Oxandrolone (Ox) and testosterone (T) are used as growth-promoting agents in the therapy of boys with constitutional delay of growth and adolescence. Although the mechanism of action of these androgens is not known, it is recognized that T enhances GH release during GH stimulation tests. We studied the effects of T and Ox on the mean concentration of GH, the pattern of GH secretion, and somatomedin-C (SmC) concentrations in boys with short stature and/or delayed sexual development to determine whether their growth-promoting effects might be mediated through endogenous GH release. Ten boys received Ox (0.1 mg/kg . day, orally) for 65 +/- 5 days (mean +/- SD), and five boys received T propionate (7.5 mg, im, for 7 days), followed by T enanthate (100 mg, im, monthly for 3 months). Serum GH was measured in samples obtained at 20-min intervals for 24 h before and 65 +/- 5 days (mean +/- SD) after the initiation of therapy. SmC levels were measured twice during the same 24-h period before and 65 +/- 5 days (mean +/- SD) after initiation of therapy. In the boys treated with T, there were significant increases in the mean concentration of GH (mean increase, 4.3-fold; range, 2-12), in the number of GH pulses 10 ng/ml or greater [1.6 +/- 2.0 vs. 4.8 +/- 1.5/24 h (mean +/- SD)], and in the SmC levels [0.82 +/- 0.46 vs. 2.3 +/- 0.4 mu/ml (mean +/- SD)]. There were, however, no significant changes in the boys treated with Ox. Both Ox and T significantly improved the growth rates; however, T increased the growth rate by 0.95 +/- 0.24 (mean +/- SD) cm/months, and Ox increased the growth rate by 0.24 +/- 0.26 (mean +/- SD) cm/month. These results indicate that T, but not Ox, at the doses tested increases GH secretion in boys with short stature and/or delayed sexual development. This increase in GH secretion may contribute to the increased growth rate in males at puberty.

To investigate the role of testosterone (T) in the pubertal elevation of somatomedin-C (SmC), six prepubertal GH-deficient boys were each given 7-day courses of GH alone (0.05 U/kg X day, im), T alone (T propionate; 25 mg/day, im), and a combination of GH and T at the same dosages. Plasma SmC levels were determined on samples drawn at the start and finish of each period, and each course was separated by a 7-day period. SmC was also measured before and after a course of T propionate (25 mg/day, im) in four GH-sufficient boys with delayed adolescence. In the GH-deficient boys, GH and the combination of GH and T resulted in comparable and significant increments of SmC (mean change, 0.68 U/ml after GH and 0.63 U/ml after the combination of GH and T). T alone caused no change in SmC in the GH-deficient boys (mean change, 0.09 U/ml), but resulted in increases in all four GH-sufficient subjects (mean change, 1.29 U/ml). In a single subject with constitutionally delayed puberty, the integrated 24-h GH concentration rose from 2.8 ng/ml before to 5.8 ng/ml after T therapy. Both the number and amplitude of GH secretory events were greater after therapy. These data show that T stimulates SmC production in prepubertal boys who can secrete GH, but not in those who are GH deficient. We postulate that the effect of T in this regard is due to its effect on pituitary GH secretion. Although the T levels were within the pharmacological range, physiological levels of T (e.g. at puberty) may be responsible for the adolescent SmC increment in men.

We report on a 17-month-old boy with Wormian bones, short stature, growth hormone deficiency, developmental delay, brachycamptodactyly, dextrocardia, cryptorchidism, midshaft hypospadias, hypoplastic left kidney, and imperforate anus. This unique combination of abnormalities has not been reported previously.

Acromegaly was diagnosed in a 37-year-old woman with classical physical and biochemical findings; an enlarged sella on computed tomography suggested the presence of a pituitary macroadenoma. Radiologic evidence of a lung mass prompted radioimmunoassay of plasma growth hormone-releasing factor (7,500 pg/ml; normal less than 100 pg/ml). After resection of a bronchial carcinoid, which stained positive for growth hormone-releasing factor, circulating growth hormone-releasing factor levels normalized. Subsequently, her clinical, biochemical, and radiologic evidence for acromegaly resolved. This case represents the first reported use of the human pancreatic growth hormone-releasing factor 1-40 radioimmunoassay to preoperatively diagnose this rare etiology of acromegaly.