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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

Yoshibayashi M, Kamiya T. Saito Y. Nakao K, Nishioka K, Temma S, Itoh H, Shirakami G, Matsuo H. Plasma brain natriuretic peptide concentrations in healthy children from birth to adolescence: marked and rapid increase after birth. Eur J Endocrinol 1995;133:207–9. ISSN 0804–4643

The aim of the present study is to establish the normal range and to determine the developmental changes of plasma brain natriuretic peptide (BNP) concentrations in children. We measured plasma BNP concentrations as well as atrial natriuretic peptide (ANP) concentrations in 58 healthy children from birth to adolescence and in the umbilical vein of 20 healthy neonates using highly sensitive immunoradiometric assays. The plasma BNP concentration was the highest at 0 days of age and descended through maturation to be almost constant and to be at the adult level at 3 months of age. The plasma BNP concentration at 0 days of age (56.7 ± 49.6 fmol/ml; mean±sd) was 25 to 30 times higher than the adult level and 21 times higher than that in the umbilical vein (2.7 ± 1.4fmol/ml), The plasma ANP concentration at 0 days of age was not significantly different from that in the umbilical vein. The ratio of BNP to ANP was also the highest at 0 days of age (1.39 ± 0.72) and decreased through maturation to be at the adult level at 3 months of age. Thus, the plasma BNP concentration in healthy subjects showed a marked, rapid and preferential increase immediately after birth, suggesting that BNP has a physiological role distinct from that of ANP in the perinatal circulatory changes from fetus to neonate.

Muneo Yoshibayashi, Department of Pediatrics, National Cardiovascular Center, 5-7-1 Fujishirodai, Suita, Osaka 565, Japan

Abstract

The frequency of hypoglycemia in 165 children with primary adrenal insufficiency, 118 of whom had Congenital Adrenal Hyperplasia and 47 Addison's Disease, was 18 %. Half of the hypoglycemic episodes occurred in the neonatal period. Hypoglycemia was isolated in 13 children, revealing the disease in 4 newborns with Congenital Adrenal Hypoplasia and in a boy with 11 B Hydroxylase deficiency.

Basal plasma cortisol levels were significantly lower in those of subjects who experienced hypoglycemia ( 47.1 ± 28.6 ng/ml vs. 106.0 ± 86.6 ng/ml, p< 0.001). A significant correlation ( p < 0.001) was found between the plasma concentration of glucose and cortisol at time of hypoglycemia.

Abstract.

Antibodies against the so called 'second colloid antigen' (CA₂ antibodies) occurred in 51% of the mothers of hypothyroid children detected by screening for neonatal congenital hypothyroidism in Quebec (N = 49) and in The Netherlands (N = 26). In The Netherlands where corresponding neonatal serum was available, 31% (8 of 26) of the infants with congenital hypothyroidism were positive for antibodies against the second colloid antigen. When during follow-up, 3 to 5 years after diagnosis, the mothers and their children were investigated, 46% (7 of 15) of the mothers were positive for antibodies against the second colloid antigen, whereas 29% (4 of 14) of the hypothyroid children were also positive. Various control groups did not show more than a 12% positivity. This presence of thyroid-reactive antibodies in a proportion of the hypothyroid children 3 to 5 years after diagnosis is not compatible with a mere transplacental passage; it indicates that the antibodies must be produced by the mothers and by the children themselves. We conclude that a thyroid autoimmune response occurs in a considerable part of infants with congenital hypothyroidism and their mothers and that this immune response seems to persist in both of them for years.

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

ABSTRACT

A female child was admitted to the hospital few days after birth with severe hypoglycemia and convulsive episodes. Plasma insulin levels were elevated and oral and intravenous administration of glucose were unable to keep blood glucose above 2 mmol/l limit. Intravenous infusion of a long acting somatostatin analog, SMS 201-995, at a dosage gradually increasing from 2 to 50 μg/24 hr, was accompanied by a dramatic fall in circulating insulin levels. Normality of glucose homeostasis was restored and convulsive spells ceased. Fasting blood glucose levels stabilized between 3.4 and 4.7 mmol/l. No rebound phenomenon was observed during short term interruptions of the SMS 201-995 infusion. A subtotal pancreatectomy was performed during SMS treatment, and the diagnosis of nesidioblastosis was confirmed by immunocytologic and electron-microscopic studies. It is concluded that this new potent and long acting somatostatin derivative may be useful in the management of hyperinsulinism in the neonate.

Abstract.

Transient neonatal hypothyroidism has been observed in three successive offspring of a mother with autoimmune thyroiditis. Thyroxine replacement therapy was initiated in a 23-year-old woman with overt clinical and laboratory findings of non-goitrous primary hypothyroidism. While on such treatment, she gave birth to three infants manifesting hypothyroidism immediately after birth. The neonates were treated with thyroxine replacement therapy which was discontinued in the three siblings at ages 2½ years, 3½ years, and 13 months. Continuous observation following cessation of therapy revealed clinical and biochemical euthyroidism in the children. Thyroid scanning during the neonatal period in the first child failed to identify functional thyroid tissue, suggesting thyroid agenesis, whereas thyroid scan performed on subsequent follow-up revealed a normal gland. Sequential serum measurements of autoantibodies directed towards the thyrotropin receptor were made in the mother and third child by a cAMP bioassay. High titres (five-six fold above normal) of blocking antibodies (tested by measuring the inhibition of TSH-stimulated cAMP production of cultured human thyroid cells by serum immunoglobulin preparations) were present in the mother and newborn 10 days after birth. The levels remained persistently high in the mother, whereas they declined and were undetectable in the child at four months. Thyroid-stimulating immunoglobulin was absent in both mother and child. The data are compatible with transient neonatal hypothyroidism caused by transplacental transfer of antibodies which block thyroid response to TSH. The half-life of the maternally-derived blocking antibody in the infant was estimated as 1-2 months. This is the first report on sequential serum measurements and estimate of half-life of the blocking antibodies performed by a cAMP bioassay (using thyroid cells of human origin). Unlike the radioreceptor assay employed so far in such cases, this assay can distinguish between stimulating and blocking TSH receptor antibodies.