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Decreased Metabolic Clearance of Endogenous Growth Hormone and Specific Alterations in the Pulsatile Mode of Growth Hormone Secretion Occur in Prepubertal Girls with Turner's Syndrome^*

JOHANNES D. VELDHUIS, JUAN F. SOTOS, BARRY M. SHERMAN and GENENTECH COLLABORATIVE GROUP

Division of Endocrinology and Metabolism, Department of Internal Medicine and National Science Foundation Science Center for Biological Timing, University of Virginia Health Sciences Center Charlottesville, Virginia 22908
the Department of Pediatrics, Children's Hospital Columbus, Ohio 43205
Clinical Research Division, Genentech, Inc. South San Francisco, California 94080

Address all correspondence and requests for reprints to: Dr. Johannes D. Veldhuis, Division of Endocrinology and Metabolism, Department of Internal Medicine, Box 202, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908.

We have used deconvolution analysis to test the hypothesis that specific facets of GH secretion and clearance differ in young patients with Turner's syndrome and normal prepubertal girls. To this end, we sampled blood at 20-min intervals for 12 h overnight in 50 girls, 37 of whom had Turner's syndrome and 13 of whom were healthy Tanner stage I controls. Deconvolution analysis revealed that the half-life of endogenous GH in Turner's syndrome was significantly prolonged at 14 ± 0.93 vs. 11 ± 0.44 min in normal girls (P = 0.029). The number of significant GH secretory bursts was reduced in Turner's patients to 4.7 ± 0.27 vs. 6.8 ± 0.60 events/12 h in healthy girls (P < 0.01). GH secretory burst half-duration was significantly prolonged in Turner's syndrome, viz. 23 ± 1.3 vs. 15 ± 0.87 min (controls; P < 0.001). The changes in GH secretory burst frequency, duration, and half-life were specific, since neither the mass of GH secreted per burst nor the maximal rate of GH secretion attained per burst (amplitude of the secretion pulse) was significantly different in the 2 study groups. Thus, although 12-h GH secretion rates corrected for body weight were similar (3.9 ± 0.76 in Turner's patients and 3.3 ± 0.76 µg/L•kg/12 h in the control girls), equivalent GH production rates were achieved by different mechanisms in the 2 groups.

We conclude that specific alterations in GH secretory burst frequency and duration and endogenous GH half-life can be documented in young girls with Turner's syndrome.

^* This work was supported in part by NIH Grant RR-00847 (to the Clinical Research Center of the University of Virginia), Research Career Development Award 1KO4-HD-00634 (to J.D.V.), Diabetes and Endocrinology Research Center Grant DK-38942, NIH-supported Clinfo Data Reduction Systems, the Pratt Foundation, the University of Virginia Academic Enhancement Fund, and the NSF Science Center for Biological Timing.

The members of the Genentech Collaborative Turner Study Group who participated in this study are: Ann Johanson (Genentech), Robert Blizzard (University of Virginia Medical Center), Barbara Lippe (UCLA Hospital, Los Angeles), and Paul Saenger (Montefiore Hospital, New York).

Received February 19, 1991.

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