Bạn đang xem bản rút gọn của tài liệu. Xem và tải ngay bản đầy đủ của tài liệu tại đây (119.4 KB, 5 trang )
Chapter 050. Hirsutism and
Virilization
(Part 3)
Hormonal Evaluation
Androgens are secreted by the ovaries and adrenal glands in response to
their respective tropic hormones, luteinizing hormone (LH) and
adrenocorticotropic hormone (ACTH).
The principal circulating steroids involved in the etiology of hirsutism are
testosterone, androstenedione, and dehydroepiandrosterone (DHEA) and its
sulfated form (DHEAS).
The ovaries and adrenal glands normally contribute about equally to
testosterone production. Approximately half of the total testosterone originates
from direct glandular secretion, and the remainder is derived from the peripheral
conversion of androstenedione and DHEA (Chap. 340).
Although it is the most important circulating androgen, testosterone is, in
effect, the penultimate androgen in mediating hirsutism; it is converted to the
more potent dihydrotestosterone (DHT) by the enzyme 5α-reductase, which is
located in the PSU.
DHT has a higher affinity for, and slower dissociation from, the androgen
receptor. The local production of DHT allows it to serve as the primary mediator
of androgen action at the level of the pilosebaceous unit. There are two
isoenzymes of 5α-reductase: type 2 is found in the prostate gland and in hair
follicles, whereas type 1 is found primarily in sebaceous glands.
One approach to testing for hyperandrogenemia is depicted in Fig. 50-2. In
addition to measuring blood levels of testosterone and DHEAS, it is also
important to measure the level of free (or unbound) testosterone.
The fraction of testosterone that is not bound to its carrier protein, sex-
hormone binding globulin (SHBG), is biologically available for conversion to
DHT and for binding to androgen receptors.
Hyperinsulinemia and/or androgen excess decrease hepatic production of