PubMed Health⌕ Search

Biomedical subjects

G E Butler

Publications and source records attributed to G E Butler.

28 records · Page 2Linked to original sources
PubMed1991

Patterns of pulsatile luteinizing hormone and follicle-stimulating hormone secretion in prepubertal (midchildhood) boys and girls and patients with idiopathic hypogonadotropic hypogonadism (Kallmann's syndrome): a study using an ultrasensitive time-resolved immunofluorometric assay.

To study the ontogeny of spontaneous pulsatile LH and FSH secretion before the onset of puberty, plasma LH and FSH were measured by an ultrasensitive time-resolved immunoflurometric assay in 16 boys and 6 girls, aged 6.5 +/- 0.2 yr (+/- SEM; range, 4.4-8.0) with short stature. Eight male patients with idiopathic hypogonadotropic hypogonadism (Kallmann's syndrome), aged 24.1 +/- 3.4 yr, were also investigated. Blood samples were withdrawn at 10- to 20-min intervals for 12 h from 2000-0800 h. Pituitary responsiveness was assessed by a standard iv LHRH challenge test. LH and/or FSH pulses were detectable in all but two prepubertal subjects. In boys, low amplitude LH (0.16 +/- 0.06 U/L) and FSH (0.19 +/- 0.03 U/L) pulses were detectable at mean frequencies of 2.19 +/- 0.37 and 2.13 +/- 0.46 pulses/12 h, respectively. In girls, low amplitude LH (0.29 +/- 0.18 U/L) pulses, but higher (P less than 0.05 compared to boys) amplitude FSH (1.62 +/- 1.05 U/L) pulses were observed at frequencies of 1.71 +/- 0.56 and 1.67 +/- 0.53 pulses/12 h, respectively. Mean FSH in prepubertal girls (1.95 +/- 0.88 U/L) was significantly (P less than 0.05) higher than that in boys (0.46 +/- 0.07 U/L), but mean LH was not different at 0.17 +/- 0.07 and 0.10 +/- 0.03 U/L, respectively. Patients with Kallmann's syndrome had mean LH and FSH levels indistinguishable from those of prepubertal boys. Nocturnal augmentation of pulsatile LH or FSH secretion was observed in 74% of children (71% in girls and 75% in boys), but in none of the eight patients with Kallmann's syndrome. A close temporal association was observed between sleep onset and the appearance of nocturnal pulsatile gonadotropin secretion. The FSH response to exogenous LHRH in prepubertal girls was significantly greater than that in patients with Kallmann's syndrome and prepubertal boys, but LH responses were not different. Our results show that pulsatile LH and FSH secretion occurs in the majority of boys and girls in midchildhood, with a robust association with nocturnal sleep onset. Between the ages of 4-8 yr, these low amplitude and low frequency pulses are unable to activate gonadal function. The regulation of FSH secretion in prepubertal girls appears to be different from that in prepubertal boys.(ABSTRACT TRUNCATED AT 400 WORDS)

Antibodies, Monoclonal↗
PubMed1990

Patterns of pulsatile luteinizing hormone secretion before and during the onset of puberty in boys: a study using an immunoradiometric assay.

To study spontaneous pulsatile LHRH/LH secretion around the onset of puberty, nocturnal plasma LH was measured by means of a highly sensitive immunoradiometric assay in 30 boys (aged 5.6-16.8 yr) investigated for potential problems with growth and/or development. Blood was withdrawn at 10- to 20-min intervals from 2000-0800 h. Pulse analysis was accomplished by a computerized peak detection algorithm. Pituitary and gonadal responsiveness was assessed by a standard exogenous LHRH challenge and testosterone. Subsequent clinical progress was monitored for a mean duration of 2.08 +/- 0.16 yr and used as the basis for classifying patients retrospectively into three groups: 1) prepubertal (n = 14), 2) peripubertal (n = 11), and 3) pubertal (n = 5). LH pulses were undetectable in 9 and present in 5 prepubertal subjects, the youngest of whom was aged 7.3 yr. In peripubertal and pubertal individuals, 2-7 LH pulses/12 h were detectable. LH pulses were detectable before sleep by midpuberty (Tanner stage 3). There was a highly significant (P less than 0.0001) increase in LH/LHRH pulse frequency from 0.93 +/- 0.38 to 4.55 +/- 0.43/12 h (mean +/- SEM) between the prepubertal and peripubertal groups and a further increase to 6.20 +/- 0.37/12 h in the pubertal group. LH pulse amplitude remained under 1.0 U/L in both the prepubertal and peripubertal groups and only increased significantly to 2.02 +/- 0.17 U/L in pubertal boys. Response to LHRH increased significantly between the prepubertal (2.47 +/- 0.49 U/L) and peripubertal (6.53 +/- 2.02 U/L) patients. T increased significantly at each stage, with the greatest rise between the peripubertal and pubertal stages.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Salivary testosterone levels and the progress of puberty in the normal boy.

