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Test ID: PRL    
Prolactin, Serum

Useful For Suggests clinical disorders or settings where the test may be helpful

Aiding in evaluation of pituitary tumors, amenorrhea, galactorrhea, infertility, and hypogonadism

 

Monitoring therapy of prolactin-producing tumors

Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

Prolactin is secreted by the anterior pituitary gland and controlled by the hypothalamus. It is structurally related to growth hormone (GH), but has few, if any, of the physiological effects of GH. The major chemical controlling prolactin secretion is dopamine, which inhibits prolactin secretion from the pituitary.

 

The only definitively known physiological function of prolactin is the stimulation of milk production. In normal individuals, the prolactin level rises in response to physiologic stimuli such as sleep, exercise, nipple stimulation, sexual intercourse, hypoglycemia, postpartum period, and also is elevated in the newborn infant.

 

Pathologic causes of hyperprolactinemia include prolactin-secreting pituitary adenoma (prolactinoma, which is 5 times more frequent in females than males), functional and organic disease of the hypothalamus, primary hypothyroidism, section compression of the pituitary stalk, chest wall lesions, renal failure, and ectopic tumors.

 

Hyperprolactinemia often results in loss of libido; galactorrhea, oligomenorrhea or amenorrhea, and infertility in premenopausal females; and loss of libido, impotence, infertility, and hypogonadism in males. Postmenopausal and premenopausal women, as well as men, can also suffer from decreased muscle mass and osteoporosis. The latter can sometimes be dramatic in a small subgroup of women who develop severe and acute onset postpartum osteoporosis that remits with cessation of breastfeeding and medical suppression of hyperprolactinemia.

Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.

Males: 3-13 ng/mL

Females: 3-27 ng/mL

Interpretation Provides information to assist in interpretation of the test results

In males, prolactin levels >13 ng/mL are indicative of hyperprolactinemia.

 

In women, prolactin levels >27 ng/mL in the absence of pregnancy and postpartum lactation are indicative of hyperprolactinemia.

 

Clear symptoms and signs of hyperprolactinemia are often absent in patients with serum prolactin levels <100 ng/mL.

 

Disease states associated with elevated serum prolactin levels include renal failure, untreated hypothyroidism, large nonprolactin-secreting pituitary tumors that have led to pituitary stalk compression, and prolactin-secreting pituitary micro- and macroadenomas.

 

Mild to moderately increased levels of serum prolactin are not a reliable guide for determining whether a prolactin-producing pituitary adenoma is present, whereas levels >250 ng/mL are usually associated with a prolactin-secreting tumor.

 

After initiation of medical therapy of prolactinomas, prolactin levels should decrease substantially in most patients; in 60% to 80% of patients, normal levels should be reached. Failure to suppress prolactin levels may indicate tumors resistant to the usual central-acting dopamine agonist therapies; however, a subset of patients will show tumor shrinkage despite persistent hyperprolactinemia. Patient who show neither a decrease in prolactin levels nor tumor shrinkage might require additional therapeutic measures.

 

Resurgent prolactin levels in patients on long-term therapy indicate, most often, noncompliance with dopaminergic therapy, but can occasionally be an indication of recurrence.

Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances

Multiple medications can cause a rise in serum prolactin level, in particular those that 1) decrease central nervous system (CNS) dopamine levels or block CNS dopamine receptors (antipsychotic drugs, antinausea/antiemetic drugs), or 2) affect CNS serotonin metabolism, serotonin receptors, or serotonin reuptake (anti-depressants of all classes, ergot derivatives, some illegal drugs such as cannabis). In addition, several antihypertensive drugs with high CNS concentrations and central action on catecholaminergic neurons or calcium fluxes can cause hyperprolactinemia, as can opiates, high doses of estrogen or progesterone, and a smattering of other drugs ranging from anticonvulsants (valporic acid) to anti-tuberculous medications (Isoniazid). Collectively, drug effects may account for the majority of mild to modest elevations in prolactin levels (2-4 times upper limit of the reference range). More pronounced prolactin elevations are only occasionally drug-related.

 

Prolactin levels are regularly transiently elevated after a grand-mal seizure, and also often after petit-mal and atypical seizures. This observation has been clinically leveraged to aid in distinguishing pseudoseizures from true epileptic seizures.

 

Exercise, stress, and sleep can transiently raise prolactin levels.

 

High-dose hook effect, leading to false-low serum prolactin measurements, is rarely observed. If a hook effect is suspected because low prolactin results are at variance with clinical presentation, then a dilution must be performed. Contact Mayo Medical Laboratories in this situation.

 

Prolactin values that exceed the reference values may be due to macroprolactin (prolactin bound to immunoglobulin). Macroprolactin should be evaluated if signs and symptoms of hyperprolactinemia are absent, or pituitary imaging studies are not informative. See MCRPL / Macroprolactin, Serum.

Clinical Reference Provides recommendations for further in-depth reading of a clinical nature

Demers LM, Vance ML: Pituitary function. In Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. Fourth edition. Edited by CA Burtis, ER Ashwood, DE Bruns. St. Louis, Elsevier Saunders Company, 2006, pp 1976-1981