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We have observed the association of transient hypoglycemia, temporary ACTH deficiency, and elements of “maternal deprivation” or parental neglect in three children. Since reversible pituitary deficiency has been documented in the syndrome of “maternal deprivation” and since hypoglycemia can be the manifestation of ACTH and/or growth hormone deficiency, we suggest that recognition of hypoglycemia in the pediatric population may sometimes lead to the discovery of an adverse environment.

In a 14-year-old girl with untreated virilizing congenital adrenal hyperplasia, growth hormone and adrenocortical steroid levels were synchronous during a 24 hour period. Therapy with intramuscular or oral cortisone failed to suppress the spontaneous release, or alter appreciably the diurnal secretory pattern of growth hormone. The similarity of the growth hormone curves on three different days several weeks apart suggests persistence of the diurnal pattern of hormonal secretions in this particular patient.

Four adolescent subjects without evidence of pituitary or adrenal disorder released GH during 24 hours in three to ten bursts, mainly during sleep. Cortisol was released periodically, but without any relationship to GH secretory episodes. These data were compared with data obtained in four clinical conditions known or presumed to affect F and/or GH secretion. In Cushing's disease cortisol was released episodically, yet the lowest concentrations were well above the normal nadir. Alternate-day administration of prednisone did not suppress the ultradian release of F on the day “of” therapy in one patient. Peak GH concentrations were lower in patients with Cushing's disease and during steroid therapy than in the four hospitalized adolescent control subjects. High mean concentrations of GH were observed during prolonged fasting in one patient and in another patient with poorly controlled diabetes mellitus, conditions which did not alter cortisol release.

The present study was undertaken to investigate the possible potentiating effect of human placental lactogen (HPL) on human growth hormone (HGH). Five preadolescent hypopituitary patients, aged 6 to 12 years received, at random, three different four month courses of therapy consisting of 1 unit of HGH, 2 units of HGH, and a combination of 1 unit of HGH and 400 mg of HPL, every other day. Linear growth was comparable on the three treatment schedules suggesting absence of growth potentiation but the diabetogenic effect of HGH appeared enhanced by HPL.

An analysis of the growth patterns of 30 children with congenital adrenal hyperplasia (CAH) treated with cortisone acetate revealed 76% to be at or below the third percentile by age 2 years. Paradoxically, the growth rate was better in the first six months of life when the dose of cortisone per unit of body surface was highest. Among this group of 30 children, a sample of six children receiving therapy intramuscularly showed no significant difference in their growth hormone response to arginine hydrochloride or insulin stimulation when compared with a group of normal children. These data are consistent with an antagonism by cortisone of the actions of growth hormone at the peripheral level rather than a central inhibition of growth hormone release. In addition, linear growth in the first 6 months of life seems relatively independent of the growth suppressing effects of glucocorticoids.