Thirty-six children with growth hormone deficiency were treated for up to 48 months with methionyl human growth hormone (hGH) synthesised by DNA recombinant methods. The growth rate for these children increased from 3·2±1·1 cm/yr to 10 · 5±2·2 cm/yr (mean±SD). This was similar to the effect of pituitary hGH in ten GH deficient children, 3·8±1·0 to 10·1±1·1 cm/yr. Serum somatomedin C rose from 0·26±0·23 U/ml to 0·79±0·53 U/ml after 6 months of methionyl-hGH therapy, similar to the effect of pituitary hGH. The incidence of antibody formation to methionyl-hGH was higher than that observed with pituitary hGH (Kabi) but poor growth was observed only in the one patient on methionyl-hGH who acquired high-titre high-binding-capacity antibodies to hGH. No consistent changes in levels of antibodies to Escherichia coli proteins were detected. No other allergic manifestations or systemic side-effects were demonstrable.

Nine hypopituitary children received human growth hormone and, subsequently, one or more prolactin compounds while ingesting a constant diet. Urinary nitrogen and calcium were measured during these periods and during control periods. Five of 6 patients receiving ovine prolactin and 4 of 4 patients receiving bovine prolactin retained nitrogen. None of 3 patients receiving porcine prolactin retained nitrogen. All patients retained more nitrogen while receiving 5 mg of HGH than while receiving 50 mg of prolactin/day. The hypercalciuria described by others in patients receiving prolactin was observed in only 1 of 9 patients. There was no significant effect exerted by prolactins on the serum urea nitrogen or insulin sensitivity. Although certain prolactins have some nitrogenretaining effect, the response was variable from patient to patient and it is concluded that animal prolactins are of limited value as human growth hormone substitutes. However, further studies are necessary to determine their effect when g...

DURING the past six years we have observed and evaluated 13 children, most of whom initially were believed to have growth failure on the basis of idiopathic hypopituitarism. However, a number of unusual features were noted in the histories that suggested emotional disturbances in the children and abnormal home environments. These were not common to the histories of patients with idiopathic hypopituitarism. When these patients were placed in a convalescent hospital, they demonstrated remarkable growth acceleration without receiving growth hormone or other agents. Detailed studies were performed before and during the period of rapid growth. This paper presents the clinical . . .

Placental lactogen (1), a hormone with somatotropic, luteotropic and lactogenic activities and which is secreted by the human placenta, has been reported to have growth hormone-like activity (2). Elsewhere in this Journal a study comparing the effects of animal prolactins with human growth hormone is reported (3). Similar studies were undertaken to determine the metabolic effects of placental lactogen as compared to human growth hormone.

Sexual precocity resulting from circulating gonadotropin is reported in a 2-year-old child with hepatoblastoma. Following removal of the tumor the sexual precocity regressed and the gonadotropin in the serum disappeared. The patient eventually succumbed to his disease as have the other four similar patients that have been reported upon. This unusual cause of sexual precocity must be considered in the differential diagnosis of isosexual precocity. The clinical signs and symptoms, and the chemical abnormalities that occur in patients of this type, are discussed. Sexual precocity resulting from circulating gonadotropin is reported in a 2-year-old child with hepatoblastoma. Following removal of the tumor the sexual precocity regressed and the gonadotropin in the serum disappeared. The patient eventually succumbed to his disease as have the other four similar patients that have been reported upon. This unusual cause of sexual precocity must be considered in the differential diagnosis of isosexual precocity. The clinical signs and symptoms, and the chemical abnormalities that occur in patients of this type, are discussed.