Administration of low-dose estrogen rapidly and directly stimulates growth hormone production
G. W. Moll Jr, R. L. Rosenfield and V. S. Fang
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
micrograms/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, greater than or equal to 7 ng/mL) to levodopa before
estrogen; all 20 children who received ethinyl estradiol priming in a dose
of 20 micrograms/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.