Salivary testosterone (ST) levels were measured in 84 boys aged 7.3-16.2 from the Edinburgh Growth Study. The correlation coefficient between matched plasma/saliva samples was 0.88. Six samples were collected over the course of one day from 0900 to 2100 h each month in the majority of the children for 4 consecutive months. Mean daily ST levels showed a significant rise between each pubertal stage (genital (G) and pubic hair (PH]. The rise in ST became more rapid once a mean testicular volume (MTV) of 10 ml had been reached. The diurnal rhythm was assessed by individual curve fitting on the log scale and by cosinor analysis. A rhythm was present prepubertally and developed into a pattern similar to that of the adult rhythm by stage G3. The monthly rate of rise of ST was greatest at stage G4. A significant rise in ST levels was detectable immediately prior to an increase in MTV to 3 ml. This allowed earlier recognition of the clinical onset of puberty at testicular volume of 3 ml, which in this group occurred at 10.9 (SD 0.9) years. ST is a non-invasive and sensitive method for the serial monitoring of gonadal function in the prepubertal and adolescent boy.

Adolescent↗
PubMedDate not supplied

The cyclical nature of prepubertal growth.

We have examined the complete longitudinal height velocity (HV) data of 135 (80 male and 55 female) chromosomally normal children from the Edinburgh Longitudinal Growth Study who were measured six-monthly between age 3 years and the onset of the adolescent growth spurt. Individual HV curves appeared to consist of a regular series of accelerations and decelerations in a cyclical fashion. After excluding variations due to measurement error, and basing the analysis on the pattern of acceleration, we were able to identify a number of spurts of regular occurrence. The mid-childhood spurt was clearly identified at ages 7.0 in boys and 6.7 years in girls, and could be identified in all children except one girl. Other spurts were also apparent; a pre-school spurt at ages 4.8 and 4.6, a late-childhood spurt at ages 9.2 and 8.6, and in children with an average-to-late onset of puberty, a prepubertal spurt at ages 10.8 and 10.0 years in boys and girls respectively. Synchronization at peak HV was performed for each spurt as described by Shuttleworth (1937) for the adolescent growth spurt. The overall pattern of growth appeared to be cyclical with a mean peak interval of 2.2 years in boys and 2.1 years in girls, the cycles appearing to continue until interrupted by the onset of the adolescent growth spurt. Sitting height velocity (SHV) and leg length velocity (LLV) curves also showed a cyclical pattern, but each varied independently. The magnitude of the HV spurts in an individual was dependent on the synchrony between the phases of SHV and LLV spurts. The cyclical pattern of prepubertal growth with its rapid changes in HV should be taken into account when assessing the growth of any child and in the response to any treatment offered.

Adolescent↗
PubMedDate not supplied

Serum leptin and leptin binding activity in children and adolescents with hypothalamic dysfunction.

Marked disturbance in eating behaviour and obesity are common sequelae of hypothalamic damage. To investigate whether these were associated with dysfunctional leptin central feedback, we evaluated serum leptin and leptin binding activity in 37 patients (age 3.5-21 yr) with tumour or trauma involving the hypothalamic-pituitary axis compared with 138 healthy children (age 5.0-18.2 yr). Patients were subdivided by BMI <2 SDS or > or = 2 SDS and healthy children and children with simple obesity of comparable age and pubertal status served as controls. Patients had higher BMI (mean 1.9 vs 0.2 SDS; p <0.001), a greater proportion had BMI > or = 2 SDS (54% vs 8%; p <0.001) and higher serum leptin (mean 2.1 vs 0.04 SDS; p <0.001) than healthy children. Serum leptin (mean 1.1 vs -0.1 SDS; p = 0.004) and values adjusted for BMI (median 0.42 vs 0.23 microg/l:kg/m2; p = 0.02) were higher in patients with BMI <2 SDS. However, serum leptin adjusted for BMI was similar in patients with BMI > or = 2 SDS compared to corresponding controls (1.08 vs 0.95; p = 0.6). Log serum leptin correlated with BMI SDS in all subject groups but the relationship in patients with BMI <2 SDS was of higher magnitude (r = 0.65, slope = 0.29, p =0.05 for difference between slopes) than in healthy controls (r = 0.42, slope = 0.19). Serum leptin binding activity (median 7.5 vs 9.3%; p = 0.02) and values adjusted for BMI (median 0.28 vs 0.48 % x m2/kg; p <0.001) were lower in patients than in healthy children. The markedly elevated leptin levels with increasing BMI in non-obese patients with hypothalamic-pituitary damage are suggestive of an unrestrained pattern of leptin secretion. This along with low leptin binding activity and hence higher free leptin levels would be consistent with central leptin insensitivity.

Adipose Tissue↗