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Biomedical subjects

C G Brook

Publications and source records attributed to C G Brook.

At least 217 records · Page 12Linked to original sources
PubMed1986

Nocturnal pulsatile growth hormone releasing hormone treatment in growth hormone deficiency.

We have treated five GH-deficient prepubertal children (4 M, 1 F) with GH releasing hormone 1-40 (GHRH1-40) in two dosage regimens over 9 months. Profiles of serum GH concentrations were obtained over 24 hours before treatment and nocturnal profiles were obtained serially throughout the study. GHRH was administered subcutaneously at night for four pulses using 1 microgram/kg/pulse in the first 3 months and 2 micrograms/kg/pulse for a further 6 months. All subjects demonstrated pituitary responsiveness to i.v. GHRH before treatment and at 3 and 6 months. GH secretion was induced in a pulsatile fashion in response to subcutaneous GHRH in three children from the first night of treatment. A self priming effect to successive GHRH pulses was evident and the response augmented with time and with the higher dose regimen. The growth velocity of these three children increased from a mean of 3.7 cm/year (range 3.7-3.8) before treatment to 5.5 cm/year (range 4.1-7.2) over the first 3 months and to 7.2 cm/year (range 4.8-9.2) over the following 6 months. In one subject entrainment of GH secretion to GHRH did not occur until the higher dose regimen and this was associated with a modest increase in growth velocity. One subject did not respond to treatment. Pulsatile administration of GHRH1-40 is effective in inducing GH secretion and promoting growth acceleration in some children with idiopathic GH deficiency. The optimal dose and mode of administration of GHRH have yet to be established.

Child↗
PubMed1986

High resolution CT scanning of the pituitary gland in growth disorders.

We have performed 217 GEC 8800 CT scans of the hypothalamus and pituitary glands of 202 children with disorders of growth and development. Pituitary morphological abnormalities were common. Intrapituitary low density lesions were found in 17% of the whole series and in 58% of children with tall stature. Seventy-seven children with idiopathic growth hormone deficiency could be divided on the basis of pituitary morphology seen on CT scan into pituitary aplasia (n = 11) and pituitary hypoplasia (n = 53). Patients with pituitary aplasia had an absent adenohypophysis which probably dated from early intrauterine life and therefore could not be related to birth trauma. We have found a high incidence of evolving endocrinopathy in children with pituitary insufficiency: thus, if a short child is investigated the initial endocrine findings need to be repeated as the pattern of pituitary insufficiency changes with time. An evolving endocrinopathy starting in later childhood is suggestive of the presence of a cerebral tumour. Children with subnormal growth velocities and a normal growth hormone response to pharmacological tests have a wide spectrum of pituitary morphological abnormalities which may be associated with growth hormone neurosecretory dysfunction.

Adolescent↗
PubMed1986

Dysgenesis of the corpus callosum and hypopituitarism.

A high resolution CT scan demonstrated the unexpected finding of dysgenesis of the corpus callosum in addition to the expected finding of pituitary hypoplasia in three children who presented with growth failure secondary to hypopituitarism. Several of the clinical features reported in association with dysgenesis of the corpus callosum may be ascribed to hypothalamo-pituitary dysfunction. These children emphasize the need to assess the endocrine function of patients with midline structural defects. It should not be assumed that the clinical manifestations are related solely to the anatomical abnormality.

Agenesis of Corpus Callosum↗
PubMed1986

Turner syndrome.

Explore the source record for details and available documents.

Adolescent↗
PubMed1986

Sleep EEG in growth disorders.

The sleep of 30 children with disorders of growth and development was studied because of the known association between sleep and the secretion of hormones. Thirty three normal children were studied for comparison. The sleep of two consecutive nights was monitored at home using a small portable electroencephalogram and electro-oculogram recorder. Within the normal group there were no significant differences between sexes nor between the first and second nights of recording. There was a significant decrease in total sleep time with increasing age due to reduction in the amounts of rapid eye movement sleep and stage IV sleep. There was no change in rapid eye movement latency or overall rapid eye movement activity between the three age groups. Children with genetic short stature and those with poor growth as a result of poor eating habits had an increased percentage of rapid eye movement sleep. A significant decrease in the percentage of stage IV sleep, increased amount of rapid eye movement sleep (especially active rapid eye movement sleep), and decreased rapid eye movement cycling time was found in five children with severe psychosocial deprivation. Children with constitutional delay of growth and puberty had an increased rapid eye movement cycling time and thus less rapid eye movement sleep over the whole night.

Adolescent↗
PubMed1986

Clinical diagnosis of disorders of puberty.

