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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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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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Gerhard Ulrich Exner, Andrea Prader, Urs Elsasser, and Max Anliker

Abstract.

125I Computed Tomography (CT) allows for the selective determination of trabecular and compact bone mineral parameters in the radius. Using this technique the effects of high dose oestrogen treatment in 11 tall girls, and of high dose testosterone treatment in 5 tall boys were monitored. In both groups trabecular bone density (TBD) increased steadily during treatment at a rate of about 1% per month. Also in both groups the compact bone mineral increased steadily. These results are compared with those from a cross sectional study on 49 normal children and 36 normal adults, in whom TBD was found to be independent of age and sex, so that the increases in TBD in both treatment groups can be attributed directly to the influence of the sex hormones. Since the compact bone mineral is higher in adults than in children it cannot yet be decided whether the increases seen in the treated patients are related to the sex hormone treatment, or reflect only the normal development of the bone during adolescence.

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D. B. GRANT, D. B. DUNGER, and E. C. BURNS

Abstract

This paper reviews the outcome in 12 children with hyperinsulinaemic hypoglycaemia who first developed symptoms between the ages of 2 and 8 months and who were treated with diazoxide (5 - 20 mg/kg/day) for 2-13 years. Two cases required subtotal pancreatectomy at the ages of 5 and 10 years because of recurrent hypoglycaemia and one girl with severe retardation died at the age of 6 years while still on diazoxide therapy. Two patients aged 3.5 and 9 years are still on treatment and in 7 cases diazoxide was discontinued between the ages of 2.5 and 14 years, indicating that spontaneous remission can be expected in a high proportion of children with post-neonatal hyperinsulinaemic hypoglycaemia. Of the 9 children who started diazoxide within 3 months of the onset of symptoms, 5 are of normal intelligence and 4 are moderately retarded (IQs 63-71). In 3 children diazoxide was started 8 months to 3 years after the onset of symptoms; two are retarded (IQs 60-70) and the third was severely retarded and died aged 6 years.

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M. H. Gons, J. H. Kok, W. H. H. Tegelaers, and J. J. M. de Vijlder

Abstract. In this paper we describe methods for the early aetiological diagnosis of congenital hypothyroidism, using beside the classical T4, T3 and TSH plasma concentrations, four additional parameters in plasma and urine. The first one is thyroglobulin (Tg). In normal children of more than one year of age and in adults, 5–35 ng/ml plasma is found, in neonates 2–3 weeks old, this level is 10–250 ng/ml. In patients with a stimulated thyroid gland, as in primary congenital hypothyroidism, plasma Tg levels increase. High Tg values are found in iodine deficiency and in organification defects. In the absence of the thyroid gland plasma Tg is undetectable. Low to normal levels are found in cases with hypoplasia of the gland. In patients with a disturbed synthesis of Tg, resulting in Tg deficiency of the gland, plasma Tg levels vary from undetectable to normal. The PBI-T4 plasma difference, which is caused by circulating abnormal iodoproteins is the second parameter. The products of thyroidal breakdown processes of the abnormal iodoproteins are excreted in the urine and used as the third parameter. We found that the excretion of this low molecular weight iodinated material (LOMWIOM) was increased only in Tg-deficient patients.

If the neonate is found to be hypothyroid, thyroid hormone substitution must be given immediately. Blood and urine sampling can be done just before or even directly after starting the therapy. The measurements extended with the determination of the total iodine excretion (fourth parameter) can be carried out within 1 week. With these additional methods it appeared to be possible to distinguish between several types of congenital hypothyroidism in neonates found by screening.

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G.J. BRUINING, A.N BOSSCHAART, R.S.R. AARSEN, S.W.J. LAMBERTS, P.J.J. SAUER, and E. DEL POZO

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.

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Paul van Trotsenburg, Thomas Vulsma, André M. Bloot, Reindert D. Van der Gaag, Jan Willem Lens, Hemmo A. Drexhage, and JanJ. de Vijlder

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.

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Y. Rakover, O. Sadeh, E. Sobel, A. Shneyour, and Z. Kraiem

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.

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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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C Evans, NJ Jordan, G Owens, D Bradley, M Ludgate, and R John

OBJECTIVE: We describe an infant with surprisingly severe neonatal hypothyroidism due to transplacental passage of thyrotrophin receptor (TSH-R)-blocking antibodies (TBAb). DESIGN AND METHODS: TBAb were detected using a cell line which stably expresses the human TSH-R and a cAMP-responsive luciferase reporter by their ability to inhibit TSH-stimulated luciferase expression. Potent TBAb were detected in maternal serum and initially in the infant's serum but, in the latter, TBAb decreased over time to within the reference range by 3-4 months of age, illustrating the transient nature of this condition. RESULTS: The thyroid function of this child did not return to normal on withdrawal of thyroxine therapy at 16 months of age when he developed transient compensated hypothyroidism. CONCLUSIONS: We propose that the presence of potent TBAb in utero and in the first weeks of life may have implications for the development of a normally sized thyroid gland. We have demonstrated the presence of TBAb in the mother's milk and, as far as we are aware, this is the first such report. However, the TBAb in the milk probably did not contribute significantly to hypothyroidism in the child, given the reducing antibody titre in his circulation.