Polycystic ovaries in childhood.
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Adolescent↗
Biomedical subjects
R Stanhope
Publications and source records attributed to R Stanhope.
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↗
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↗
Gonadotrophin, growth hormone and prolactin secretion in children with primary hypothyroidism.
We have studied eight children with primary hypothyroidism (6F, 2M) aged 6.7 to 14.2 years. The girls were prepubertal and the boys had early normal pubertal development. Overnight secretion of LH, FSH, TSH, PRL and GH, and ovarian ultrasound morphology were assessed before and up to 9 months after commencing thyroxine treatment. Serum FSH concentrations in all the girls were increased above LH levels and severe hypothyroidism was associated with reduced GH secretion. These abnormalities reversed with thyroxine treatment. The boys had less severe hypothyroidism and did not demonstrate abnormal gonadotropin or GH secretion. We conclude that primary hypothyroidism in childhood is associated with widespread disturbance of pituitary function, including increased FSH secretion often without signs of early sexual maturation.
Adolescent↗
Physiological growth hormone (GH) secretion during the recovery from psychosocial dwarfism: a case report.
We describe a 6.4 year old boy who had reversible GH insufficiency secondary to psychosocial dwarfism. On removal to a more favourable environment we observed the recovery of physiological GH secretion by progressive increase in GH pulse amplitude. These observations are relevant to our understanding of the control of GH secretion in that GH pulse frequency appears invariable and alteration in GH secretion is by pulse amplitude modulation.
Child↗
Abnormal pubertal development in primary hypothyroidism.
We have studied three patients (1M, 2F), age range 10.9 to 15.5 years, who had abnormal sexual maturation secondary to primary hypothyroidism. The boy had inappropriately large testes for his stage of puberty, the girls had isolated breast development and there was absence of pubertal growth acceleration. FSH, LH, TSH and GH secretion, pituitary imaging and ovarian ultrasound morphology were studied before and during thyroxine treatment. In the hypothyroid state, FSH levels were elevated with abnormal pulsatility and LH:FSH concentrations were reversed.
Adolescent↗
Growth, growth hormone and sex steroid secretion in girls with central precocious puberty treated with a gonadotrophin releasing hormone (GnRH) analogue.
We have treated 14 girls with central precocious puberty for a mean period of 2.3 years (range, 0.5-3.9) with intranasal (D-Ser6) GnRH analogue administered in a mean dose of 28 micrograms/kg/day (range, 15-56). With the onset of treatment there was an initial increase in sitting height compared to subischial leg length, but overall there was no significant change in height standard deviation score for bone age. In this respect our results were indistinguishable from untreated children with central precocious puberty. There was a decrease in physiological GH secretion, associated with decreased sex steroid secretion, which probably accounts for the growth deceleration which has been described during GnRH analogue therapy. The effect of this growth deceleration combined with slowing of the rate of epiphyseal maturation may explain the absence of alteration in height prognosis.
Administration, Intranasal↗
Double blind placebo controlled trial of low dose oxandrolone in the treatment of boys with constitutional delay of growth and puberty.
Nineteen boys, mean age 14.4 years (range 12.9-16.3), with constitutional delay of growth and puberty were randomised into two groups in a double blind fashion for a three month period. Ten boys received oxandrolone, 2.5 mg per day (mean dose 0.072 mg/kg/day), and nine boys were treated with placebo. Mean growth velocity increased from 4.5 cm/year in the oxandrolone treated group to 9.6 cm/year in three months, and this was sustained at 8.6 cm/year after cessation of treatment. In the placebo treated group, growth rate showed no alteration from 5.1 cm/year to 5.2 cm/year; boys in this group were then treated with oxandrolone, 2.5 mg a day (mean dose 0.073 mg/kg/day) for three months and growth velocity accelerated to 8.6 cm/year. Serum concentrations of insulin-like growth factor -1/somatomedin-C (IGF-1) increased during oxandrolone treatment and continued to rise after treatment had ceased. There was no change in serum IGF-1 concentration during treatment with placebo. Oxandrolone, when used in an appropriate regimen, is an effective, safe treatment for boys with constitutional delay of growth and puberty.
Adolescent↗
Management of constitutional delay of growth and puberty.
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Adolescent↗
Precocious or early puberty and growth failure in girls treated for acute lymphoblastic leukaemia.
We have studied 41 children with early or precocious puberty who have been treated for acute lymphoblastic leukaemia with prophylactic cranial irradiation (1,800-2,400 cGy) accompanied by intrathecal methotrexate and systemic chemotherapy. Mean age at radiotherapy was 3.9 years (range 1.7-7.7) in the girls and 4.8 years (range 2.6-7.8) in the boys. Mean age at the onset of puberty was 8.6 years (range 6.7-9.7) in the girls and 9.3 years (range 7.8-10.3) in the boys. Of the 41 children with early puberty (greater than 1.4 SD from the mean) 36 were females and 5 were males. 21 of the 36 girls had an absent or inadequate growth acceleration of puberty. 7 of 12 girls who had a pharmacological test of growth hormone (GH) secretion had GH insufficiency (peak level less than 20 mU/l). Early or precocious puberty combined with GH insufficiency may produce severe growth failure and we have used a treatment regimen of a gonadotrophin-releasing hormone analogue, in order to reduce the rate of epiphyseal maturation, combined with biosynthetic GH to increase or sustain growth rate. We have treated 4 girls in this manner. During a mean treatment period of 0.86 years, height SDS for bone age rose from a mean of -1.06 to -0.59. Longer treatment periods will be required to assess the effect on final height.
