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    Clomid (clomiphene) is a non-steroidal fertility medicine. It causes the pituitary gland to release hormones needed to stimulate ovulation (the release of an egg from the ovary). Clomid is used to cause ovulation in women with certain medical conditions (such as polycystic ovary syndrome) that prevent naturally occurring ovulation. Clomid may also be used for purposes not listed in this medication guide. You should not use Clomid if you have: liver disease, abnormal vaginal bleeding, an uncontrolled adrenal gland or thyroid disorder, an ovarian cyst (unrelated to polycystic ovary syndrome), or if you are pregnant. You should not use Clomid if you are allergic to clomiphene, or if you have: Do not use Clomid if you are already pregnant. Talk to your doctor if you have concerns about the possible effects of Clomid on a new pregnancy. Clomiphene can pass into breast milk and may harm a nursing baby. Less common effects (1-10% of people) include visual symptoms (blurred vision, double vision, floaters, eye sensitivity to light, scotomata), headaches, vasomotor flushes (or hot flashes), light sensitivity and pupil constriction, abnormal uterine bleeding and/or abdominal discomfort. Clomifene can lead to multiple ovulation, hence increasing the chance of twins (10% of births instead of ~1% in the general population) and triplets. Some studies have suggested that clomifene citrate if used for more than a year may increase the risk of ovarian cancer. The incidence of fetal and neonatal abnormalities for patients on clomifene for fertility is similar to that seen in the general population. There is no data to suggest a higher rate of congenital anomalies or spontaneous abortions after using this drug. Compared to letrozole, another drug used for ovarian stimulation, a study found no significant difference in the rate of overall abnormalities, but found that congenital cardiac anomalies was significantly higher in the clomifene group compared to the letrozole group. Clomifene is a nonsteroidal SERM that inhibits estrogen receptors in the hypothalamus, inhibiting negative feedback of estrogen on gonadotropin release, leading to up-regulation of the hypothalamic–pituitary–gonadal axis.

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