After stabilization of tumor size is documented, the MRI scan is repeated 6 months later and, if stable, yearly for several years. This examination may be performed earlier if new symptoms develop or if there is no improvement in symptoms. Serum prolactin levels are measured every 6 months.
Because tumors may enlarge despite normalized prolactin values, a reevaluation of symptoms at regular intervals (6 months) is prudent. Normalized prolactin levels or resumption of menses should not be taken as absolute proof of tumor response to treatment (306,308).
Surgical Intervention Tumors that are unresponsive to bromocriptine or that cause persistent visual field loss require surgical intervention. Some neurosurgeons have noted that a short (2-to 6-week) preoperative course of bromocriptine increases the efficacy of surgery in patients with larger adenomas (291). Unfortunately, despite surgical resection, recurrence of hyperprolactinemia and tumor growth is common. Complications of surgery include cerebral carotid artery injury, diabetes insipidus, meningitis, nasal septal perforation, partial or panhypopituitarism, spinal ﬂuid rhinorrhea, and third nerve palsy. Periodic MRI scanning after surgery is indicated, particularly in patients with recurrent hyperprolactinemia.
Occasionally, patients with hypothyroidism exhibit hyperprolactinemia with remarkable pituitary enlargement caused by thyrotroph hyperplasia. These patients respond to thyroid replacement therapy with reduction in pituitary enlargement and normalization of prolactin levels (309).
Hyperprolactinemia occurs in 20% to 75% of women with chronic renal failure. Prolactin levels are not normalized through hemodialysis but are normalized after transplantation (310–312). Occasionally, women with hyperandrogenemia also have hyperprolactinemia. Elevated prolactin levels may alter adrenal function by enhancing the release of adrenal androgens such as DHEAS (313).
Numerous drugs interfere with dopamine secretion and can be responsible for hyperprolactinemia and its attendant symptoms (Table 31.9). If medication can be discontinued, resolution of hyperprolactinemia is uniformly prompt. If not, endocrine management should be directed at estrogen replacement and normalization of menses for those with disturbed or absent ovulation. Treatment with dopamine agonists may be utilized if ovulation is desired and the drug-inducing hyperprolactinemia cannot be discontinued.
Use of Estrogen in Hyperprolactinemia
In rodents, pituitary prolactin-secreting adenomas occur with high-dose estrogen administration (314). Elevated levels of estrogen, as found in pregnancy, are responsible for hypertrophy and hyperplasia of lactotrophic cells and account for the progressive increase in prolactin levels in normal pregnancy. The increase in prolactin during pregnancy is physiologic and reversible; adenomas are not fostered by the hyperestrogemia of pregnancy. Pregnancy may have a favorable inﬂuence on preexisting prolactinomas (315,316). Estrogen administration is not associated with clinical, biochemical, or radiologic evidence of growth of pituitary microadenomas or the progression of idiopathic hyperprolactinemia to an adenoma status (317–320). For these reasons, estrogen replacement or OC use is appropriate for hypoestrogenic patients with hyperprolactinemia secondary to microadenoma or hyperplasia.
Prolactin-secreting microadenomas rarely create complications during pregnancy. Monitoring of patients with serial gross visual field examinations and funduscopic examination is recommended. If persistent headaches, visual field deficits, or visual or funduscopic changes occur, MRI scanning is advisable. Because serum prolactin levels progressively rise throughout pregnancy, prolactin measurements are rarely of value.