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Journal of Clinical Endocrinology & Metabolism Vol. 66, No. 1 16-23
doi:10.1210/jcem-66-1-16
Copyright © 1988 by the Endocrine Society.
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Treatment of Acromegaly with the Long-Acting Somatostatin Analog SMS 201-995*

ARIEL L. BARKAN{dagger}, ROBERT P. KELCH, NANCY J. HOPWOOD and INESE Z. BEITINS

Divisions of Endocrinology and Metabolism, Departments of Medicine and Pediatrics, Veterans Administration Medical Center, and University of Michigan Hospitals Ann Arbor, Michigan 48105

Address all correspondence and requests for reprints to: Ariel L. Barkan, M.D., Endocrine Section, Veterans Administration Medical Center, 2215 Fuller Road, Ann Arbor, Michigan 48105.

Current treatment of acromegaly (surgery, radiation, and bromocriptine) is often unsatisfactory, and a sizeable proportion of patients with this disease continue to have GH hypersecretion after all therapeutic modalities have been exhausted. Fifteen patients with active acromegaly (8 previously treated and 7 newly diagnosed) were treated with the long-acting somatostatin analog SMS 201-995 (Sandoz; 50–250 pg, sc, every 6–8 h for up to 21 months). The mean daily plasma GH concentration was significantly suppressed in 13 patients, and it became normal in 10. Two patients, however, did not have GH suppression by SMS 201-995 treatment alone; in 1, a significant decline in mean daily GH was achieved after the addition of bromocriptine. As expected, suppression of GH secretion was associated with normalization of plasma somatomedin-C values and significant clinical improvement. Plasma GH responses to synthetic GHRH-(l–44) and TRH were either abolished or blunted by SMS 201-995. Thyroid function remained normal, and glucose tolerance did not change. Significant shrinkage of pituitary tumors occurred in 7 previously untreated and 2 previously treated patients. Side-effects were minimal. SMS 201-995 is an effective agent for the treatment of acromegaly. Further studies are necessary to establish guidelines for identification of nonresponders and to examine the effect of preoperative tumor shrinkage on subsequent surgical outcome.

* This work was supported by the V.A. Research Service, and NIH grants HD-16000 (to RPK) and 5MO1-RR-42 (Clinical Research Center).

{dagger} Recipient of the Career Development Research Associate Award from the V.A.

Received April 13, 1987.




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