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 orde rliness of 24-h growth hormone (GH) secretion in adult Turner syndrome ; (2) study the impact of sex steroid replacement therapy in adult Tur ner syndrome on these measures of GH secretion, and in addition examin e the differential effect of oral vs transdermal estrogen administrati on on GH secretion patterns. To these ends, we used deconvolution anal ysis and approximate entropy (ApEn) to quantify GH release over 24 h i n 21 patients with Turner syndrome before and during sex hormone subst itution, compared to an age-matched control group. Deconvolution analy sis revealed that the mass of GH secreted per burst and production rat e was significantly lower in Turner patients compared to controls, res ulting in a significantly lower integrated 24-h GH concentration. Howe ver, multiple stepwise regression revealed that lean body mass (LBM) a nd maximal oxygen uptake were significant discriminative variable, exp laining 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 admini stration of sex hormones, a significant increase was seen in basal sec retion 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 a nd production rate. The reduction in mass and production rate could be explained by differences in body composition and maximal oxygen uptak e compared to relevant controls, while the irregularity of GH secretio n was unexplained by the measured variables. We hypothesize that the i ncreased irregularity could be attributable to low levels of circulati ng androgens or an increased biological age in the Turner patients. (C ) 1998 Churchill Livingstone.