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Biomedical subjects

C G Brook

Publications and source records attributed to C G Brook.

At least 163 records · Page 9Linked to original sources
PubMed1989

Growth velocity, growth hormone therapy, and serum concentrations of the amino-terminal propeptide of type III procollagen.

The relationship between serum concentrations of the amino-terminal propeptide of type III procollagen (PIIINP) and growth was assessed in 307 healthy subjects and 82 children with disorders of growth (41 with insufficient growth hormone, 23 with short stature and normal endocrinologic studies, 18 with tall stature) by means of a recently developed, simplified PIIINP radioimmunoassay. The PIIINP value appeared to be related to height velocity; in healthy children of each sex, the pattern of change with age mirrored the shape of the standard height velocity curve; in children with disorders of growth, there was a statistical correlation (p less than 0.001) between PIIINP concentration and height velocity. However, measurement of serum PIIINP alone had no diagnostic value because there was considerable overlap of PIIINP values in children with growth hormone insufficiency, short stature, normal stature, and tall stature. The most appropriate application of PIIINP may be in the monitoring of prepubertal children receiving exogenous growth hormone therapy; in these patients, increases in height velocity were reflected by increases in PIIINP, and early increases in PIIINP may have predictive value.

Body Height↗
PubMed1989

The half-life of exogenous growth hormone after suppression of endogenous growth hormone secretion with somatostatin.

We have estimated the half-life of serum growth hormone (GH) in six subjects on 14 occasions following an intravenous bolus injection of either 50 or 500 mU of biosynthetic human growth hormone (B-hGH) while endogenous GH secretion was suppressed by a continuous infusion of somatostatin. The disappearance curve of serum GH was mono-exponential and the mean half-life was 8.9 min (SD 1.5). This is less than previously reported and has important implications for the performance of GH profiles, which should be performed with 10-15 min sampling intervals, and the calculation of pituitary GH secretion rates.

Adolescent↗
PubMed1989

The infancy-childhood-puberty model of growth: clinical aspects.

The infancy-childhood-puberty (ICP) growth model describes human growth from the latter half of the intrauterine life to maturity as three additive and partly superimposed components--infancy, childhood and puberty. Each component can be analysed mathematically and appears to be controlled by distinct biological mechanisms. The infancy component is largely nutrition dependent, the childhood component is mostly dependent on growth hormone (GH) and the pubertal component depends on the synergism between sex steroids and GH. The ICP model offers a method for detecting abnormalities in the three components, so that early intervention can be targeted and therapy monitored.

Adolescent↗
PubMed1989

Use of continuous subcutaneous growth hormone-releasing hormone (GHRH (1-29)NH2) infusions to augment growth hormone secretion and to promote growth.

It has previously been shown that an 8-day continuous subcutaneous infusion of GHRH (1-29)NH2 in adult males augments growth hormone (GH) secretion with no evidence of desensitization of the response. The present report details the results of treatment with continuous subcutaneous infusions of GHRH (1-29)NH2 in eight children aged 6-9 years with partial GH insufficiency. All the children showed augmentation of GH secretion and an increase in growth velocity after 3 and 6 months of therapy.

Child↗
PubMed1989

Growth hormone secretion in Turner's syndrome and influence of oxandrolone and ethinyl oestradiol.

We investigated 24 hour growth hormone secretion by intermittent 20 minute blood sampling in 34 prepubertal patients with Turner's syndrome, aged 4.3-12.4 years. Growth hormone profiles were analysed by the PULSAR programme and results expressed as the sum of growth hormone pulse amplitudes. Six patients had abnormal growth hormone pulse frequencies. In the remaining 28, growth hormone pulse amplitudes declined significantly with increasing age, but there was no correlation between growth hormone pulse amplitudes and growth rates. Concentrations of insulin like growth factor-1 (IGF-1) rose with age but did not correlate with either growth rates or growth hormone secretion. Fifteen patients were given oxandrolone and 11 low dose ethinyl oestradiol. Both agents increased height velocity without increasing growth hormone secretion. We conclude that the relation between growth hormone secretion and growth in Turner's syndrome is less certain than in normal children. End organ resistance is probably due to a skeletal dysplasia. Both oxandrolone and low dose ethinyl oestradiol improve the growth of girls with Turner's syndrome, but their mechanism of action remains uncertain.

