Abstract
OBJECTIVE: In girls with Turner's syndrome a positive effect of growth hormone (GH) therapy on statutal growth has been well documented, in spite of the fact that the levels of GH and IGF-I in these patients are usually within the normal range. It is known that plasma levels of sex hormone-binding globulin (SHBG) are negatively associated with growth hormone (GH) and with [GF-I.
Limited data on SHBG levels in these patients and only scarce reports on other than gonadal steroids in these patients are available so far. The major aim of this study was to find out whether SHBG does respond to GH treatment.
METHODS: Plasma levels of SHBG, estradiol, progesterone, testosterone and the adrenal steroids and their precursors, namely cortisol, 17alpha-hydroxyprogesterone, androstenedione, dehydroepiandrosterone and its sulfate were determined in 65 patients aged 2-23 years with Turner's syndrome. The patients were divided into 4 groups according to their actual treatment (untreated, sex steroids only, GH only, GH and sex steroids) and the differences between the groups were evaluated.
With respect to dependence of SHBG and of steroids studied on age (with exception of cortisol), their values were expressed as per cents of medians of the physiological values. RESULTS: As expected, low levels of sex steroids were found.
As to the adrenal steroids, in general, their average levels were lower than in healthy subjects but still within the physiological limits. With one exception (androstenedione), no significant differences were found between the groups.
The levels of cortisol were undistinguishable from healthy subjects. Absolute as well as relative SHBG levels in untreated group and in the group treated with estrogens were normal or even lower than those reported for normal subjects of the same chronological age.
Significantly reduced absolute as well as relative SHBG levels in comparison to all other groups were found in GH treated children. CONCLUSION: The results indicate that SHBG may serve as a sensitive biochemical marker of the response to the GH administration.