Twenty-two hypopituitary boys treated with human GH were studied longitudinally before and during puberty. Eight patients entered spontaneous puberty at a mean bone age of 12.4 +/- 1.0 (+/- SD) yr. Height velocity reached a mean peak of 6.8 cm/yr during the second year of spontaneous puberty. In these patients, the mean total height gain throughout puberty was 22.8 +/- 5.2 cm, and the mean final height was 158.6 +/- 7.2 cm. Fourteen patients received testosterone enanthate (100 mg/month, im) starting at a mean bone age of 13.6 +/- 1.1 yr. Height velocity was maximal (7.5 cm/yr) during the first year of therapy. The mean final height was 162.9 +/- 5.0 cm, with a mean pubertal gain of 15.9 +/- 3.8 cm. Genital development, peak height velocity, and increase in plasma testosterone levels occurred earlier during testosterone therapy than during spontaneous puberty. In both groups of patients, there was a positive correlation between the bone age at onset of puberty and the height at onset of puberty (r = 0.65). There was also a negative correlation between bone age and total pubertal height gain (r = -0.73). This reduction in pubertal height increase was less than expected for bone age at onset of puberty, which can be explained by a decrease in bone age velocity in relation to bone age at onset of puberty (r = -0.81). Therefore, advancement in bone age at the onset of testosterone therapy did not impair final height, whereas it may increase height at onset of puberty, which is the major factor in final height. We conclude that in GH- and gonadotropin-deficient boys 1) a reduced dosage of testosterone enanthate (25 mg twice a month, im) should be used to induce pubertal development, and 2) the major criterion to decide when to give testosterone is height reached at that time regardless of bone age.

These results suggest that early puberty is a critical period for the development of diabetic cardiac autonomic dysfunction. Therefore, all type 1 diabetic patients should be screened for this complication by HRV analysis beginning at the first stage of puberty regardless of illness duration, microalbuminuria, and level of metabolic control.

Melanocytic naevi may grow more rapidly during human growth hormone (hGH) therapy. With standardised skin photographs, the growth rate of the naevi was two-fold greater in 14 hypopituitary and 5 Turner's syndrome girls treated with hGH than in untreated patients or controls. HMB-45 immunoreactivity, a marker of stimulated melanocytes, was absent in naevi from 18 of 19 individuals not treated with hGH, including 5 Turner's syndrome patients studied 2-43 months after stopping hGH. In naevi from 39 hGH-treated patients, 22 showed unusual HMB-45 reactivity in dermal naevocytes. During administration of hGH, melanocytic naevi grow faster and there is reversible stimulation of naevocytes.

SUMMARY The release of gonadotrophin following the injection of synthetic LH‐RH (Hoechst) was studied in various physiological and experimental circumstances. In the male, 25 μg of LH‐RH led to simultaneous release of FSH and LH prior to and during puberty. In adults, on the other hand, the same dose led only to an increase in LH while FSH levels remained unchanged. At higher doses there was FSH release and an increase in LH proportional to the amount of LH‐RH injected. When FSH was released the increase was clearly less than that of LH and often occurred considerably later. In the female, 25 μg of LH‐RH led to a clear‐cut release of FSH and a small release of LH prior to puberty. After the onset of puberty the degree of response was inverted: the increase in LH was greater than that of FSH. In normally menstruating women the FSH and LH response was greater during the luteal phase than during the preovulatory phase. Treatment with non‐sequential hormonal contraceptives blocked FSH and LH release normally produced by the injection of 50 μg of LH‐RH. There was no effect when a dose of 100 μg was injected. In post‐menopausal women, only LH rose following the administration of 25 μg of LH‐RH. After 5 days of treatment with 200 μg ethinyl oestradiol the same dose of LH‐RH led to simultaneous release of LH and of FSH. From the above studies it can be concluded that the secretory response of the gonadotrophins to LH‐RH is influenced by the endocrine equilibrium and more particularly by the interaction of the gonadal steroids which can alter the synthesis and/or the release of the pituitary gonadotrophins.

In boys with constitutional delay of growth and puberty, adult height may be inconsistent with parental (target) height. We aimed at studying which period of growth was important to account for adult height being above or below target height. In this retrospective study, adult height measured after 20 years in 39 patients was compared with target height and height data obtained at about 6 and 12 years of age and at diagnosis of delayed puberty (mean 14.6 years). Twenty-eight patients were untreated while 11 received testosterone enanthate (50 or 100 mg/month for 6 months). The growth data from both groups were pooled since they were not different. On average, the adult height standard deviation score (–0.6 ± 0.8, mean ± SD) was similar to target height (–0.5 ± 0.6). There were, however, marked individual differences since adult height varied between 1.7 SD (11 cm) below target height and 1.4 SD (9.5 cm) above target height. Multiple regression analysis showed that the most significant determinant of the difference between adult height and target height was height catch up during puberty (p < 0.002). We conclude that the magnitude of height catch up during puberty is a significant determinant of adult height in boys with constitutional delay of growth and puberty. Thus, optimizing pubertal growth may be a relevant therapeutic aim for adult height in boys with short stature and delayed puberty.