, and thickness and degree of pigmentation of individual hairs. The history should focus on the onset and duration of symptoms (faster growth is associated with tumors of adrenal and ovary, whereas slow onset since menarche more likely is PCOS). The severity of symptoms should be characterized (e.g., virilization is rare and usually is associated with androgen-secreting tumors). The regularity of the menses and symptoms of thyroid disease should be sought. Physical examination should focus on the location of hair growth and its severity, thyromegaly. body shape and habitus, presence of breast discharge, skin changes (acanthosis or abdominal striae), adnexal or abdominal masses, and external genitalia. Helpful laboratory tests include assays for serum testosterone, DHEA-S, 17-hydroxyprogesterone (which is elevated with congenital adrenal hyperplasia), prolactin, and thyroid-stimulating hormone. A markedly elevated testosterone level suggests an andro-gen-secreting ovarian tumor, such as a Sertoli-Leydig cell tumor. With a high DHEA-S level, the examiner should be suspicious of an adrenal process, such as adrenal hyperplasia or a tumor.

The differential diagnosis for hirsutism (Table 59-1) includes anovulation, late-onset adrenal hyperplasia, androgen-secreting tumors (adrenal or ovarian in origin), Cushing's disease, medications, thyroid disease, and hyperpro-lacUnemia. A genetic defect in the enzyme 21-hydroxylase causes most of the cases of congenital adrenal hyperplasia (CAH). Whereas classic CAH is the

Table 59-1

DIFFERENTIAL DIAGNOSIS OF HIRSUTISM

Table 59-1

DIFFERENTIAL DIAGNOSIS OF HIRSUTISM

DISEASE

HISTORY

PHYSICAL EXAMINATION

LABORATORY TEST

TREATMENT

Cushing's syndrome

Glucose intolerance

Hypertension, buffalo hump, central obesity

Dexamethasone suppression test

Surgical

Adrenal tumor

Rapid-onset virilism

Abdominal mass

DHEA-S

Surgical

Congenital adrenal hyperplasia

Ambiguous genitalia, family history

17-hydroxy-

progesterone

Replace Cortisol and mineralocorticoid

Polycystic ovarian syndrome

rarely virilization

Elevated LH-FSH ratio

Oral contraceptive pills

Sertoli-Leydig Rapid onset Hirsutism. Elevated Surgical cell tumor virilism. testosterone adnexal mass level

Sertoli-Leydig Rapid onset Hirsutism. Elevated Surgical cell tumor virilism. testosterone adnexal mass level most common cause of ambiguous genitalia in the newborn, late onset of non-classic CAH can present in adult females with symptoms of hirsutism and anovulation. An elevated morning fasting 17-hydroxyprogesterone level is highly suggestive of CAH. Treatment depends on the etiology; however, in general, the goal is to decrease the amount of DHT available. This can be accomplished by inhibiting adrenal or ovarian androgen secretion, changing SHBG binding, impairing peripheral conversion of androgen to active androgen, and inhibiting activity at target tissues. Treatment options include weight loss, combined oral contraception pills, spironolactone (a diuretic that is an androgen antagonist), progesterone-containing medications, electrolysis, laser vaporization, waxing, and shaving. The patient must be warned that there is a slow response to treatment with medications (average 6 months). To help with more immediate results, nonmedical therapies (waxing and shaving) can be used initially until the new medication begins to work effectively.

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