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Departments of Medicine, VA Hospital, Bronx, N.Y., Mount Sinai School of Medicine, Cornell University Medical College, and Columbia University College of Physicians and Surgeons New York, N.Y
Reprints: Eckehart Wiedemann, M.D., VA Hospital, 130 W. Kingsbridge Road, Bronx, New York 10468. Received August 7, 1975.
Estrogen (E) reduces bioassayable GH-dependent serum somatomedin (SM) activity in acromegalics without affecting plasma growth hormone (GH) levels and inhibits the rise of SM activity normally produced by GH administration in GH-deficient subjects. We have now investigated the effect of E administration on serum SM activity and on plasma GH and prolactin (PRL) in 6 adult male subjects without pituitary pathology. Chronic E administration (ethinyl estradiol 0.5 mg/day for 7 to 70 days) reduced serum SM activity by 40 to 62% in each of 4 subjects (P < 0.02 to <0.001). In 3 of the subjects, basal GH levels increased by 75 to 300% (P < 0.05 to <0.001) and basal PRL levels increased by 90 to 200% (P < 0.01 to <0.001). While iv administration of normal saline did not significantly affect either SM or GH, iv administration of E (bolus injection of 25 mg conjugated estrogens, USP) to 5 subjects resulted in: a) a 46 to 80% decrease in serum SM activity in all subjects, proceeding with an apparent half-life of 2 hours, becoming significant (P < 0.05) at 2 hours (1 subject) to 3 hours (4 subjects), maximal at 6 hours, and persisting for 12 to 24 hours; b) GH elevation to 3 to 16 times baseline level (P < 0.01) at 2 to 3 hours in 4 subjects; and c) no significant change of PRL levels in any subject. The mean GH response to iv E was maximal at a time (2 hours) when the mean SM activity had decreased only 20% and subsided well before the nadir of SM activity. The one patient without GH response to chronic or acute E administration may have been affected by absorption of triamcinolone being applied topically during the study.
These results demonstrate that in males with normal pituitary function, E reduces serum SM activity, enhances basal GH and PRL secretion, and, upon iv injection, stimulates acute GH release. Although opposite chronic E effects upon GH and SM activity support a putative negative SM-GH feed-back mechanism, iv E administration apparently provokes acute GH release by a different mechanism. The halflife of serum SM activity in the human is probably much shorter than previously estimated.
Supported by the Veterans Administration (project no. 8392) and by USPHS Grant CA-11704. Dr. Wiedemann was a Clinical Investigator of the Veterans Administration.
Presented in part at the National Meeting of the American Federation for Clinical Research, Atlantic City, N.J., May 3, 1975.
Received August 7, 1975.
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