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Biomedical subjects

M A Preece

Publications and source records attributed to M A Preece.

At least 145 records · Page 8Linked to original sources
PubMed1988

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↗
PubMed1988

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↗
PubMed1988

Adolescent growth and pubertal progression in the Silver-Russell syndrome.

The pattern of growth and development of 18 adolescent children with the Silver-Russell syndrome was studied. Mature height was about -3.6 standard deviation scores in both sexes. This is comparable to the height reduction at diagnosis, which has been reported previously. The pattern of puberty and adolescent growth was essentially normal and occurred at a marginally earlier time than normal, although in this small series the differences were not significant. In the girls there was a tendency to gain subcutaneous fat after puberty. This trend was not apparent in the boys.

Adolescent↗
PubMed1988

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↗
PubMed1988

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↗
PubMed1988

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↗
PubMed1988

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↗
PubMed1988

Prediction of adult height: methods and problems.

The three commonly used methods of height prediction employ various combinations of anthropometric data and bone age. In normal children, the regression type methods are preferable, though they do not perform well in the more severe disorders of growth. They are extremely dependent upon the limitations of the method of bone age determination that is used. A major source of error is the inability to predict the timing or the intensity of the adolescent growth spurt. Until this proves possible it is unlikely that significant improvements can be made.

Adolescent↗
PubMed1988

Somatomedin-C/IGF-I measured by radioimmunoassay and somatomedin bioactivity in adolescents with insulin dependent diabetes compared with puberty matched controls.

Plasma concentrations of insulin like growth factor-I in the adolescent diabetic remain controversial. IGF-I levels were determined by radioimmunoassay in 81 insulin dependent adolescent diabetics (49 boys and 32 girls) and compared with 75 puberty stage matched normal controls. Plasma somatomedin bioactivity was determined by cartilage bioassay in a smaller group of 10 normal and 25 diabetic subjects. IGF-I concentrations increased in the normals during puberty and there were no observed differences between the sexes. (P1, 0.77 +/- 0.08; P2, 1.33 +/- 0.2; P3, 1.59 +/- 0.16; P4, 1.76 +/- 0.16; P5, 2.24 +/- 0.09). IGF-I also increased in the diabetics reaching a peak level at stage three in both girls and boys. Combining the data from both sexes the diabetics had significantly lower levels of IGF-I compared to controls at stages; (P1, 0.67 +/- 0.05, ns. P2, 0.92 +/- 0.1, p less than 0.05; P3, 1.16 +/- 0.09, p less than 0.01; P4, 0.73 +/- 0.11, p less than 0.001; P5, 1.13 +/- 0.11, p less than 0.001). Plasma somatomedin bioactivity was elevated in the normals but inhibitory responses were observed in all but two of the diabetic subjects, highlighting the presence of inhibitory factors in diabetic plasma. HbA1C levels rose in the diabetics during puberty, however using covariance analysis there was no relationship between IGF-I and HbA1C when changes relating to puberty were excluded. The importance of controlling for pubertal stage as opposed to age is noted when assessing IGF-I status in the diabetic adolescent.

Adolescent↗
PubMed1987

Treatment of growth-hormone deficiency with growth-hormone-releasing hormone.

18 prepubertal growth-hormone (GH)-deficient children were treated with twice-daily subcutaneous injections of a growth-hormone-releasing hormone analogue, GHRH (1-29) NH2. In 12 of the children the height velocity rose on GHRH treatment, and 8 were judged to have shown a worthwhile response to therapy in that their height velocities during the first 6 months of treatment increased by greater than 2 cm/yr (range 2.7-11.2 cm/yr). These 8 children have now been treated for 6 to 18 months and their increase in height velocity has been maintained. In the 14 patients who had previously received human GH (hGH) height velocity on hGH correlated with that on GHRH. 4 of these patients showed growth deceleration with GHRH, for unknown reasons. A pretreatment peak serum GH response of above 30 mU/l during an intravenous GHRH test was predictive of a good growth response to GHRH but a lower peak did not preclude a growth response. There was no consistent evidence of a priming or desensitisation effect of therapy on the GH responses to GHRH. Although anti-GHRH antibodies developed in 14 patients, these did not seem to have adverse effects on either growth or the GH responses to GHRH. GHRH (1-29) NH2 therapy is an alternative to conventional hGH in the treatment of some GH-deficient children. Ideal dose regimens need to be established.

