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Patients with hyperprolactinemia present with ovulatory dysfunction, galactorrhea, delayed pubescence, or signs of a polyendocrinopathy. Four principal causes of hyperprolactinemia are pituitary hyperplasia, which may be the result of dopamine dysfunction; prolactinomas, which are characterized as microadenomas (<10 mm in size) or macroadenomas (>10 mm in size); hypothyroidism; and drug intake. Other causes of hyperprolactinemia are listed below.

The origin of prolactinomas has received intense study. Prolactinomas have been demonstrated to have a blood supply that may be independent from the normal hypothalamic portal anatomy.

The workup of the patient with hyperprolactinemia should consist of the measurement of prolactin levels on multiple occasions. Unfortunately, prolactin assays are subject to great variation. In the past, radioimmunoassays were done with polyclonal antibodies; today, monoclonal antibodies are often used, and chemiluminescence has at times replaced isotopes as an indicator.

The evaluation of hyperprolactinemia is further complicated by the fact that prolactin is a dynamic hormone that is believed to be affected by stress, breast examination, exercise, and sleep. Therefore, it has been suggested that samples be drawn in the late morning at least 1 hour before or after meals or in the early afternoon. However, recent observations have demonstrated that breast examination in normal cycling.

The use of visual field examinations is to be discouraged except in patients with macroadenomas. Macroadenomas generally do not produce chiasmatic suppression, and patients who have lesions of 10 mm or greater present with superior bitemporal hemianopsia only 68% of the time. It should be recalled that prolactinomas often behave like meningiomas and grow along dural planes, they frequently grow into the cavernous sinus, and they do not produce compression of the optic chiasm. Radiographic imaging is generally restricted to either computed tomography or magnetic resonance imaging.

Treatment of the patient with hyperprolactinemia hinges on several factors: 1) symptoms, 2) the desire for pregnancy, 3) whether the patient has a microadenoma or a macroadenoma, and 4) whether the patient is hypoestrogenic. When the cause of hyperprolactinemia can be determined, specific therapy should be instituted. For instance, hypothyroidism resolves in patients treated with replacement therapy. Patients who take medications that induce hyperprolactinemia should have the medication discontinued if the symptoms warrant such a move. Women with functional hyperprolactinemia who have slightly elevated prolactin levels.

When dopamine agonist therapy is used, patients often have side effects such as nausea, nasal congestion, lethargy, and dysphoria. Several factors may help improve the tolerance to dopamine agonist therapy. The first is to begin medication at a subtherapeutic dose and slowly increase the dose over the next few weeks. It has been suggested that vaginal administration of dopamine agonists will reduce sustained levels of the drug and minimize side effects. The vaginal delivery of bromocriptine results in a slower rise of the serum dopamine agonist level and a slower clearance, but patients who appear to be hypersensitive to dopamine agonists are, in general, intolerant to either route of delivery. The long- and short-acting injectable forms of bromocriptine that are available in Europe are not approved for use in the United States. An alternate form of therapy is to treat the patient with pergolide mesylate. Pergolide mesylate is approved in the United States for the treatment of Parkinson's disease.