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Milo Zachman

In recent years, it became evident that the hypothalamo-pituitary-gonadal axis is functioning in boys already between the neonatal period and the onset of puberty. With sensitive techniques, testosterone and gonadotropines have been detected in the plasma and urine of prepubertal boys. It is now believed that, during this period of life, the axis is active, but that either the feedback mechanisms are adjusted to a different level, the hypothalamic centers being more sensitive to androgens and keeping the testicular androgen production low, or that the gonads are more refractory to the effect of gonadotropins.

The androgen levels in biological fluids from normal prepubertal boys are extremely low. It is therefore impossible to distinguish the basal values of children with defective steroid production from those of normal children. Recently, several investigators have, however, shown that stimulation of the testicular interstitial cells is possible, if human chorionic gonadotropin is administered for several

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George W. Clayton


Patterns of growth of 30 children with Congenital Adrenal Hyperplasia of the 21-hydroxylase type were studied from infancy to maturity. These children were compliant as to therapy. Intramuscular (I.M.) Cortisone (40mg/M2) given every three days resulted in growth failure after the first year of life. A marked increase in height velocity occurred when oral Cortisone (20-25mg/M2) was given at approximate] 3 years. Growth was relatively normal during childhood in both boys and girls but there was a marked increase in mean weight in both sexes.

Pubertal growth spurt occurred normally in males but was delayed in females. Weight decreased in both sexes at puberty but not to normal. Better methods of monitoring this condition should result in therapeutic regimes which allow normal growth patterns as well as normal mature height.

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N Benhadi, W M Wiersinga, J B Reitsma, T G M Vrijkotte, and G J Bonsel


To examine the relationship between maternal TSH and free thyroxine (FT4) concentrations in early pregnancy and the risk of miscarriage, fetal or neonatal death.


Cohort study of 2497 Dutch women. TSH, FT4, and thyroid peroxidase antibodies concentrations were determined at first booking. Child loss was operationalized as miscarriage, fetal or neonatal death. Women with overt thyroid dysfunction were excluded.


Twenty-seven cases of child loss were observed. The mean TSH and FT4 level in the women with child loss was 1.48 mU/l and 9.82 pmol/l compared with 1.11 mU/l and 9.58 pmol/l in women without child loss. The incidence of child loss increased by 60% (OR=1.60 (95% confidence interval (CI): 1.04–2.47)) for every doubling in TSH concentration. This association remained after adjustment for smoking, age, parity, diabetes mellitus, hypertension, previous preterm deliveries, and previous preterm stillbirth/miscarriage (adjusted odds ratio=1.80 (95% CI: 1.07–3.03)). This was not true for FT4 concentrations (OR=1.41 (95% CI: 0.21–9.40); P=0.724).


In a cohort of pregnant women without overt thyroid dysfunction, the risk of child loss increased with higher levels of maternal TSH. Maternal FT4 concentrations and child loss were not associated.

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Susan M. Scott, Carmela Guardian, Cathy Rogers, Pam Angelus, and Sher Werner


We have previously demonstrated that changes in urinary epidermal growth factor/creatinine ratios relate to gestational age and gender. It is unclear what controls this developmental pattern although chronic renal disease and thyroid aberrations have significant effects on epidermal growth factor and creatinine excretion in childhood and in adults. Therefore, we chose to explore the effects of these disease states on epidermal growth factor excretion during the perinatal time period. We collected urine samples from 8 infants with congenital renal disease and 45 infants with low T4 and normal TSH values who 'failed' the newborn screen. In addition, 2 infants with hypothyroidism and 2 infants with neonatal Grave's disease had urine samples examined. Values were compared with the epidermal growth factor and creatinine excretion from 190 infants. We demonstrated that epidermal growth factor excretion increased earlier in gestation than does creatinine excretion. In infants with renal disease or hypothyroidism, epidermal growth factor excretion was decreased while hyperthyroidism enhanced excretion. Epidermal growth factor excretion increased with relief of an obstruction but still remained low and creatinine excretion was unchanged. We confirm that in preterm infants as in childhood there are similar effects of thyroid and renal diseases on epidermal growth factor excretion.

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S.-I. Björklund and C. C. Jensen

During the neonatal period infants of diabetic mothers often have attacks of cyanosis, temporary cardiac murmurs and arrhythmia. Electrocardiographic changes have been observed both in the presence and in the absence of such disturbances, but in none of the children with any of these disturbances was the electrocardiogram normal (Björklund, 1953 b). The hypothesis has been advanced that the clinical symptoms and electrocardiographic changes are caused by hypokalaemia, secondary to hyperinsulinism with concomitant hyperfunction or dysfunction of the adrenal cortex (Björklund, 1953 a, b).

