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" Data were abstracted from Vessey et al. (1982). b The data concerning the number of women in the United States that employ the indicated contraceptive procedure were abstracted from Mosher, W. D., and Pratt, W. F. (1990). Contraceptive use in the United States. Patient Education Council 16, 163.

c Periodic abstinance from coital activity during periods of presumed fertility.

" Data were abstracted from Vessey et al. (1982). b The data concerning the number of women in the United States that employ the indicated contraceptive procedure were abstracted from Mosher, W. D., and Pratt, W. F. (1990). Contraceptive use in the United States. Patient Education Council 16, 163.

c Periodic abstinance from coital activity during periods of presumed fertility.

wedge resection. Clomiphene is an antiestrogen compound that blocks the binding of estrogen to its receptor. Clomiphene's effectiveness as an inducer of ovulation is believed to occur as a consequence of it functioning as an analogue of circulating estradiol. This permits GnRH to be secreted, leading to pituitary release of LH and FSH.

Polycystic ovary disease is the most common form of anovulation and is often associated with hirsutism. The hirsutism results from excessive androgen production that is in some unknown way linked with the inability to ovulate.

C. Hirsutism

Hirsutism or the heavy, abnormal growth of hair in the female is a medical problem of endocrine origin. Hair may be classified as either terminal hair (coarse and pigmented) or vellus hair (fine, soft, and unpig-mented). The hair follicle may produce either terminal or vellus hair in response to appropriate stimuli. In hirsutism there is an androgen-dependent transition to the production of terminal hair. Androgens neither increase the number of hair follicles nor increase the mitotic rate of the cells of the connective tissue of the papillae of the hair follicle. Instead, androgens mediate an increase in the number and size of the cells of the papilla, which leads to an increase in hair growth rate and diameter.

Most commonly hirsutism results from inappropriately high plasma levels of testosterone and its precursors. If the elevated plasma level of testosterone is extensive over a prolonged time interval (e.g., years), virilization (masculinization) may also occur. The most common causes of elevated levels of testosterone in the female are congenital adrenal hyperplasia (see Chapter 10) or the presence of a tumor in the adrenal cortex, hyperplasia of the androgen-producing cells (the stromal and thecal cells) of the ovaries or an ovarian tumor, and occasionally polycystic ovary disease. Hirsutism may result from the inappropriate production of testosterone or the testosterone precursors dehydroepiandrosterone, 3a-androstanediol, or androst-4-ene-3,17-dione (see Figure 2-22).

D. Primary Amenorrhea

Amenorrhea is the absence of expected menstrual periods. When the menarche has not occurred by age 16, it is appropriate to seek an explanation. If there has been no change in the growth of breasts, appearance of pubic hair, or changes in vaginal smears, this suggests a tentative diagnosis of primary amenorrhea. The disorder can be due to either extra-gonadal or gonadal problems. One retrospective analysis found that gonadal dysgeneses and primary gonadal failure in phenotypic females who were genetic males accounted for about 40% of the patients with primary amenorrhea. An additional 20% have a gonadal dysfunction (e.g., polycystic ovaries) or "resistant ovary syndrome." In about 40% of cases, the etiological basis for the amenorrhea could be attributed to dysplasia of the Miillerian ducts or hypogonadotropic states.

E. Breast Cancer

The topic of breast cancer is reviewed at the end of Chapter 14.

F. Menopause

Cessation of reproductive activity is associated with a number of bodily changes, resulting from changes in the circulating levels of estrogen, progesterone, FSH, and LH. A major problem can be the development of the bone disease osteoporosis. Osteoporosis is a thinning of the skeleton that, if it occurs over a long enough time interval, incurs the definite risk of increased accidental or spontaneous fracture. In the view of many,

figure 13-21 Structures of steroids used as oral contraceptives: (A) combination pills containing an estrogen + progestin; (B) the progestin-only pill; (C) RU-486 or mifepristone, which can be utilized as an abortifacient.

the onset of osteoporosis is initiated by the absence of estradiol (see Chapter 9).


A. Books

Knobil, E., and Neill J. D. (1994). "The Physiology of Reproduction," 2nd ed., Vol. 2. Raven Press, New York.

B. Review Articles

Burger, H. G. (1992). Inhibin. Reprod. Med. Rev. 1,1-20. Djerassi, C. (1995). The mother of the pill. In "Recent Progress in Hormone Research" (C. W. Bardin, ed.), Vol. 50, pp. 1-17. Academic Press, San Diego.

Gaddy-Kurten, D., Tsuchida, K., and Vale, W. (1995). Activins and the receptor serine kinase superfamily. In "Recent Progress in Hormone Research" (C. W. Bardin, ed.), Vol. 50, pp. 109-129. Academic Press, San Diego. Gorski, J., Furlow, J. D., Murdock, F. E., Fritsch, M., Kaneko, K., Ying, C., and Maleeyer, J. R. (1993). Perturbations in the model of the estrogen receptor regulation of gene expression. Biol. Re-prod. 48, 8-14.