Body Height↗
PubMed1989

Thyroid dysfunction after radiotherapy and chemotherapy of brain tumours.

We investigated thyroid function in 119 survivors of treatment for brain tumours not involving the hypothalamo-pituitary region. Cranial irradiation did not effect thyroid function but 11 of 47 children (23%) who had spinal irradiation had raised concentrations of thyroid stimulating hormone. Chemotherapy further increased the incidence of thyroid dysfunction: two of four patients who had cranial irradiation and chemotherapy and 20 of 29 patients (69%) who had spinal irradiation and chemotherapy had increased thyroid stimulating hormone concentrations. Only six patients with raised thyroid stimulating hormone concentrations had low serum thyroxine concentrations. Four children had secondary hypothyroidism. Thyroid function should be monitored in children who have received chemotherapy or radiotherapy. A rise in thyroid stimulating hormone concentrations is the most sensitive indicator of thyroid dysfunction. Children with raised thyroid stimulating hormone concentrations should be treated with thyroxine.

Brain Neoplasms↗
PubMed1989

Monitoring treatment in congenital adrenal hyperplasia.

We report results of monitoring treatment in 41 patients with congenital adrenal hyperplasia controlled over 0.3-13.1 years using standard auxological techniques alone. Doses of glucocorticoid (15-25 mg/m2/day) and mineralocorticoid (0.15 mg/m2/day) replacement were determined initially using biochemical indices and thereafter adjusted according to surface area. Monitoring was solely directed at maintaining a 50th centile height velocity for chronological age. Of 41 patients, 32 were referred after the newborn period. Nearly half of these patients were either overtreated or undertreated before their referral. Of the nine treated from birth, all but one were in good control and only two have had a second hospital admission. Present height standard deviation scores (SDS) for chronological age range from -1.60 to -0.26. Height SDS for bone age were compared with midparental heights in 33 patients: 15 treated with early emphasis on growth had a height prognosis exceeding midparental values; patients who had experienced appreciable prior overtreatment or undertreatment fared less well. In the long term management of congenital adrenal hyperplasia correction of salt loss is of primary importance. Doses of glucocorticoid required in addition to mineralcorticoid replacement should be continuously assessed and adjusted to maintain a normal growth velocity. This is most conveniently achieved by standardising replacement doses on surface area.

Adrenal Hyperplasia, Congenital↗
PubMed1989

The measurement and effect of growth hormone in the presence of growth hormone-binding antibodies.

We have developed methods for measuring the concentrations of free GH in plasma using a polyethylene glycol (PEG) separation procedure to remove antibody-bound GH within 1 h of collection. Total GH concentrations were obtained by acidification of the GH-antibody complex to release the GH followed by PEG precipitation of the antibody. The plasma GH assay had a within-assay coefficient of variation (C.V.) of 6.8% at 4.6 mU/l and a between-assay C.V. of 9.2% at 4.0 mU/l. The PEG-modified assay had a within-assay C.V. of 4.3% at 6.3 mU/l and a between-assay C.V. of 10.9% at 5.3 mU/l. Both assays had a sensitivity of 1.3 mU/l. There was good correlation between plasma and free GH concentrations in 24-h profiles in two tall children (r = 0.98; P less than 0.001) and between total and free GH in the same profiles (r = 0.97; P less than 0.001). GH antibodies were measured using a highly sensitive radioimmunoassay. In children who did not develop GH antibodies there was no difference between total, plasma and free GH concentrations. In contrast, in those who developed GH antibodies both total and plasma GH concentrations were markedly increased compared with free GH concentrations. The presence of GH antibodies did not affect the growth, plasma insulin-like growth factor-I concentrations or fasting serum insulin concentration responses to 1 year of therapy with biosynthetic human GH.

Autoantibodies↗
PubMed1988

The effect of gonadotrophin releasing hormone analogue on height prognosis in growth hormone deficiency and normal puberty.

