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

Abstract.

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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A. Parra, S. Villalpando, E. Junco, B. Urquieta, S. Alatorre, and G. García-Bulnes

Abstract.

Serum thyrotrophin (TSH), thyroxine (T4), triiodothyronine (T3), thyroxine-binding globulin (TBG) and reverse T3 (rT3) were measured by radioimmunoassay in 175 girls and 187 boys aged 6.0 to 16.9 years, who were clinically healthy, and had negative serum antithyroglobulin and antimicrosomal antibodies. All the children had normal weight and height and were grouped at 12 months' intervals. In girls, TSH levels ranged between 5.3 ± 0.4 and 6.9 ± 0.5 μU/ml without significant changes with age; serum T4 decreased up to 13.9 years and rose afterwards; serum TBG was constant up to 13.9 years, decreased subsequently and rose after 15.9 years; serum T3 levels were lower after 13.0 years than previously; serum rT3 decreased between 11.0 and 11.9 years and rose thereafter; the calculated serum free T4 (FT4) and free T3 (FT3) concentrations had a significant rise from 14.0 to 15.9 years followed by a sharp decline; T3:T4, rT3:T3 and rT3:T4 ratios were constant up to 11.9 years, then a rise was seen in T3:T4 and a fall in the later ratios, followed by a drop in T3:T4 ratio and a sustained rise in rT3:T3 and rT3:T4 ratios. In boys, TSH levels were constant between 5.2 ± 0.4 and 6.6 ± 0.4 μU/ml; serum T4 decreased with increasing age; serum TBG was constant up to 13.9 years, and had a sustained fall thereafter; serum T3 was constant over the age range studied; serum rT3 levels decreased up to 13.9 years and rose thereafter; FT4 had no changes with increasing age while FT3, although constant up to 13.9 years, had a sustained rise afterwards; T3:T4 ratio did not change with age, while rT3:T3 and rT3:T4 ratios, although constant up to 13.9 years, showed a tendency toward a sustained rise thereafter. These sex-different variations in serum thyroid hormone concentrations might be related to the fact that girls mature at an earlier chronological age than boys and may represent a partial response of the body to the qualitatively and quantitatively different energy needs in girls as compared with boys, consecutive to the differences in body composition first appearing at puberty.

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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.

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E. M. de Wijn and R. Steendijk

Abstract.

In 4 girls and 1 boy with pseudo-hypoparathyroidism growth and physical maturation were followed longitudinally for 7 – 13 years until adult height had been reached. As a result of early puberty and cessation of growth all patients were relatively shorter as adults than in their childhood years. The difference between average height at the age of 8.0 years and average adult height was 2.25 sd. This observation offers an explanation for the finding in the literature that short stature is more common in adults with this disease than in children. Skeletal age was advanced in all cases and the development of the tubular bones of the hand was more advanced than the development of the round bones. It is possible that this difference resulted from inappropriately early closure of the epiphyseal discs of disproportionally short metacarpals and phalanges. On the other hand it may be an aspecific phenomenon of advanced skeletal maturation.

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Olav Trygstad

ABSTRACT

This study was carried out in order to determine whether children with a transitory type of growth hormone deficiency showed an accelerated growth in height velocity on treatment with human growth hormone (HGH).

Following careful diagnostic routine procedures 13 extremely short children were diagnosed as having isolated growth hormone deficiency, and were successfully treated with HGH. A true isolated growth hormone deficiency was present in 5 of the children, whereas 8 showed a normal increase in serum growth hormone on repeated growth hormone stimulation tests after their development of puberty and termination of HGH treatment. Three boys with bone ages of 5.5, 8.0 and 9.5 years showed an undisputable effect following HGH administration. They showed an initial growth at the start of treatment, and a second growth spurt during development of puberty. Two of the boys reached final statures of 14 cm taller than the predicted heights. The other patients, including the children with true isolated growth hormone deficiency showed an initial spurt of growth at the start of the HGH treatment immediately followed by a pubertal growth spurt. The mean acceleration of height velocity for the children with true isolated growth hormone deficiency was from 3.4 cm during the year before treatment to 7.0 cm during the first year on treatment, as compared to 2.8 and 7.4 cm, respectively, for the children with transitory growth hormone deficiency. A girl with severe anorexia nervosa who had a transitory growth hormone deficiency, showed an accelerated high velocity from 1.1 cm to 7.6 cm during the first year following treatment with HGH.

