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The approval of GH treatment of adults with GH deficiency (GHD) raises issues regarding continuation of GH treatment in the GH-deficient child following achievement of near adult height. The transition period begins in late puberty and ends with full adult maturation and includes hormonal and many lifestyle changes. Children treated with GH should be retested near the time of reaching adult height to determine if they have persistence of GHD. Although most children with organic causes of GHD will again be found to have GHD on retesting, most of those with idiopathic GHD will not. Retesting usually involves measurement of IGF-I and stimulation with insulin-induced hypoglycemia or arginine-GHRH, but important questions remain about adjustment of established cut-offs for age and body mass index. Most studies have shown the benefit of GH treatment in young adults with GHD in body composition, especially the achievement of peak bone mass. It is important for pediatric endocrinologists to discuss the potential need for continued treatment beyond achievement of adult height at the time of initiation of GH treatment, especially in those children with organic causes of GHD.

During a systematic study of women with idiopathic galactorrhea, we observed several patients with normal random serum prolactin (PRL) levels and normal menses, but abnormal sellar tomograms characteristic of a pituitary adenoma. To test the hypothesis that these women might have intermittent PRL hypersecretion, we studied PRL secretion by sampling blood every half hour for 24 h in 10 patients and for 17.5 h in another, and compared the findings to those of a group of 5 normal women. The mean 24-h PRL of the 10 patients (16.8 ± 7.8 ng/ml; mean ± SD) was not significantly different from that of the normal women (13.6 ± 3.2 ng/ml), and each patient showed a normal sleep-associated PRL increment. Three individuals exhibited an abnormally elevated 24-h PRL (> 20 ng/ml). Increased PRL secretion occurred primarily at night or in the afternoon. Thyrotropin releasing hormone (TRH) administration caused normal or exaggerated PRL responses in all patients tested. High resolution CT scanning of two of the hypersecre-tors suggested a microadenoma in one case. In another case whose PRL was normal over 17.5 h, transsphenoidal surgery, carried out because of the tomographic findings and the symptom of headaches, demonstrated a 5-mm chromophobe adenoma that did not contain PRL by immuno-histochemistry. Postoperatively the galactorrhea persisted. We conclude that most women with galactorrhea, normal PRL., normal menses, and abnormal tomograms have normal PRL secretion. However, a minority of patients with this syndrome do demonstrate intermittent PRL hypersecretion. The etiology of intermittent PRL hypersecretion and its relevance to galactorrhea have not been determined. Furthermore the clinical and pathological significance of the “abnormal” tomograms and their relevance to PRL secretion and galactorrhea are not clear.

To test the hypothesis that PRL is able to feedback negatively on its own secretion (short-loop feedback) in humans via augmentation of the turnover of tuberoinfundibular dopamine (TIDA), the effects of the administration of purified hPRL on endogenous LH, FSH and TSH were assessed. Purified hPRL, given in an iv loading dose of 90 μg followed by a continuous infusion of 1.39 μg/min to 4 normal male volunteers resulted in a tripling of PRL levels (10.5±1.9 μg/L increasing to 30.9±3.6 μg/L) at the end of 90 min. There were no changes in LH, FSH or TSH levels, however, during or following the infusion. Purified hPRL was also given in 1 and 8 μg/kg doses IM to 5 normal male volunteers. Although PRL levels did not rise significantly with the 1 μg/kg dose, levels almost doubled with the 8 μg/kg dose (9.5±2.2 μg/L increasing to 17.4±1.5 μg/L). Again, LH, FSH and TSH levels did not change significantly over the three hour period of sampling with either dose. In conclusion, in this study we found that a 2–3 fold increase of circulating PRL levels maintained for 1.5–3 h exerted no apparent effects on the secretion of endogenous LH, FSH and TSH. This study provides direct evidence against the existence of a short-loop feedback occurring via TIDA activation in humans over this time interval but does not rule out the possibility that such feedback may occur with more prolonged states of hyperprolactinemia or via other mechanisms or the possibility of an effect on the hypothalamic pulse generator.