We have treated seven pubertal children, five (three female, two male) with growth hormone deficiency and two (one female, one male) with constitutional short stature with intranasal (D-Serine6) gonadotrophin releasing hormone (GnRH) analogue (Buserelin) for a mean of 0.84 years (range, 0.5-1.3). Treatment was successful in arresting pubertal development but there was no improvement in final height prognosis.

Administration, Intranasal↗
PubMed1988

Long-term auxologic effects of human growth hormone.

Seventy-eight children with idiopathic growth hormone deficiency treated with human growth hormone continuously for up to 5 years were studied; 58 were prepubertal at the start of treatment, and remained so throughout the treatment period, and 20 were showing pubertal signs at the start of treatment. Height velocity increased markedly in the prepubertal group over the first year of therapy, with a gradual decrease in the following years. The increased growth rate of the first treatment year continued in the pubertal group. Height standard deviation score for chronologic age increased significantly throughout all treatment years, but for bone age did not change in either group. The more frequent the treatment regimen, the better was the growth response; a dose effect independent of frequency was identified. Thus human growth hormone treatment cannot make up a deficit in height prognosis already present at diagnosis, but prevents further loss of stature, which is why early diagnosis is important.

Adolescent↗
PubMed1988

Growth hormone secretion in children determined by time series analysis.

Mid childhood growth has been studied in 26 short children (18M;8F) aged between 5.2 and 11.9 years growing with height velocity standard deviation score (SDS) between 0 and -0.8 and 24 short children (17M;7F) growing with height velocity SDS less than 0.8. Twenty-four hour GH profiles were analysed by an iterative method of pulse detection and subjected to time series analysis to determine dominant periodicity within the data arrays. Children aged less than 7 years displayed no dominant periodicity but after this age a periodicity of 200 min emerged. In the whole sample, differences between growth rate could be explained entirely by pulse amplitude. Nevertheless, the normal decline in height velocity over this age period occurred despite a significant shift in periodicity and an increase in GH pulse amplitude. This modulation of childhood growth by GH pulse amplitude persisted into puberty and the pubertal growth spurt of 14 tall girls was shown to be amplitude modulated with the periodicity unchanged. We conclude that mid childhood and pubertal growth is GH pulse amplitude modulated with a periodicity of approximately 200 min.

Age Factors↗
PubMed1988

The mechanism of the adolescent growth spurt induced by low dose pulsatile GnRH treatment.

We have used GnRH administered in a pulsatile fashion to treat 26 patients (12M:14F) with delayed puberty. Treatment was for a mean of 1.05 years (range, 0.3-1.6). Mean age at the onset of treatment was 16.4 years in the girls (range, 12.7-28.2) and 15.8 years in the boys (range, 13.8-17.8). At different stages of sexual maturation, overnight serum samples for growth hormone (GH) were taken at 15 min intervals between 2000 h and 0600 h. The girls had a peak growth velocity which occurred between breast stages 2 and stage 3 (B2/3). GH secretion (both sum of the GH peaks and area under the GH pulse) increased at B2 and reached a peak at B3. Growth acceleration in the boys started at the attainment of a 9-10 ml testicular volume and reached a peak at 11-15 ml. The boys demonstrated an initial fall in GH secretion with the onset of treatment until the attainment of 9-10 ml testicular volume; peak GH secretion occurred at the attainment of 11-12 ml testicular volume. There was no change in GH pulse frequency during treatment in either sex. These observations and the maintenance of the normal relationship of the growth spurts to the appearance of secondary sexual characteristics are relevant to the mechanisms and timing of the adolescent growth spurts in normal girls and boys.

Circadian Rhythm↗
PubMed1988

Cholinergic muscarinic blockade produces short-term suppression of growth hormone secretion in children with tall stature.

We have studied the effects of oral pirenzepine (50 mg twice daily) on growth and growth hormone (GH) secretion in 10 children with tall stature (9F, 1M). Suppression of GH secretion was observed in all children for 2-3 h after drug administration but was followed by rebound secretion of GH after 4-6 h. Consequently there was little overall change in GH secretion. In the dose regimen used the disruption of normal pulsatile GH secretion was not sufficiently significant to change final or predicted heights.

Adolescent↗