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Journal of Clinical Endocrinology & Metabolism Vol. 51, No. 3 438-445
doi:10.1210/jcem-51-3-438
Copyright © 1980 by the Endocrine Society.
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Rapid Regression of Pituitary Prolactinomas during Bromocriptine Treatment*

MICHAEL O. THORNER, WILLIAM H. MARTIN, ALAN D. ROGOL, J. LEON MORRIS, RICHARD L. PERRYMAN, BRIAN P. CONWAY, STUART S. HOWARDS, MARK G. WOLFMAN and ROBERT M. MACLEOD

Division of Endocrinology and Metabolism, Departments of Internal Medicine, Ophthalmology, Pediatrics, Radiology, and Urology, University of Virginia Medical Center Charlottesville, Virginia 22908 Department of Radiology Suburban Hospital, Bethesda, Maryland 20016

Address requests for reprints to: Dr. Michael O. Thorner, Box 252, Department of Internal Medicine, University of Virginia Medical Center, Charlottesville, Virginia 22908

herapy for large prolactinomas remains controversial. Surgery is often unsuccessful in restoring endocrine function to normal. However, medical therapy with bromocriptine, a dopamine agonist, not only suppresses PRL levels, but may also lead to a reduction in tumor size. Previous reports have demonstrated radiographic evidence of tumor regression only after 3 or more months of bromocriptine therapy. We have now documented, for the first time, objective evidence of extremely rapid reduction in tumor size in two patients harboring large PRL-secreting pituitary tumors (mean pretreatment serum PRL levels, 2350 and 3900 ng/ml) who were prospectively treated with bromocriptine (7.5 mg/day) in preference to surgical intervention despite marked visual impairment in one of the patients. After 2 and 6 weeks of therapy, respectively, marked reduction in tumor size was demonstrated radiographically in both patients. Headache, visual acuity, and visual fields had improved after only 3 days.

Although the mechanism of bromocriptine's antitumor activity is unclear, we believe that a large prospective trial to study the effects of bromocriptine therapy on the size of PRL-secreting macroadenomas is urgently needed to determine whether medical therapy should become the primary modality of treatment to reduce tumor size as well as restore endocrine function.

* This work was supported in part by Research Grant CA-07535 from the National Cancer Institute, USPHS General Clinical Research Grant RR-847, Grant RCDA5-K04-AM00153 (to A.D.R.), and a research grant from Sandoz Pharmaceuticals, East Hanover, N.J.

Received February 4, 1980.




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