On day 21 of the menstrual cycle, high levels of estrogen and progesterone cause negative feedback inhibition at the hypothalamus and anterior pituitary. As a result, decreased LH levels leads to atrophy of the corpus luteum, subsequently leading to decreased production of estrogen and progesterone. This will release the feedback inhibition of the hypothalamus and anterior pituitary, causing the FSH level to rise again at day 22.
Clomiphene is given at day 2 menses. By that time, FSH level is rising steadily, causing development of a few follicles. Follicles in turn produce the estrogen, which circulates in serum. Clomiphene acts by inhibiting the action of estrogen on the hypothalamus. Zuclomifene, the more active isomer (see below), binds to estrogen receptors and stays bound for long periods of time. This prevents normal receptor recycling and causes an effective reduction in hypothalamic estrogen receptor number. As a result, the body perceives a low level of estrogen, similar to day 22 in the previous cycle. Since estrogen can no longer effectively exert negative feedback on the hypothalamus, GnRH secretion becomes more pulsatile, which results in increased pituitary gonadotropin (FSH, LH) release. Increased FSH level causes growth of more ovarian follicles, and subsequently rupture of follicles resulting in ovulation.
Thursday, November 19, 2009
Monday, November 16, 2009
Clomid - Clinical Pharmacology
Action
Clomid is a drug of considerable pharmacologic potency. With careful selection and proper management of the patient, Clomid has been demonstrated to be a useful therapy for the anovulatory patient desiring pregnancy.
Clomiphene citrate is capable of interacting with estrogen-receptor-containing tissues, including the hypothalamus, pituitary, ovary, endometrium, vagina, and cervix. It may compete with estrogen for estrogen-receptor-binding sites and may delay replenishment of intracellular estrogen receptors. Clomiphene citrate initiates a series of endocrine events culminating in a preovulatory gonadotropin surge and subsequent follicular rupture. The first endocrine event in response to a course of clomiphene therapy is an increase in the release of pituitary gonadotropins. This initiates steroidogenesis and folliculogenesis, resulting in growth of the ovarian follicle and an increase in the circulating level of estradiol. Following ovulation, plasma progesterone and estradiol rise and fall as they would in a normal ovulatory cycle.
Available data suggest that both the estrogenic and antiestrogenic properties of clomiphene may participate in the initiation of ovulation. The two clomiphene isomers have been found to have mixed estrogenic and antiestrogenic effects, which may vary from one species to another. Some data suggest that zuclomiphene has greater estrogenic activity than enclomiphene.
Clomiphene citrate has no apparent progestational, androgenic, or antiandrogenic effects and does not appear to interfere with pituitary-adrenal or pituitary-thyroid function.
Although there is no evidence of a "carryover effect" of Clomid, spontaneous ovulatory menses have been noted in some patients after Clomid therapy.
Clomid is a drug of considerable pharmacologic potency. With careful selection and proper management of the patient, Clomid has been demonstrated to be a useful therapy for the anovulatory patient desiring pregnancy.
Clomiphene citrate is capable of interacting with estrogen-receptor-containing tissues, including the hypothalamus, pituitary, ovary, endometrium, vagina, and cervix. It may compete with estrogen for estrogen-receptor-binding sites and may delay replenishment of intracellular estrogen receptors. Clomiphene citrate initiates a series of endocrine events culminating in a preovulatory gonadotropin surge and subsequent follicular rupture. The first endocrine event in response to a course of clomiphene therapy is an increase in the release of pituitary gonadotropins. This initiates steroidogenesis and folliculogenesis, resulting in growth of the ovarian follicle and an increase in the circulating level of estradiol. Following ovulation, plasma progesterone and estradiol rise and fall as they would in a normal ovulatory cycle.
Available data suggest that both the estrogenic and antiestrogenic properties of clomiphene may participate in the initiation of ovulation. The two clomiphene isomers have been found to have mixed estrogenic and antiestrogenic effects, which may vary from one species to another. Some data suggest that zuclomiphene has greater estrogenic activity than enclomiphene.
Clomiphene citrate has no apparent progestational, androgenic, or antiandrogenic effects and does not appear to interfere with pituitary-adrenal or pituitary-thyroid function.
Although there is no evidence of a "carryover effect" of Clomid, spontaneous ovulatory menses have been noted in some patients after Clomid therapy.
Sunday, October 11, 2009
What is Clomid?
Clomid is the brand name for the fertility drug clomiphene citrate. Clomiphene citrate may also be sold under the brand name Serophene. Whether you’re taking the brand name Clomid, Serophene, or a generic version of clomiphene citrate, it’s all the same drug.
Subscribe to:
Posts (Atom)