beard Male voice

Hair on chest


Rhomboid pubic hair

Feminization of the male due to testosterone deficiency


Masculinization of the female due to testosterone excess

- Hyper-trophic clitoris

Release of Female Sex Hormones

The gonadotropic hormones FSH and LH are released from the anterior lobe of the pituitary gland in a pulsative manner (every 60 to 90 min for 1 min) after pulsatile stimulation by GnRH from the hypothalamus at the same frequency (^ A2; see also p. 272). FSH and LH are essential for the maturing of the follicles and for the temporal coordination of the production of female sex hormones. In the female organism FSH promotes the maturation of the follicles and estrogen production in the granulosa cells of the follicles (^ A2). The estrogens (estrone, estradiol, estriol) at first stimulate the further release of gonadotropins (positive feedback) until the maturation of a follicle leads to ovulation and corpus luteum formation. Progestogens (progesterone and analogs), formed by the corpus luteum under the influence of LH, and the estrogens (after ovulation) inhibit further release of gonadotropins (^A3). The concentration of gonadotropins falls again, as does, after some delay, that of the estrogens and progestogens (^ A4). As a rule this cycle takes 28 days, although the interval between menstruation and ovulation varies greatly. The granulosa cells also form in-hibin and activin, while the theka cells form the androgens androstenedione and testosterone. Activin promotes gonadotropin release, while inhibin suppresses it (see p. 272 for the effect of testosterone). Prolactin produced in the anterior pituitary inhibits the pulsatile release of gonadotropins. It also decreases the ovary's responsiveness to gonadotropins.

An excess of female sex hormones is usually due to an exogenous supply (contraceptive pills). In addition, some tumors produce sex hormones.

A lack of estrogens and progestogens is frequently the result of a decreased GnRH release in severe psychological or physical stress (e.g., malnutrition, serious systemic disease, highperformance sport). GnRH release can also be reduced through the influence of the neuro-transmitters norepinephrine, dopamine, serotonin, and endorphins (^A1).

However, it is not only reduced, but also persistently high concentrations of GnRH (or its analogs) that decrease the release of gonado-tropins (down-regulation of the GnRH recep tors). Even if the hypothalamus is undamaged, gonadotropin release can be impaired by damage to the pituitary (hemorrhage, ischemia, inflammation, trauma), by displacement of go-nadotropin-producing cells by tumors, or by inhibition due to a raised concentration of sex hormones (ovulation inhibitors, anabolic substances with androgen action, tumors, adreno-genital syndrome; ^ p. 264).

Ifandrogen production is raised, the release of FSH is inhibited and follicle maturation is thus interrupted. Polycystic ovaries are formed. Some of the androgens are transformed into estrogens which, via stimulation of LH release, promote further formation of ovarian andro-gens.

It is relatively common for a reduction in gonadotropin release to be due to raised prolactin secretion, for example, as a result of the absence of inhibition of pituitary secretion of prolactin or a prolactin-producing pituitary tumor (^ p. 260). Gonadotropin release can be inhibited by dopaminergic drugs that cause a rise in prolactin secretion. Lastly, gonadotro-pin release can be inhibited by damage to the pituitary through head trauma, abnormal anlage or maturation, radiation, tumors, degenerative or inflammatory disease, or defective biosynthesis.

The formation of estrogens and/or proges-togens can be impaired by ovarian insufficiency caused by an abnormal development (^ p. 278) or by damage (e.g., radiation, chemo-therapeutic agents). Inadequate follicular maturation or transformation in the corpus lu-teum (corpus luteum insufficiency) can cause the deficiency. Lack of estrogen can also be due to an enzyme defect. In the resistant ovary syndrome the ovaries are refractory to the action of gonadotropins. This may be caused by defective receptors or inactivating antibodies. The result is a lack of estrogens despite an increased release of gonadotropins.

i— A. Release of Female Sex Hormones -


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