Venning et al. (1949) found in 2 premature infants of diabetic mothers, delivered by Caesarean section, increased glucocorticoid excretion during the first few days of life. Normalization of the excretion occurred on about the fifth day. Since these 2 infants had atelectasis and cyanosis, Venning et al. considered that the stress to which these babies were exposed was the cause of the increased function of the

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R. G. Edwards

The presentation made by Dr. Verbickij is important in several respects. First, it is an excellent piece of work on the immunology of pregnancy. Next, it shows how a model can be established in a non-human primate to facilitate research on clinical problems.

There has been a great amount of interest in the immunology of pregnancy in recent years. The stimulus to much of the early research was the development of methods to prevent rhesus haemolytic disease in human neonates. We are all familiar with the great progress being made in these studies following the introduction of the use of anti-Rh serum (Clarke 1968). There has been a significant reduction in the incidence of afflicted children, and this progress seems bound to continue as more experience is gained on the best ways of using the antiserum.

Yet there are still many cases of sensitised mothers carrying foetuses at risk of

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J. L. C. Ch'ng, A. Kaiser, J. Lynn, and G. F. Joplin

Abstract. Total parathyroidectomy is required to cure neonatal primary hyperparathyroidism (NPH) as any parathyroid remnant quickly becomes hyperplastic, causing recurrent hypercalcaemia. We present a patient with NPH who had total removal of his eutopic parathyroid glands but continued to have parathyroid hormone secretion from presumed ectopic parathyroid tissue. Hypercalcaemia initially recurred but normal calcium homeostasis was established as the child grew older. We postulate that the underlying defect in NPH is decreased sensitivity to the serum ionic calcium feedback inhibition at the parathyroid receptor level and that this sensitivity can improve with age.

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David B. Dunger, Janet A. Perkins, Terence P. Jowett, Philip R. Edwards, Leslie A. Cox, Michael A. Preece, and Roger P. Ekins


Thyroid hormones are essential for normal pubertal growth, yet the changes in total and, especially, free thyroid hormones and thyroxine-binding globulin during puberty have not been adequately defined. Serum from 39 normal children (20 girls, 19 boys) between the ages of 10 and 15 years were assayed for total T4, free T4, free T3 and thyroxine-binding globulin at 6-monthly intervals; the free hormone assays were valid, non-analogue methodologies. In the girls, free T4 levels fell from 15.7±0.6 pmol/l at 10 years to 13.0±0.6 (p<0.001) at 12.5 years before rising to 15.9±0.7 at 15 years; this nadir occurred at puberty stages 3-4. Changes in total T4 followed a similar pattern with a slight delay in the nadir (13 years, puberty stage 4). In the boys, free T4 fell from 16.3±0.6 pmol/l at 10 years to 14.3±0.3 at 13.5 years, then rising to 15.4±0.5 at 15 years; the nadir again occurred at puberty stages 3-4. The corresponding nadir in total T4 which occurred at puberty stages 4-5 was not apparent by age analysis. Thyroxine-binding globulin concentrations remained unchanged in the girls, but fell slightly in the boys during later puberty. Free T3 concentrations in the girls showed a progressive fall after 12.5 years which was significant by the age of 14 when most had been in puberty stage 5 for more than 1 year. The boys showed no change of free T3 concentration throughout the study. These data demonstrate important differences in the levels of free thyroid hormones in males and females during puberty. Normal ranges for girls and boys between the ages of 9.5 and 15.5 years are presented.

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Liora Lazar, Rivka Kauli, Celia Bruchis, Jardena Nordenberg, Avinoam Galatzer, and Athalia Pertzelan

Lazar L, Kauli R, Bruchis C, Nordenberg J, Galatzer A, Pertzelan A. Early polycystic ovary-like syndrome in girls with central precocious puberty and exaggerated adrenal response. Eur J Endocrinol 1995;133:403–6. ISSN 0804–4643

