For those women who become pregnant while taking bromocriptine to treat a return of spontaneous ovulations, discontinuation of bromocriptine is recommended. This does not preclude subsequent use of bromocriptine during the pregnancy to treat symptoms (visual field defects, headaches) that arise from further enlargement of the microadenoma (301,321–323).
Bromocriptine did not exhibit teratogenicity in animals, and observational data do not suggest harm to pregnancy or fetus in humans.
Pregnant women with previous transsphenoidal surgery for microadenomas or macroadenomas may be monitored with monthly Goldman perimetry visual field testing. Periodic MRI scanning may be necessary in women with symptoms or visual changes. Breastfeeding is not contraindicated in the presence of microadenomas or macroadenomas (301,321–323). The use of bromocriptine and presumably other dopaminergic agents that may cause blood pressure elevation during the postpartum period is contraindicated (324–328).
Thyroid disorders are 10 times more common in women than men. Approximately 1% of the female population of the United States will develop overt hypothyroidism (329). Even prior to the discovery of the long-acting thyroid stimulator (LATS) in women with Graves disease in 1956, numerous investigations demonstrated a link between these autoimmune thyroid disorders and reproductive physiology and pathology (330).
Thyroid Hormones Iodide is a critical component of the class of hormones known as thyronines, among which the most important are triiodothyronine (T3) and thyroxine (T4). Iodide obtained from dietary sources is actively transported into the thyroid follicular cell for the synthesis of these hormones. The sodium–iodide symporter (NIS) is a key molecule in thyroid function. It allows the accumulation of iodide from the circulation into the thyrocyte against an electrochemical gradient. The NIS requires energy that is supplied by Na-K ATPase, and iodine uptake is stimulated by TSH or thyrotropin. The enzyme thyroid peroxidase (TPO) then oxidizes iodide near the cell-colloid surface and incorporates it into tyrosyl residues within the thyroglobulin molecule, which results in the formation of monoiodotyrosine (MIT) and diiodotyrosine (DIT). T3 and T4, formed by secondary coupling of MIT and DIT, are catalyzed by TPO. The membrane-bound, heme-containing oligomer, TPO, is localized in the rough endoplasmic reticulum, Golgi vesicles, lateral and apical vesicles, and on the follicular cell surface. Thyroglobulin, the major protein formed in the thyroid gland, has an iodine content of 0.1% to 1.1% by weight. About 33% of the iodine is present in thyroglobulin in the form of T3 and T4, and the remainder is present in MIT and DIT or found as unbound iodine. Thyroglobulin provides a storage capacity capable of maintaining a euthyroid state for nearly 2 months without the formation of new thyroid hormones. The thyroid antimicrosomal antibodies found in patients with autoimmune thyroid disease are directed against the TPO enzyme (331,332).