Increased disorderliness and decreased mass and daily rate of endogenous growth hormone secretion in adult Turner syndrome: The impact of body composition, maximal oxygen uptake and treatment with sex hormones

The objectives of this study were to (1) quantify pulsatility and orderliness of 24-h growth hormone (GH) secretion in adult Turner syndrome; (2) study the impact of sex steroid replacement therapy in adult Turner syndrome on these measures of GH secretion, and in addition examine the differential effect of oral vs transdermal estrogen administration on GH secretion patterns. To these ends, we used deconvolution analysis and approximate entropy (ApEn) to quantify GH release over 24 h in 21 patients with Turner syndrome before and during sex hormone substitution, compared to an age-matched control group. Deconvolution analysis revealed that the mass of GH secreted per burst and production rate was significantly lower in Turner patients compared to controls, resulting in a significantly lower integrated 24-h GH concentration. However, multiple stepwise regression revealed that lean body mass (LBM) and maximal oxygen uptake were significant discriminative variable, explaining a large part of the variation in mass secreted per burst (r= 0.72, P< 0.0005) and production rate (r= 0.73, P < 0.0005), while group (Turner or control) did not explain any of the difference. There was a significant difference in ApEn between Turner patients and controls, denoting more disorderly GH release in Turner syndrome. During administration of sex hormones, a significant increase was seen in basal secretion and GH secretory burst half-duration, as well as in integrated 24-h GH concentration. No change in ApEn was evident. We conclude that GH secretion in adult Turner syndrome is irregular, reduced in mass and production rate. The reduction in mass and production rate could be explained by differences in body composition and maximal oxygen uptake compared to relevant controls, while the irregularity of GH secretion was unexplained by the measured variables. We hypothesize that the increased irregularity could be attributable to low levels of circulating androgens or an increased biological age in the Turner patients. (C) 1998 Churchill Livingstone.