Child↗
Physiological growth hormone secretion in children with short stature and intra-uterine growth retardation.
31 prepubertal children with short stature [mean height standard deviation score (SDS) -2.84] and low birth weight (mean -2.82 SDS) were studied. Mean age was 6.0 years and mean height velocity SDS was -0.76. Patients were classified as having either the clinical characteristics of Russell-Silver syndrome (RSS) (4 F, 13 M) or not (4 F, 10 M). All children had an overnight profile of spontaneous growth hormone (GH) secretion. 4 children achieved a maximum GH concentration of less than 20 mU/l. 9 children with RSS secreted only one large GH peak during the night. Most of the non-RSS group had normal GH pulse frequency but 3 boys had a fast-frequency pattern. Abnormal GH secretion may contribute towards growth failure in children with low birth weight/RSS.
Body Height↗
An evaluation of hormonal changes at puberty in man.
The pulsatile nature of the secretion of gonadotrophins, sex steroids and growth hormone are important in both the onset and maintenance of sexual maturation. The night-time is intimately related to the endocrine events which result in puberty, such that hormone measurements during the daytime have little meaning. This relationship between the night-time and gonadal function is not restricted to puberty but continues in adult life; the onset of the preovulatory LH surge occurs in the early hours of the morning. Girls seem more sensitive to small changes in GnRH concentrations than boys, which is why the physical signs of puberty appear slightly earlier in them. Low levels of oestradiol appear to assist growth hormone secretion, whereas higher levels of testosterone are required for the same effect. This probably explains the sex differences in the timing of the pubertal growth spurts.
Adolescent↗
Growth and growth hormone secretion.
Growth hormone pulse amplitude is intimately connected with growth in childhood. Its effects are most clear in middle childhood, although the influence of adrenal androgens is probably also important. In infancy, nutrition plays an important part and, in the adolescent growth spurt, the synergism with sex steroids is important. Detailed attention needs now to be focussed on the mechanisms by which growth hormone is secreted and has its action; these include the effects of GHRH, somatostatin, insulin and IGF-I.
Adolescent↗
New concepts of the growth spurt of puberty.
The timing of the growth spurt of normal children does not affect their final height attainment. Growth rate during the growth acceleration of puberty correlates with changes in GH, and not sex steroid, secretion. GH secretion during puberty is pulse amplitude, and not frequency, modulated. In both central precocious puberty and normal puberty suppressed with a GnRH analogue, the rate of epiphyseal maturation is decreased as are GH pulse amplitude and growth, but with no influence on final height.
Adolescent↗
Evolution of polycystic ovaries in a girl with delayed menarche. A case report.
A 17-year-old girl had delayed growth secondary to low birth weight. Although she entered puberty at 12.5 years, she had delayed menarche. She underwent serial ovarian ultrasound scans, and a change in ovarian morphology was observed, from a normal multicystic appearance to one typical of polycystic ovaries (PCOs). We hypothesize that normal ovarian morphology may change to PCOs during the peripubertal period because of a change in the endocrine milieu.
Adolescent↗
Induction of puberty by pulsatile gonadotropin releasing hormone.
15 girls and 17 boys with delayed or arrested puberty were treated with gonadotropin releasing hormone (GnRH) for a mean of 1.04 years. GnRH was administered subcutaneously in a pulsatile fashion at 90 min intervals, and the dose was increased as required to maintain progression of puberty, initially only at night and subsequently over 24 h. Initial GnRH dose was 1-2 micrograms per pulse in the girls and 2-4 micrograms per pulse in the boys. The effect of treatment was monitored by serial overnight gonadotropin profiles in all patients and with pelvic ultrasound in the girls. The clinical features, growth acceleration, endocrinology, and ovarian ultrasound morphology of puberty were those seen in normal children. Measurement of spontaneous gonadotropin pulsatility after treatment had been discontinued allowed the distinction between 20 patients with hypogonadotropic hypogonadism and 12 who had constitutional delay of growth and puberty. 2 girls and 6 boys did not respond to the treatment regimen. These findings indicate that normal puberty is GnRH dependent.
Adolescent↗
The effect of cyproterone acetate on the growth of children with central precocious puberty.
We have examined the growth and skeletal maturation of 19 children (6 male, 13 female) with central precocious puberty. The aetiology in nine patients (5 male, 4 female) was secondary to a hypothalamic hamartoma. Six children (2 male, 4 female) received no treatment whereas 13 children (4 male, 9 female) were treated with cyproterone acetate in a mean dose of 68 mg/m2 per day (range, 34-260) for a mean duration of 4.5 years (range, 0.8-7.9). There was no significant difference between height SDS for bone age at the beginning and end of observation in either treated or untreated groups. No significant relationship between the mean dose of cyproterone acetate used and change in height SDS for bone age could be determined. We conclude that cyproterone acetate has no beneficial effect on the growth prognosis of children with central precocious puberty.
Body Height↗
The evolution of polycystic ovaries in a girl with hypogonadotropic hypogonadism before puberty and during puberty induced with pulsatile gonadotropin-releasing hormone.
We describe a girl of 12.7 years who had GnRH deficiency after surgery and radiotherapy for a craniopharyngioma at age 5 years. She had large cystic ovaries with a small uterus in the absence of spontaneous gonadotropin pulsatility. Puberty was induced by low-dose pulsatile GnRH treatment over a 1.5-year period. In the perimenarcheal period, ovarian morphology became typical of PCO with abnormal diurnal pulsatile gonadotropin secretion. These data suggest that PCO is primarily a disorder of the ovary and that the observed gonadotropin abnormalities are secondary to the ovarian lesion.
Child↗