The question whether HGH treatment should be made available to all short children with no known syndrome, and presenting a height less than −3.5 sds, a bone age/chronological age ratio of less than ⅔, and a height velocity less than −2 sds is discussed. The only way to know if a child will respond to HGH treatment is to give it for a trial period of at least six months. At least a physiological stimulus to growth hormone secretion should be decisive in the selection of growth retarded children for HGH treatment. Different mechanisms seem to be responsible for physiological growth hormone secretion to sleep or exercise, and the secretion obtained with pharmacological stimuli.

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C Ankarberg-Lindgren, J Dahlgren, B Carlsson, S Rosberg, L Carlsson, KA Wikland, and E Norjavaara

OBJECTIVE: To investigate the levels and diurnal rhythm of serum leptin in healthy children, and to investigate the association between leptin levels and sex steroids. METHODS: Four girls and four boys, all healthy volunteers, were followed longitudinally throughout puberty. Their chronological ages ranged from 8.7 to 19.5 years, and body composition, expressed as weight-for-height standard deviation scores (SDS), ranged between -1.7 and +2.4. Serum leptin, oestradiol and testosterone concentrations were measured by radioimmunoassay at 1000, 1400, 1800, 2200, 0200 and 0600 h. RESULTS: In all girls and boys, both prepubertally and during pubertal development, serum leptin levels increased during the night, with no difference in relative peak amplitude. In boys, the leptin concentrations increased until the initiation of puberty and then declined, whereas in girls, the concentrations increased throughout puberty. The inter-individual variation in mean leptin levels among girls decreased to 11% at the time of menarche. A positive correlation was found for both oestradiol and testosterone versus leptin in girls throughout puberty (r=0.64 and r=0.71 respectively, P<0.001). A negative correlation was found between leptin and testosterone in boys in mid- and late puberty (r=-0.66, P<0.01). No correlation was found between oestradiol and leptin in boys or between testosterone and leptin in pre- and early pubertal boys. CONCLUSION: Serum leptin concentrations show diurnal variation throughout pubertal development in both girls and boys. The changes in leptin levels during puberty follow a gender-specific pattern, probably due to an influence of sex steroids on leptin production.

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J Bellone, G Aimaretti, MR Valetto, S Bellone, C Baffoni, E Arvat, S Seminara, F Camanni, and E Ghigo

Bellone J. Aimaretti G, Valetto MR, Bellone S, Baffoni C, Arvat E, Seminara S, Camanni F, Ghigo E, Acute administration of recombinant human growth hormone inhibits the somatotrope responsiveness to growth hormone-releasing hormone in childhood. Eur J Endocrinol 1996:135: 421–4. ISSN 0804–4643

In adulthood the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) is inhibited by previous acute administration of either GH or GHRH and it is restored by substances that inhibit hypothalamic somatostatin release. Because in children the GH response to GHRH is not affected by previous neurohormone administration, it has been suggested that in childhood a GH increase is not able to trigger the somatostatin-mediated negative GH autofeedback mechanism. To verify this hypothesis, in 25 children (8 girls and 17 boys; 15 prepubertal and 10 in pubertal stages II–IV) with familial short stature (normal height velocity and insulin-like growth factor I levels) we studied the effect of acute iv administration of different recombinant human GH doses (group 1, N = 5, 0.06U/kg; group 2, N = 6, 0.01 U/kg; group 3, N = 7, 0.005 U/kg at −150 min or saline on the GH response to GHRH (1 μg/kg iv at 0 min). In another group (N = 7), we studied the effect of 0.005 U/kg iv recombinant human GH or saline on the GH response to GHRH combined with arginine (0.5 g/kg iv over 30 min), which likely inhibits hypothalamic somatostatin release. Serum GH increases after recombinant human GH were dose-dependent (GH peak, mean±sem, 171.7 ± 24.4, 33.3 ± 3.9 and 21.8 ± 5.1 μg/l, respectively). The administration of recombinant human GH strongly inhibited the GHRH-induced GH rise in all groups (group 1, 7.1 ± 1.7 vs 23.1 ± 7.6 μg/l, p < 0.05; group 2, 9.5 ±2.8 vs 26.9±8.5 μg/l, p < 0.05; group 3, 9.1 ±2.7 vs 34.8 ± 7.2 μg/l, p< 0.02). The GH response to arginine + GHRH (56.9 ± 13.3 μg/l) was higher than that to GHRH alone recorded in group 1 (p < 0.005), group 2 (p < 0.01) and group 3 (p < 0.01), while exogenous recombinant human GH failed to inhibit it (45.0 ± 9.4 μg/l). Our results demonstrate that in childhood, as well as in adulthood, recombinant human GH administration inhibits the somatotrope responsiveness to GHRH. This inhibitory effect is likely to be mediated by hypothalamic somatostatin release.

