TAILIEUCHUNG - 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. | 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 5a-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 5a-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 SHBG resulting in levels of total testosterone within the high-normal range whereas the unbound hormone is more substantially elevated. Although there is a decline in ovarian testosterone production after menopause ovarian .

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