Adolescent↗
PubMed1987

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↗
PubMed1987

Physiological growth hormone secretion during slow-wave sleep in short prepubertal children.

The usefulness of a limited nocturnal GH profile has been evaluated for the assessment of physiological GH secretion. We have analysed the complete overnight GH and sleep profiles of 20 short prepubertal children, sampled at 15-min intervals. The mean age was 9.1 years (range 4.3-11.7 years) and mean height velocity standard deviation score (SDS)-1.0 (range -2.4 to +0.4). The sleep stage in which the maximal GH value was reached varied considerably between the patients. Only 55% achieved the maximal GH value during the first slow-wave sleep period, and 65% in the first 2 h of sleep. The maximal values during the first slow-wave period correlated weakly with the sum of the nocturnal peak values and the total area under the curve of the complete GH profile. None of these parameters correlated with height velocity. We conclude that at present there is no substitute for complete overnight or 24 h GH profiles for the assessment of physiological GH secretion, but the clinical significance of the variations seen remains unclear.

Body Height↗
PubMed1987

Growth hormone releasing hormone in the assessment and long-term treatment of growth hormone deficiency.

The secretion of hGH after the administration of the analogue of growth hormone releasing hormone, GHRH (1-29)NH2, to 8 normal adults and 41 short children has been studied. The children were classified on the basis of their hGH response to insulin-induced hypoglycaemia; 28 had severe hGH deficiency (peak serum hGH less than 7 mIU/litre) and 13 had simple short stature (peak serum hGH greater than 15 mIU/litre). The hGH response to GHRH was similar in normal adults and short stature children, but significantly lower in the hGH deficient children. In 23 (82%) of the hGH deficient children the peak serum hGH in response to GHRH was greater than 7 mIU/litre (the maximum value seen during hypoglycaemia), and in 14 (50%) the peak serum hGH in response to GHRH was greater than 15 mIU/litre. This suggests that in the majority of hGH deficient children the defect in hGH secretion results from hypothalamic GHRH deficiency. The hGH responses of the short stature children to insulin-induced hypoglycaemia were mainly in the low range of normal, and the majority showed normal hGH responses to GHRH. Eighteen prepubertal children with definite hGH deficiency have been treated for 3-18 months with twice daily, subcutaneous injections of GHRH. This has promoted linear growth in 12 children, of whom 8 showed an increment in height velocity of 2-11 cm/year. GHRH provides a valuable method for the assessment of hGH secretion, but by itself it cannot be used to establish deficient hGH secretion; this requires a stimulation test that promotes hypothalamic GHRH secretion, such as insulin-induced hypoglycaemia. GHRH is a practical alternative therapy to hGH for some hGH-deficient children.

Adult↗
PubMed1987

Growth hormone deficiency in adults--an indication for therapy?

Case studies are presented for two patients, one with isolated hGH deficiency and one with multiple hormone deficiencies. The patients were studied 3 months before, and 3 and 9 months after discontinuing hGH therapy, at 19 and 18 years of age, respectively. Strength in the quadriceps femoris, cross-sectional area of the quadriceps muscles and cross-sectional muscle fibre area were measured. In the patient with multiple hormone deficiencies, clear decreases in all three parameters were evident after discontinuing hGH treatment. There were no significant changes in the other patient. Reasons for these differences are discussed.

Adolescent↗
PubMed1987

Cushing's disease and craniopharyngioma.

A 14-year old girl presented with growth failure and Cushing's disease. Histological examination confirmed a craniopharyngioma but failed to show that the tumour secreted adrenocorticotrophic hormone. We suggest that her Cushing's disease was caused by hypothalamic dysfunction associated with increased corticotrophin-releasing hormone secretion, secondary to the craniopharyngioma.

Adolescent↗