Search Results

You are looking at 101 - 110 of 1,616 items for

  • Abstract: adolescen* x
  • Abstract: boy* x
  • Abstract: child* x
  • Abstract: girl* x
  • Abstract: neonat* x
  • Abstract: paediatric x
  • Refine by Access: All content x
Clear All Modify Search
Restricted access

H Kanety, A Silbergeld, B Klinger, A Karasik, RC Baxter, and Z Laron

A minority of patients with Laron syndrome have normal serum GH binding protein (GHBP), indicating that the defect is elsewhere than in the extracellular domain of the GH receptor. We have evaluated the effect of long-term IGF-I treatment on serum IGF-binding protein (IGFBP)-3 and the acid-labile subunit (ALS) in three sibling with Laron syndrome caused by a GH post-receptor defect and with normal GHBP. The children (a boy aged 3 years, a girl aged 4 years and a boy aged 10 years) were treated by daily s.c. injection of IGF-I in a dose of 150 micrograms/kg. IGFBP-3 was measured by RIA and Western ligand blotting, ALS by RIA. Based values of IGFBP-3 and ALS were low. During IGF-I treatment, the IGFBP-3 concentrations in the girl gradually increased, whereas in the boys there was a 60% decrease during the first week, followed by gradual increase towards baseline. The ALS concentrations followed a similar pattern. We conclude that IGF-I treatment induces and initial suppression and then an increase in the IGFBP-3 and ALS concentrations, confirming data from animal experiments that IGFBP-3 synthesis is not solely under GH control. The differences in responsiveness between the female and male siblings may reflect genetic differences, or lower circulating concentrations of IGF-I in the boys compared with the girl.

Restricted access

T. Torresani, E. Schuster, and R. Illig

Abstract. Luteinizing hormone (LH) bioactivity was determined by an in vitro microbioassay in 65 plasma samples from 26 infants and young children between 10 days and 6.5 years of age. In addition LH was measured by radioimmunoassay. For both, LH preparation LER-907 was used as standard.

Biologically measured LH values (bio-LH) were always higher than radioimmunologically determined LH values (RIA-LH) as reflected by bio/RIA ratios greater then 1.0.

In male infants bio-LH was elevated up to 7 months of age. Thereafter, it decreased and remained low over the age range of our study. In female infants bio-LH was also elevated, but decreased after 1 month and showed a slight tendency to rise in the age group 3–6.5 years.

The results of RIA-LH showed approximately the same pattern, but at a lower level. In boys RIA-LH levels were highest around 1 month of age, decreased steadily between 2 and 7 months and remained constant thereafter. Girls had rather constant RIA-LH values between 2 months and 3 years of age. In contrast to bio-LH, there is a clear-cut drop of RIA-LH in the age group 3–6.5 years, resulting in a statistically significant increase of the bio/RIA ratio.

In boys the time course of the bio-LH changes coincides with the known elevation of testosterone during the first months of life.

In girls the elevated bio-LH levels observed during the first month are not so far associated with a known steroid correlate.

Our study shows an increased biological activity of circulating LH and a marked dissociation of biologically and radioimmunologically active LH during early infancy, analogous to observations during puberty.

Restricted access

Peter Christiansen


The influence of ovine follicle stimulating hormone (NIH-FSH-S-3) on ovine luteinizing hormone (NIH-LH-S-8) in the Ventral Prostate Weight method (VPW) was studied. Adding of NIH-FSH-S-3 to NIH-LH-S-8 at ratios of 1:1, 4:1 and 10:1 gave no significantly higher responses than did NIH-LH-S-8 alone.

Urinary extracts from 2 women, hypophysectomized for metastasizing mammary carcinoma and from 3 children between 2 and 5 years old (1 boy, 2 girls) gave no positive response with the doses employed (1/4 of a 24 hours urine sample total per rat). It is concluded that the Ventral Prostate Weight method in hypophysectomized rats is specific for the assay of luteinizing hormone.

Restricted access

L. A. Nilsson

Cytologic aspiration biopsy of the thyroid was used in 48 of 63 children being the material of juvenile atoxic goitre (aged 10–15 years) from the last 31/2 years in Gothenburg. Cytologic signs of lymphoid thyroiditis were found in 23 girls and 3 boys.

Clinical signs and symptoms in 35 children with auto-immune thyroiditis are reported. One third had no complaints apart from the goitre, 12 were more or less hypothyroid and the rest had chiefly mild and diffuse symptoms. Increased firmness of the goitre was found in 27 of 32 cases, the surface was nodular or bosselated in 15.

Thyroid function: PBI was low only in 3 cases with myxedema, was above the upper normal limit in several cases. The difference between the PBI- and the BEI-levels was disproportionately great in most cases examined. The thyroid uptake of I131 showed abnormal discharge of iodide in every fourth patient.