Exaggerated adrenal response (ExAR), i.e. hypersecretion of both 17-hydroxypregnenolone (170HPreg) and 17-hydroxyprogesterone(17OHP) in response to adrenocorticotropic hormone (ACTH) stimulation, is frequently found in women with polycystic ovary (PCO) syndrome who had precocious adrenarche. In an earlier study we found an abnormal adrenal response in girls with idiopathic true central precocious puberty (CPP) at early stages of puberty. On follow-up it was noted that a significant number of girls with CPP develop PCO-like syndrome at a relatively young age. The aim of the present study was to determine if there is an association between ExAR and early PCO in girls with a history of CPP. Included were 49 girls with a history of CPP, 34 of whom were treated with gonadotropin-releasing hormone (GnRH) analog. All 49 were evaluated at full maturity, at ages 12.5–14 years, 0.5–4 years after menarche or resumption of menses. Of the 49 girls, 20 had at least 3/4 clinical signs of PCO (irregular menses, hirsutism, acne and obesity) and were defined as PCOlike+, whereas 29 did not fulfil the criteria and were considered PCO-like -. Girls with a definite enzyme deficiency were excluded from the study. All participants underwent a combined iv ACTHGnRH test at early follicular phase. The PCO-like + girls all revealed ExAR, i.e. an elevated stimulated 17OHPreg of 63.4 ± 9.6 nmol/l (normal 28.6 ± 9.2 nmol/l) and a normal stimulated 17OHPreg/ 17OHP ratio of 7.1 ± 1.8 (normal 6.2 ± 2.7), whereas all the PCO-like – had a normal adrenal response (30.0 ±8.7 and 5.3 ± 2.0 nmol/l, respectively). Compared to the PCO-like – girls, those with PCO-like± had significantly higher levels of testosterone (1.8 ± 0.7 vs 1.0 ± 0.5 nmol/l; p < 0.001), androstenedione (6.6 ±3.2 vs 4.7 ± 1.8 nmol/l; p < 0.02) and dehydroepiandrosterone sulfate (7.8 ± 4.7 vs 4.2 ± 2.5 μmol/l; p < 0.004), and a trend toward inappropriate luteinizing hormone secretion. The prevalence of ExAR (40.8%) in the mature CPP girls (confined to only PCO-like ±) was similar to that previously found by us in another group of girls with CPP at early puberty (44.6%). In conclusion, our findings indicate that the pattern of adrenal response remains unchanged from early puberty to adulthood and is probably inherent. As only the girls with CPP who developed early PCO syndrome showed ExAR, it is suggested that ExAR in early puberty may serve as a predictive marker for the eventual development of PCO.

A Pertzelan, Institute of Pediatric and Adolescent Endocrinology, Children's Medical Center of Israel, Beilinson Medical Campus, Kaplan Street, Petah Tiqva 49202, Israel

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CL Boguszewski, C Jansson, MC Boguszewski, S Rosberg, KA Wikland, B Carlsson, and LM Carlsson

The proportion of non-22 kDa GH isoforms was evaluated in 93 healthy children (48 boys aged 6.8-18.4 years and 45 girls aged 3.9-18.4 years) of normal stature (height +/- 2 s.d. score) at different stages of puberty. In addition, correlations among the proportion of non-22 kDa GH isoforms, auxology, spontaneous GH secretion and biochemical measurements were investigated. Serum non-22 kDa GH levels, expressed as percentage of total GH concentration in the samples, were determined by the 22 kDa GH exclusion assay, in which monomeric and dimeric 22 kDa GH are removed from serum and the non-22 kDa GH isoforms are quantitated using a polyclonal antibody GH assay. Samples were selected from spontaneous GH peaks in 24-h GH profiles. For boys, the median proportion of non-22 kDa GH isoforms was 8.5% (range 3.2-26.6%) and for girls it was 9.6% (1.8-17.4%), with no influence of age and no sex-related difference in prepubertal (boys, 7.2%; girls, 8.8%) or pubertal children (boys, 9.1%; girls, 9.9%). However, the median proportion of non-22 kDa GH isoforms was significantly higher in pubertal boys (9.1%) than in prepubertal boys (7.2%; P = 0.03). In pubertal boys, height S.D. scores (SDS) were inversely correlated to the proportion of non-22 kDa GH isoforms (r = -0.38; P = 0.02), especially at mid-puberty (r = -0.7; P = 0.01), indicating that the presence of increased amounts of circulating non-22 kDa GH isoforms was associated with less growth. In prepubertal children, positive correlations between non-22 kDa GH and weight SDS (r = 0.46; P = 0.03), weight-for-height SDS (r = 0.51; P = 0.01) and body mass index (r = 0.42; P = 0.04) were observed. No significant correlations were seen with spontaneous GH secretion or measurements of IGF-1, IGF-binding protein-3, insulin and leptin. These findings in normal children indicate that the proportion of circulating non-22 kDa GH isoforms may have physiologic significance for growth and metabolism in different stages of development, and emphasize the importance of evaluating the circulating ratio of 22 kDa and non-22 kDa GH in children with growth disorders.