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CLINICAL CASE SEMINAR |
Division of Endocrinology, Metabolism, and Molecular Medicine (M.P.G., M.E.M.), Northwestern University, The Feinberg Medical School, Chicago, Illinois 60611; and Cedars-Sinai Medical Center (S.M.), University of California at Los Angeles School of Medicine, Los Angeles, California 90048
Address all correspondence and requests for reprints to: Mark E. Molitch, M.D., Division of Endocrinology, Metabolism, and Molecular Medicine, Northwestern University, The Feinberg Medical School, 303 East Chicago Avenue, Tarry 15, Chicago, Illinois 60611. E-mail: molitch{at}northwestern.edu.
Abstract
Most prolactinomas respond rapidly to low doses of dopamine agonists. Occasionally, stepwise increases in doses of these agents are needed to achieve gradual prolactin (PRL) reductions. Approximately 50% of treated men remain hypogonadal, yet testosterone replacement may stimulate hyperprolactinemia.
A 34-yr-old male with a pituitary macroadenoma was found to have a PRL level of 10,362 µg/liter and testosterone level of 3.5 nmol/liter. Eleven months of dopamine agonist therapy at standard doses lowered PRL levels to 299 µg/liter. Subsequent stepwise increases in cabergoline (3 mg daily) further lowered PRL levels to 71 µg/liter, but hypogonadism persisted. Initiation of testosterone replacement resulted in a rise and discontinuation in a fall of PRL levels. Aromatization of exogenous testosterone to estradiol and subsequent estrogen-stimulated PRL release was suspected. Concomitant use of cabergoline with the aromatase inhibitor anastrozole after resuming testosterone replacement resulted in the maintenance of testosterone levels and restoration of normal sexual function, without increasing PRL. Ultimately, further reduction in PRL on this therapy permitted endogenous testosterone production. Thus, novel pharmacological maneuvers may permit successful medical treatment of some patients with invasive macroprolactinomas.
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