The value of assessing basal steroids in children presenting with premature adrenarche is demonstrated in this series with 5.7% being diagnosed with 21-hydroxylase deficiency and 9.1% with 'exaggerated adrenarche'. No relation was found between adrenal steroids and clinical features except for the acceleration of bone age. The relation between 'exaggerated adrenarche' and future ovarian hyperandrogenism needs further evaluation.

SUMMARY Four previously healthy children acquired skin problems that were treated with topical or intralesional fluorinated corticosteroids. Three developed signs that suggested Cushing's syndrome 1-4 months after initial treatment. Investigation showed low plasma cortisol levels and inadequate response to corticotrophin stimulation. After 7 months of treatment with topical steroids the fourth child presented with failure to thrive; during a febrile illness he had a convulsion followed by acute hypotension which responded to parenteral corticosteroid administration. Adrenal function was not studied in this patient. Although fluorinated corticosteroids seldom lead to overt adrenal suppression in children, they may impair pituitary-adrenal responses in some. Such patients should be given oral or parenteral steroid cover in the event of illness or trauma.

We have reported that the mouse ventro-lateral hypothalamus releases a humoral factor in vitro which stimulates insulin secretion by isolated islets (Idahl & Martin, 1971). We report here similar studies extended to rats, and attempts to isolate this hypothalamic factor and to demonstrate its presence in blood.Ventro-lateral (VLH) and ventro-medial hypothalami (VMH) of 16 rats were separated and extracted with 3 ml Gey & Gey (1936) buffer at 37 \ s=deg\ Cfor 30 min. Aliquots (0\m=.\4ml) of the extract were tested for stimulatory capacity by incubation (20 min at 37 \ s=deg\ C) with five islets of Langerhans. The incubation medium contained glucose (3\m=.\3 mmol/l and albumin (1 mg/ml), in a final volume of 0\m=.\5 ml Gey & Gey buffer. The amount of insulin released into the medium was compared with the amount released by the same islets during a preliminary 20-min incubation in a medium without the extract (baseline). Insulin concentration was measured by immunoassay (Herbert, Lau, Gottlieb & Bleicher, 1965). Results of a typical experiment, expressed in ng insulin/islet incubated for 20 min, were (mean and range of five observations): baseline, 2-0 (1-5-2-6); islets in VLH extract, 5-9 (3-8-8-4); islets in VMH extract, 1-8 (0-5-2-6). The VLH extract stimulated insulin release while the VMH extract had no effect. Isolation of this islet-stimulating material was attempted by fractionation of the VLH extract through a Sephadex G-100 column. Figure la shows that the islet-stimulating activity resides in fractions in the descending portion of the second peak.The presence of the islet-stimulating factor in plasma was examined by passing dialysed rat plasma through a Sephadex G-100 column, as shown in Fig. 16: the fractions eluted in the shoulder of the albumin peak stimulated insulin release. The elution volume of this fraction was identical with that of the active fraction from the VLH extract. Further purification ofthis fraction by acrylamide gel electrophoresis and electrofocusing is in progress.The VLH origin of the plasma material was indicated by the following experiment : plasma from normal rats and from rats 48 h after the electrolytic destruction of the VLH (Steffens, Mogenson & Stevenson, 1972) were investigated for their islet stimu¬ lating capacity. Both normal and VLH-lesioned rats were tube-fed for 10 days before the operation and thereafter until the time of killing. The plasma was dialysed and 0-4-ml aliquots from each animal were tested. Table 1 shows that the plasma from the VLH-lesioned animals failed to stimulate the islets while the plasma from the controls remained fully active.

Benign intracranial hypertension (BIH) is reported in three children from Australia and one from New Zealand, who were being treated with recombinant human growth hormone (rhGH). Three males and one female, aged between 10.5 and 14.2 y, developed intracranial hypertension within 2 weeks to 3 months of starting treatment. A national database, OZGROW, has been prospectively collecting data on all 3332 children treated with rhGH in Australia and New Zealand from January 1986 to 1996. The incidence of BIH in children treated with growth hormone (GH) is small, 1.2 per 1000 cases overall, but appears to be greater with biochemical GHD (<10IUml ‐1), i.e. 6.5/1000 (3 in 465 cases), relative risk 18.4, 95% confidence interval 1.9‐176.1, than in all other children on the database. The incidence in patients with Turner's syndrome was 2.3/1000 (1 in 428 cases). No cases in patients with partial GHD (10–20 IUml ‐1) or chronic renal failure were identified. Possible causative mechanisms are discussed. The authors’practice is now to start GH replacement at less than the usual recommended dose of 14IUm‐2 week‐1 in those children considered to be at high risk of developing BIH. Ophthalmological evaluation is recommended for children before and during the first few months following commencement of rhGH therapy and is mandatory in the event of peripheral or facial oedema, persistent headaches, vomiting or visual symptoms. The absence of papilledema does not exclude the diagnosis.

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