Ezio Ghigo, Divisione di Endocrinologia, Ospedale Molinette, C.so Dogliotti 14, 10126 Torino, Italy

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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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Salvador Villalpando, Ignacia Cisneros, Guadalupe García-Bulnes, Bárbara Urquieta, Lourdes Mondragón, Elisa Junco, and Adalberto Parra

Abstract.

Anti-thyroid antibodies are frequently found in otherwise normal populations (4.5–25.8%); however, there is scanty information about thyroid function status in affected individuals. In this report, the serum concentrations of TSH, T3, T4, rT3 and TBG and the titre of anti-thyroglobulin and anti-microsomal antibodies (haemagglutination technique) were studied in 520 healthy school children (260 boys and 260 girls) aged 6.0–17.9 years. Titres equal or greater than 1:16 of one or both antibodies were detected in 58 boys and in 77 girls (in 33 boys and in 24 girls with, and in 25 boys and 43 girls without, associated abnormalities in the serum concentrations of one or several hormones). The age distribution of thyroid antibodies followed a trimodal pattern with peaks at 7, 11 and 16–17 years in both sexes. The most striking finding was an abnormally elevated T3 concentration in 22 boys and 5 girls with positive antibodies, with no symptoms of thyroid dysfunction and with no clear relationship with simultaneous abnormalities in TSH, T4 or rT3; however, in 5 boys the TBG serum levels were increased. Serum from these patients was incubated with [125I]T3 before free radioactivity was precipitated with dextran-coated charcoal and the aliquots were analyzed by paper electrophoresis. Serum samples with high T3 levels bound significantly more radioactivity than normal or T3-free serum (P < 0.001) and an abnormal peak of radioactivity was present in the gamma globulin fraction, in the former but not in the latter two types of sera. The presence of high serum T3 levels in the absence of clinical symptoms of hyperthyroidism was probably due to sequestration of T3 by the anti-thyroglobulin antibody, which may have cross-reactivity with T3 and T4, as has previously been demonstrated both in animals and humans.

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K. W. Kastrup, J. Sandahl Christiansen, J. Koch Andersen, and H. Ørskov

Abstract. The effect of more frequent (daily) injections of human growth hormone (hGH) on growth rate was studied in 16 growth hormone deficient children (12 boys, 4 girls) during 2 years. All had previously been treated with im injection of hGH 2–3 times weekly and in the majority of the patients a waning growth response was observed.

For a total weekly dose of 12 IU hGH a daily dose of 2 IU was injected sc at night before sleep. This dosage has been shown by us to imitate the average nocturnal hGH profile in plasma.

Growth response on the im treatment was 5.2 ± 1.2 cm/year (sd) in boys and 5.4 ± 0.9 cm/year in girls. A significant increase was seen during the first year of sc treatment to 7.9 ± 2.7 cm in boys and 6.3 ± 2cm in girls. During the second year the growth response was still significantly increased in boys (7.2 ± 1.9 cm). Bone age was more advanced and the period of previous im treatment was longer in girls (6.7 vs 3.6 years) which may be the main cause of the waning second year response (4.7 ±1.3 cm/year). Pubertal development occurred in 9 children during treatment. However, the highest growth rates were not found in these children.

Absence of antibodies against hGH and local reactions at the injection site is evidence of the safety of the treatment, which was very well accepted by the children.

Daily sc injections thus represent an effective alternative to conventional im injections ensuring high acceptance in children with growth hormone deficiency.