Hall, J. E., and Crowley, W. F., Jr. (1995). Gonadotropins and the gonad: normal physiology and their disturbances in clinical endocrine diseases. In "Endocrinology" (L. J. DeGroot, M. Besser,

H. G. Burger, J. L. Jameson, D. L. Loriaux, J. C. Marshall, W. D. Odell, J. T. Potts, Jr., and A. H. Rubenstein, eds.), 3rd ed., Vol.

I, Chapter 15, pp. 242-258. W. B. Saunders Company, Philadelphia, PA.

Mathews, L. S. (1994). Activin receptors and cellular signaling by the receptor serine kinase family. Endocr. Rev. 15, 310-325.

McEwen, B. S. (1991). Steroid hormones and thyroid hormones modulate a changing brain. /. Steroid Biochem. Mol. Biol. 40, 1-14.

Odell, W. D. (1979). The reproductive system in women. In "Endocrinology" (L. J. DeGroot, et al, eds.), Vol. 3, p. 1385. Glunt & Stratton New York.

Parker, M. G. (1995). Structure and function of estrogen receptors. Vitamins Hormones 51, 267-287.

Richards, J. S. (1994). Hormonal control of gene expression in the ovary. Endocr. Rev. 15, 725-751.

Tsai, J.-J., and O'Malley, B. W. (1994). Molecular mechanisms of action of steroid/thyroid receptor superfamily members. Annu. Rev. Biochem. 63, 451-486.

C. Research Papers

Billig, H., Furuta, I., and Hsueh, A. J. W. (1993). Estrogens inhibit and androgens enhance ovarian granulosa cell apoptosis. Endocrinology 133, 2204-2212.

Chen, C. L. (1993). Inhibin and activin as paracrine/ autocrine factors. Endocrinology 132, 4-5.

Conn, M. P., and Crowley, W. F. (1994). Gonadotropin releasing hormone and its analogs. Annu. Rev. Med. 45, 391-405.

DePaolo, L. V., Bicsak, T. A., Erickson, G. F., Shimasaki, S., and Ling, N. (1991). Follistatin and activin: a potential intrinsic regulatory system within diverse tissues. Proc. Soc. Exp. Biol. Med. 198, 500-512.

Fitzpatrick, S. L., and Richards, J. S. (1994). Identification of a cyclic 3',5'-monophosphate response element in the rat aromatase promoter that is required for transcriptional activation in rat granulosa cells and R2C Leydig cells. Mol. Endocrinol. 8, 1309-1319.

Hashimoto, M., Nakamura, T., Inoue, S., Kondo, T., Yamada, R., Eto, Y., Sugino, H., and Muramatsu, M. (1992). Follistatin is a developmentally regulated cytokine in neural differentiation. /. Biol. Chem. 267, 7303-7306.

Heckert, L. L., Daley, I. J., and Griswold, M. D. (1992). Structural organization of the follicle stimulating receptor gene. Mol. Endocrinol. 6, 70-80.

Hill, N. C. W., Furguson, J., and MacKenzie, I. Z. (1990). The efficacy of oral mifepristone (RU 38,486) with a prostaglandin E! analog vaginal pessary for the termination of early pregnancy: Complications and patient acceptability. Am. J. Obstet. Gynecol. 162, 414-417.

Inouye, S., Guo, Y., DePaolo, I., Shimonaka, M., Ling, N., and Shimasaki, S. (1991). Recombinant expression of human follistatin with 315 and 288 amino acids: Chemical and biological comparison with native porcine follistatin. Endocrinology 129, 815-822.

Marshall, J. A. (1968). A field trial of the basal body temperature method of regulating births. Lancet 2, 8-10.

Michel, U., Farnworth, P., and Findlay, J. K. (1993). Follistatins: more than follicle-stimulating hormone suppressing proteins. Mol. Cell. Endocrinol. 91, 1-11.

Nakamura, T., Takio, K., Eto, Y., Shibai, H., Titani, K., and Sugino, H. (1989). Activin-binding protein from rat ovary is follistatin. Science 247, 836-838.

Robertson, D. M., Foulds, L. M., Prisk, M„ and Hedger, M. P. (1992). Inhibin/ activin b subunit monomer: Isolation and characterization. Endocrinology 130, 1680-1687.

Shimonaka, M., Inouye, S., Shimasaki, S., and Ling, N. (1991). Follistatin binds to both activin and inhibin through the common beta-subunit. Endocrinology 128, 3313-3315.

Thomsen, G., Woolf, T., Whitman, M., Sokol, S., Vaughan, J., Vale, W., and Melton, D. A. (1990). Activins are expressed early in Xeropus embryogenesis and can induce axial mesoderm and anterior structures. Cell 63, 485-493.

Ueno, N., Ling, N., Ying, S. Y., Esch, F., Shimasaki, S., and Guillemin, R. (1987). Isolation and partial characterization of follistatin: A single chain Mr 35,000 monomeric protein that inhibits the release of follicle stimulatory hormone. Proc. Natl. Acad. Sci. USA 84, 8282-8286.

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