Prolactin

• Thyroid-stimulating Hormone (TSH)

• Female: 4.8-23.3 ng/mL

The release of prolactin is promoted physiologically by suckling and stress. In addition, elevated serum prolactin concentrations are caused by a number of pharmaceuticals (eg, dibenzodiazepines, phenothiazine), TRH, and estrogen.^1-3 The release of prolactin is inhibited by dopamine, L-dopa, and ergotamine derivatives.

In patients receiving therapy with high biotin doses (ie, >5 mg/day), no sample should be taken until at least eight hours after the last biotin administration.⁴ As with all tests containing monoclonal mouse antibodies, erroneous findings may be obtained from samples taken from patients who have been treated with monoclonal mouse antibodies or who have received them for diagnostic purposes.⁴ In rare cases, interference due to extremely high titers of antibodies to ruthenium can occur.⁴ Extremely high titers of antibodies to streptavidin can occur in isolated cases and cause interference.⁴

Patients with hyperprolactinemia may have the multiple endocrine neoplasia syndrome, MEN-1.⁵ Provocative tests used in work-up of hyperprolactinemia include metyrapone stimulation of ACTH-2 and TRH provocative test.⁶

Antipsychotic drugs may elevate serum prolactin. Antipsychotics block dopamine, thereby elevating serum prolactin levels. Hyperprolactinemia is present in many patients receiving neuroleptics with an occasional patient developing amenorrhea, galactorrhea, and/or decreased libido. Amoxapine, a dibenzoxazepine type of tricyclic with antidepressant and antipsychotic characteristics, has been found to cause galactorrhea and oligomenorrhea with hyperprolactinemia. Amoxapine may have a dopamine blocking action.⁷ The prolactin level may rise significantly but only briefly. Point prolactin level determinations during therapy may be within normal range while total integrated 24-hour secretion is significantly increased. It has been recommended that patients who develop amenorrhea and/or galactorrhea during neuroleptic therapy should be observed regularly for possible emergence of a pituitary tumor.

Persistent elevations of plasma prolactin levels may be observed with, and after withdrawal from, chronic cocaine abuse, and may reflect a cocaine-induced derangement in the neural dopaminergic regulatory systems.⁸

2. Müller EE, Locatelli V, Cella S, et al, “Prolactin-Lowering and -Releasing Drugs, Mechanism of Action and Therapeutic Applications,” Drugs, 1983, 25(4):399-432.PubMed 6133737

3. Pontiroli AE, Falsetti L, Bottazzo G, et al, “Clinical, Endocrine, Roentgenographic and Immune Characterization of Hyperprolactinemic Women,” Int J Fert, 1987, 32(1):81-5.PubMed 2880822

4. Prolactin on Elecsys 1010/2010 and Modular Analytics E170, package insert 2007-09, V 2, Indianapolis, IN: Roche Diagnostics, 2007.

5. Levine JH, Sagel J, Rosebrock G, “Prolactin-Secreting Adenoma as Part of the Multiple Endocrine Neoplasia − Type 1 (MEN-1) Syndrome,” Cancer, 1979, 43(6):2492-6.PubMed 36978

6. Randall RV, Laws ER Jr, Abboud CF, et al, “Transsphenoidal Microsurgical Treatment of Prolactin-Producing Pituitary Adenomas. Results in 100 Patients,” Mayo Clin Proc, 1983, 58(2):108-21.PubMed 6681646

7. Gelenberg AJ, Cooper DS, Doller JC, et al, “Galactorrhea and Hyperprolactinemia Associated With Amoxapine Therapy. Report of a Case,” JAMA, 1979, 242(17):1900-1.PubMed 573343

8. Mendelson JH, Teoh SK, Lange U, et al, “Anterior Pituitary, Adrenal, and Gonadal Hormones During Cocaine Withdrawal,” Am J Psychiatry, 1988, 145(9):1094-8.PubMed 3414852

Berczi I, Cosby H, Hunter T, et al, “Decreased Bioactivity of Circulating Prolactin in Patients With Rheumatoid Arthritis,” Br J Rheumatol, 1987, 26(6):433-6. PubMed 3690137

Burrow GN, Wortzman G, Rewcastle NB, et al, “Microadenomas of the Pituitary and Abnormal Sellar Tomograms in an Unselected Autopsy Series,” N Engl J Med, 1981, 304(3):156-8. PubMed 7442734

Fujimoto VY, Clifton DK, Cohen NL, et al, “Variability of Serum Prolactin and Progesterone Levels in Normal Women: The Relevance of Single Hormone Measurements in the Clinical Setting,” Obstet Gynecol, 1990, 76(1):71-8. PubMed 2359568

Kelly PA, Djiane J, Postel-Vinay MC, et al, “The Prolactin/Growth Hormone Receptor Family,” Endocr Rev, 1991, 12(3):235-51. PubMed 1935820

Kletzky OA, Davajan V, “Hyperprolactinemia: Diagnosis and Treatment,” Infertility, Contraception & Reproductive Endocrinology, 2nd ed, Mishell DR Jr, Davajan V, eds, Oradell, NJ: Medical Economics Books, 1986, 275-301.

Schlechte J, Dolan K, Sherman B, et al, “The Natural History of Untreated Hyperprolactinemia: A Prospective Analysis,” J Clin Endocrinol Metab, 1989, 68(2):412-8. PubMed 2918052

Smith CR, Butler J, Hashim I, et al, “Serum Prolactin Bioactivity and Immunoactivity in Hyperprolactinaemic States,” Ann Clin Biochem, 1990, 27(Pt 1):3-8. PubMed 2310154

Tippet PD, Simon JA, Rifka SM, et al, “Luteal Phase Hyperprolactinemia During Ovulation Induction With Human Menopausal Gonadotropins: Incidence, Recurrence, and Effect on Pregnancy Rates,” Obstet Gynecol, 1989, 73(4):613. PubMed 2494621

Veldhuis JD, Evans WS, Stumpf PG, “Mechanisms that Subserve Estradiol’s Induction of Increased Prolactin Concentrations: Evidence of Amplitude Modulation of Spontaneous Prolactin Secretory Bursts,” Am J Obstet Gynecol, 1989, 161(5):1149-58.PubMed 2589434