The basic principle is to limit fetal exposure to the drug to as little time as possible. In untreated individuals, optic cross compression occurs in approximately 5% of pregnancies with PRL microadenomas, whereas the likelihood of this risk in patients with macroadenomas after pregnancy is 25% or more. Therefore, patients with PRL adenomas should use contraception other than oral contraceptives when treated with dopamine agonists. Patients with microadenomas prior to pregnancy should discontinue bromocriptine after pregnancy is clearly established because the risk of tumor enlargement is less. Blood PRL levels and visual field examinations should be measured periodically after discontinuation. PRL levels can increase about 10-fold after pregnancy in normal individuals. Patients with blood PRL levels significantly exceeding pretreatment PRL levels should be closely monitored for blood PRL and increased density of visual field examination. Once visual field defects or cavernous sinus syndrome are detected, the immediate addition of bromocriptine can be expected to improve the relief within 1 week. If no improvement is seen, surgery should be considered. In women with macroadenomas that extend beyond the pyriform saddle, pregnancy when bromocriptine alone is used can result in clinically significant tumor enlargement in 20% to 25%; there is no definitive best treatment, and the patient must make a highly individualized choice after multiple treatment options have been clearly discussed and documented. Patients with macroadenomas who must become pregnant are allowed to do so only after the adenoma has shrunk with bromocriptine therapy (PRL), and bromocriptine should be given continuously throughout the pregnancy. Women taking bromocriptine have been found to be pregnant, and the available information establishes that the recommendation for therapeutic abortion is not warranted. Although, as noted earlier, radiotherapy before pregnancy (followed by bromocriptine) reduces the risk of tumor enlargement to only 4.5%, radiotherapy is rarely curative. Radiotherapy can also lead to long-term hypopituitarism, so this treatment is less acceptable and is not recommended. All patients with pituitary PRL adenomas in combination with pregnancy need to be evaluated every 2 months during pregnancy. If the tumor enlarges during pregnancy and causes appropriate symptoms, bromocriptine can be given again to control tumor growth, and the medication may have less impact on the mother and fetus than surgery. Medication requires close monitoring, and in the absence of response to bromocriptine and progressive deterioration of visual field, treatment should be by pterosynovial surgery and delivery at the earliest possible time (near full term). Clomiphene is used to promote ovulation in patients who do not ovulate despite normalization of PRL on medication. For patients who have normal PRL levels on medication but have not recovered ovarian function and are seeking to have children, treatment to promote the recovery of ovarian function should be used aggressively. Conventional ovulation promotion treatment with clomiphene (CC). Clomiphene (Cloniphene, CC for short) is also known as clomiphene, clostebolamine. It is a non-steroidal anti-estrogen, similar in structure to estrogen, and has both anti-estrogenic and weak estrogenic activities. It indirectly promotes the release of gonadotropin releasing hormone (GnRH) from the pituitary gland by inhibiting the negative feedback effect of endogenous estrogen on the hypothalamus, stimulating the secretion of gonadotropins from the pituitary gland, exciting the activity of the ovaries and promoting the development of follicles. CC also has a weak estrogenic effect, which can act directly on the ovaries of the pituitary gland to increase their sensitivity and responsiveness, and promote the activity of the ovarian sex hormone synthesis system, increase the synthesis and secretion of sex hormones, and promote the positive feedback effect of estradiol (E2). Due to the appearance of blood E2 peak before ovulation, it exerts a positive feedback effect on the hypothalamic-pituitary-ovarian axis (HPOA), stimulates the pituitary LH peak and promotes ovulation. CC for ovulation is only suitable for patients with certain pituitary function, if the pituitary macroadenoma or surgical destruction of pituitary tissue is more serious, the pituitary function is impaired then CC for ovulation is ineffective. Postoperative hypogonadotropic patients using gonadotropic hormones to promote ovulation When CC ovulation is ineffective, or the pituitary gland tissue is destroyed after surgery for pituitary adenomas, the function of the pituitary gland is impaired, resulting in hypogonadotropic amenorrhea, the patient can use exogenous human gonadotropin (Gn) to promote ovulation. Gn is divided into human pituitary gonadotropin and human chorionic gonadotropin (hCG). Human pituitary gonadotropin is divided into follicle stimulating hormone (FSH) and luteinizing hormone (LH). Low Gn after pituitary tumor surgery should be human postmenopausal urinary gonadotropin (HMG, each containing 75 IU FSH and 75 IU LH) ovulation treatment is appropriate to promote follicular development and maturation, and use HCG to induce ovulation. Due to individual differences in ovarian sensitivity to gonadotropins, low-dose HMG should be used, generally starting with HMG 75 IU once daily for 5-7 days to monitor follicular development, and if there is no obvious follicular development, increase the dosage of HMG by 75 IU/day every 5-7 days, and do not increase the dosage of Gn too fast to prevent severe ovarian hyperstimulation syndrome (OH). Do not increase Gn too fast to prevent severe ovarian hyperstimulation syndrome (OHSS). HCG was injected when the diameter of the largest follicle reached 18mm.