INTRODUCTION

Lactotroph adenomas (prolactinomas) usually cause infertility because of the inhibitory effect of prolactin on gonadotropin secretion and sometimes because of the mass effect of a macroadenoma. However, our ability to treat both of these abnormalities allows most women with this disorder to become pregnant. Management during pregnancy is based on knowledge of the risks to the mother and the fetus.

The management of women with lactotroph adenomas during pregnancy will be reviewed here. Other aspects of hyperprolactinemia and lactotroph adenomas are reviewed separately. (See "Clinical manifestations and diagnosis of hyperprolactinemia" and "Causes of hyperprolactinemia" and "Treatment of hyperprolactinemia due to lactotroph adenoma and other causes".)

OVERVIEW

Goals of treatment — Treatment of women with lactotroph adenomas should begin before conception with advice to the woman and her partner about the risks of pregnancy to her (adenoma growth) and the fetus (exposure to dopamine agonists). Current data suggest that bromocriptine use during the first month of pregnancy (eg, ovulation induction) does not harm the fetus. Data for cabergoline are reassuring as well. However, insufficient data are available about the use of either drug later in pregnancy. The main goals of treatment for women with lactotroph adenomas considering pregnancy include:

• Women with microadenomas – Lower serum prolactin into the normal range to induce ovulation.
• Women with macroadenomas – Administer dopamine agonists or perform transsphenoidal surgery to decrease tumor size before attempting to conceive.
• During pregnancy, all women should be monitored for possible adenoma growth; growth that affects visual function should be treated with dopamine agonists or, if necessary, surgery (only in second trimester).

Effect of pregnancy on tumor size — The principal risk during pregnancy to a mother with a lactotroph adenoma is an increase in adenoma size sufficient to cause neurologic symptoms, most importantly visual impairment. The theoretical basis for an increase in size during pregnancy is that hyperestrogenemia causes lactotroph hyperplasia. As an example of the normal effect of estrogen, a study of 20 normal nonpregnant women and 32 normal pregnant women showed a progressive increase in pituitary size, as assessed by MR imaging, throughout pregnancy, so that the volume during the third trimester was more than double that in nonpregnant women (figure 1) [1]. Similarly, in women with lactotroph adenomas who become pregnant, the hyperestrogenemia of pregnancy may increase the size of the adenoma.