The endocrine disorders encountered most frequently in gynecologic patients are those related to disturbances in the regular occurrence of ovulation and accompanying menstruation. The most prevalent are those characterized by androgen excess, often with insulin resistance, including what is arguably the most common endocrinopathy in women— polycystic ovary syndrome (PCOS). Other conditions leading to ovulatory dysfunction, hirsutism, or virilization, and common disorders of the pituitary and thyroid glands associated with reproductive abnormalities, are reviewed in this chapter.
Hyperandrogenism most often presents as hirsutism, which arises as a result of androgen excess related to abnormalities of function in the ovary or adrenal glands, constitutive increase in expression of androgen effects at the level of the pilosebaceous unit, or a combination of the two. By contrast, virilization is rare and indicates marked elevations in androgen levels. An ovarian or adrenal neoplasm that may be benign or malignant commonly causes virilization.
Hirsutism Hirsutism, the most frequent manifestation of androgen excess in women, is defined as excessive growth of terminal hair in a male distribution. This refers particularly to midline hair, side burns, moustache, beard, chest or intermammary hair, and inner thigh and midline lower back hair entering the intergluteal area. The response of the pilosebaceous unit to androgens in these androgen responsive areas transforms vellus hair (fine, nonpigmented, short) that is normally present into terminal hair (coarse, stiff, pigmented, and long).
Androgen effects on hair vary in relation to specific regions of the body surface. Hair that shows no androgen dependence includes lanugo, eyebrows, and eyelashes. The hair of the limbs and portions of the trunk exhibits minimal sensitivity to androgens. Pilosebaceous units of the axilla and pubic region are sensitive to low levels of androgens, such that the modest androgenic effects of adult levels of androgens of adrenal origin are sufficient for substantial expression of terminal hair in these areas. Follicles in the distribution associated with male patterns of facial and body hair (midline, facial, inframammary) require higher levels of androgens, as seen with normal testicular function or abnormal ovarian or adrenal androgen production. Scalp hair is inhibited by gonadal androgens, in varying degrees, as determined by age and genetic determination of follicular responsiveness, resulting in the common frontal-parietal balding seen in some males and in virilized females. Hirsutism results from both increased androgen production and skin sensitivity to androgens. Skin sensitivity depends on the genetically determined local activity of 5α-reductase, the enzyme that converts testosterone to dihydrotestosterone (DHT), the bioactive androgen in hair follicles.
Hair demonstrates cyclic activity between growth (anagen), involution (catagen), and resting (telogen) phases. The durations of both the growth and resting phases vary according to region of the body, genetic factors, age, and hormonal effects. The cycles of growth, rest, and shedding are normally asynchronous, but when synchronous entry into telogen phase is triggered by major metabolic or endocrine events, such as pregnancy and delivery, or severe illness, dramatic (although transient) hair loss may occur in the following months (telogen efﬂuvium).
Hirsutism is a relative, rather than absolute, designation. What is normal in one setting may be considered abnormal in others; social and clinical reactions to hirsutism can vary significantly, reﬂecting ethnic variation in skin sensitivity to androgens and cultural ideals. Androgen-dependent hair (excluding pubic and axillary hair) occurs in only 5% of premenopausal white women and is considered abnormal by white women of North America, whereas considerable facial and male pattern hair in other areas may be more common and more often considered acceptable and normal among such groups as the Inuit and women of Mediterranean background.