The authors emphasize the orderly sequence of events (consonance) characteristic of normal puberty. Loss of consonance of normal puberty indicates an underlying endocrine disorder.

Adenoma↗
PubMed1985

Comparison between a physiological and a pharmacological stimulus of growth hormone secretion: response to stage IV sleep and insulin-induced hypoglycaemia.

Peak growth hormone (GH) response to insulin-induced hypoglycaemia was compared with peak GH concentration during the first cycle of stage IV sleep in 75 children. 65 children had concordant results: in 38 GH concentrations were greater than 15 mU/l and in 27 less than this value. Results were discordant in 10 children. Results of sleep sampling under electroencephalographic control of the assessment of GH secretion are comparable to conventional pharmacological studies in terms of efficiency, sensitivity, and percentage false-negatives. Sleep sampling has the advantage of being a physiological test of secretion.

Adolescent↗
PubMed1985

Inhibition of physiological growth hormone secretion by atropine.

We have investigated the effects of atropine (specific muscarinic cholinergic inhibition) on the nocturnal secretion of GH during the first cycle of stage IV sleep in six normal volunteers and three tall adolescents. Atropine was administered orally in a dose of 0.6 mg (n = 8) or 1.8 mg (n = 4) 30 min before expected sleep and the sampling repeated. Peak GH level without atropine was 45.3 mU/l (range 5.7 to 92.0): both doses of atropine abolished sleep associated GH secretion. Spontaneous daytime GH secretion was demonstrated during five 6 h sampling periods in three normal adults. There was a significant decrease in spontaneous daytime GH secretion when the sampling was repeated after atropine 0.6 mg or 1.8 mg. We conclude that inhibition of GH secretion using anticholinergic drugs should be further investigated in the management of excessive growth hormone secretion.

Adolescent↗
PubMed1985

The treatment of central precocious puberty using an intranasal LHRH analogue (buserelin).

Eight girls and one boy with precocious puberty were treated with intranasal (D-Ser6)-LHRH (buserelin) for 0.5-2.3 years (mean 1.2 years). Treatment regimen varied between 17 and 40 microgram/kg/d in the girls to 10 micrograms/kg/d in the boy in two or three divided doses. Gonadotrophin-dependent clinical signs showed arrest or regression whereas those of adrenarche progressed. Serial pelvic ultrasound assessment was used to monitor treatment in four girls. Although peak stimulated gonadotrophins reduced to prepubertal levels, basal gonadotrophins became elevated on treatment. The mode of action of buserelin was the abolition of gonadotrophin pulsatility. Initial data suggest an improved growth prognosis. We concluded that intranasal therapy is an alternative route of administration of LHRH analogue in the treatment of precocious puberty.

Administration, Intranasal↗
PubMed1985

Single dose dexamethasone suppression test in children: dose relationship to body size.

We have performed an overnight single dose dexamethasone suppression test in 15 children at different dosages to determine the minimum dose required to suppress the 0800 h serum cortisol level. With a dexamethasone dose of 0.1 mg/m2 two of seven children showed suppression. When the dose was increased to 0.3 mg/m2 all of six patients showed suppression as did three given dexamethasone 0.5 mg/m2. We recommend that doses of dexamethasone should be calculated in terms of body surface area when assessing the hypothalamo-pituitary axis in children and that a dose of 0.3 mg/m2 should be used for suppression tests.

Body Surface Area↗
PubMed1985

Alteration in the nocturnal pulsatile release of GH during the induction of puberty using low dose pulsatile LHRH: a case report.

A 16.4 year old girl with idiopathic hypogonadotrophic hypogonadism had successful induction of puberty by administration of low dose LHRH by pulsatile subcutaneous infusion at night. Peak serum GH was increased with therapy but more importantly, pulsatile secretion of GH which was minimal before treatment, was restored after one week of LHRH treatment.

Adolescent↗
PubMed1985

Spontaneous gonadotrophin pulsatility and ovarian morphology in girls with central precocious puberty treated with cyproterone acetate.

We have studied four girls with central precocious puberty treated with cyproterone acetate for a mean of 3.6 years (range 1.5-6.3 years). Pelvic ultrasound assessment demonstrated suppression of the ovarian morphology of central precocious puberty despite the presence of spontaneous pulsatile gonadotrophin secretion at night. We suggest that the previously reported effects on gonadotrophin secretion induced by cyproterone acetate therapy, administered in recommended doses, are minor and that the predominant effect of cyproterone acetate in the treatment of girls with central precocious puberty is direct inhibition of ovarian steroidogenesis.

Child↗