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George Wm. Moll, Jr, MD, PhD; Robert L. Rosenfield, MD; Victor S. Fang, PhD

Am J Dis Child. 1986;140(2):124-127.

Abstract
• We tested the concept that estrogen directly stimulates growth hormone (GH) production by determining whether low-dose treatment with ethinyl estradiol increases the GH reserve, as assessed by levodopa administration, without inhibiting somatomedin-C (Sm-C) levels. Twenty-three prepubertal short normal children underwent levodopa tests before and after being treated with ethinyl estradiol. One bedtime dose of ethinyl estradiol (20 to 40 µg/sq m, n = 8) resulted in a significant increase in GH levels during levodopa testing, with no significant change in Sm-C levels (0.27±0.03 vs 0.36±0.1 units/mL). Two days of a comparable ethinyl estradiol dose (n=12) raised the mean basal GH level (2.4±0.4 vs 9±3 ng/mL) and had a similar effect on peak GH response, without affecting the mean Sm-C level. Eighteen of the 23 patients responded (maximum GH level, 7 ng/mL) to levodopa before estrogen; all 20 children who received ethinyl estradiol priming in a dose of 20 µg/sq m or more also responded. We conclude that low-dose estrogen therapy rapidly stimulates GH production without decreasing Sm-C plasma levels. These results support the concept that the estrogen effect is direct. This action may be important for the stimulation of growth by estrogen. This effect can be conveniently employed to enhance the specificity of the levodopa test for profound GH deficiency.

(AJDC 1986;140:124-127)

Author Affiliations
From the Departments of Pediatrics (Drs Moll and Rosenfield), and Medicine (Dr Fang), The University of Chicago Pritzker School of Medicine. Dr Moll is currently with Emory University, Atlanta.

Footnotes
Accepted for publication Sept 24, 1985.

A preliminary report of this work was presented at the Midwest Society for Pediatric Research Annual Meeting, Chicago, Nov 3, 1984.

Reprint requests to Wyler Children's Hospital, 5825 S Maryland Ave, Chicago, IL 60637 (Dr Rosenfield).

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