Thyroid antibodies:

Restricted access

J. W. Honour, C. J. H. Kelnar, and C. G. D. Brook


Normal ranges for daily urine steroid excretion rates in childhood are reported for the first time by gas chromatographic analysis using capillary columns and flame ionisation detector. Longitudinal data came from a study over 3 years of 127 normal boys (aged 7.5-15.6 years) studied on 5 occasions and 14 pubertal girls studied over 2 years. Cross-sectional data were collected from 115 hospitalized patients (58 males, 57 females) aged 2.9 to 14 years with normal adrenal function. The excretion rate of cortisol metabolites was constant for body size, whereas androgen metabolite excretion rates rose sharply in childhood to approach adult levels at the end of puberty. The new data will enable better interpretation of pediatric patient data.

Restricted access

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. High prevalence of abnormal adrenal response in girls with central precocious puberty at early pubertal stages. Eur J Endocrinol 1995;133:407–11. ISSN 0804–4643

Abnormal adrenal response is often observed in girls with precocious adrenarche (1). We studied the adrenal response in 112 girls with idiopathic true central precocious puberty (CPP) at early stages of puberty compared to that in 21 girls with normal puberty (controls). The aims of this study were to determine the prevalence of abnormal adrenal response at early stages of puberty, the possible correlation of abnormal adrenal response with pubertal signs at onset of puberty and with plasma androgen levels, and a possible association with the activity of the hypothalamic-pituitary-gonadal (HPG) axis. All participants underwent a combined iv adrenocorticotropic hormone (ACTH)gonadrotropin-releasing hormone (GnRH) test at Tanner stage 2-3: 62 of the CPP girls before and 50 during treatment with GnRH analog. The stimulated levels of 17-hydroxypregnenolone (17OHPreg) and the stimulated 17OHPreg/17-hydroxyprogesterone ratio were analyzed and compared to previously reported norms. The result revealed three patterns of adrenal response: normal (17OHPreg ⩽24 nmol/l and 17OHPreg/17OHP ratio ⩽7) in 50/112 (44.6%) CPP patients and 17/21 (80.9%) controls; exaggerated (17OHPreg> 24 nmol/l, 17OHPreg/17OHP ratio ⩽ 7) in 50/112 (44.6%) CPP patients and 3/21 (14.3%) controls; and non-classical 3β-hydroxysteroid dehydrogenase deficiency (17OHPreg> 24 nmol/l and 17OHPreg/17OHP ratio > 7) in 12/112 (10.8%) CPP patients and 1/21 (4.8%) controls. The clinical features at onset of puberty were comparable in all girls with the CPP in spite of the different adrenal response patterns. The levels of androstenedione and testosterone were within normal range in all cases. Dehydroepiandrosterone sulfate was significantly elevated only in 3β-hydroxysteroid dehydrogenase deficiency, 4.8 ± 2.7 (p < 0.03) as expected. The adrenal response was not affected by GnRH analog therapy. In conclusion, an abnormal adrenal response was found in 55.4% of girls with CPP in early puberty. This response did not cause clinical signs and laboratory findings of a hyperandrogenic state at early stages of puberty and was not affected by the activity of the HPG axis. Its role in evoking precocious puberty remains to be explored further.

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

Free access

B Gyorffy, B Vasarhelyi, D Krikovszky, L Madacsy, A Tordai, T Tulassay, and A Szabo

OBJECTIVE: Recent data have indicated the significance of vitamin D receptor (VDR) polymorphisms in type 1 diabetes mellitus (T1DM). We have studied the association of five known restriction enzyme polymorphisms of the VDR gene in patients with T1DM. DESIGN AND METHODS: One hundred and seven children with T1DM (T1DM for 5 Years; age, 1-14 Years; boys/girls, 57/50; body mass index, 17.0+/-2.3 kg/m(2); haemoglobin A(Ic) (HbA(Ic)), 7.87+/-1.05) and 103 healthy subjects were enrolled. The VDR polymorphisms ApaI, BsmI, FokI, TaqI and Tru9I ("a", "b", "f", "t" and "u" alleles respectively) were investigated. RESULTS: The "t" and "T" alleles miss the Hardy-Weinberg equilibrium (P<0.01) in control and diabetic populations; we therefore excluded this polymorphism from further analysis. We did not find a difference in the allele prevalence in T1DM patients and controls of any of the five polymorphisms. However, when the "b", "a" and "u" alleles were simultaneously compared in girls, there was a significantly higher prevalence in patients with diabetes compared with controls ("b"+"a"+"u" present/absent: healthy, 0/53; diabetic, 13/37; P<0.005). In boys the prevalence of "b"+"a"+"u" genotype was similar in T1DM and controls. CONCLUSIONS: The impact of the "t" allele cannot be investigated in this study population. Not a single VDR polymorphism increases the susceptibility to T1DM. The common presence of the "b", "a" and "u" alleles greatly increases the probability of T1DM in girls.

Restricted access

Maria N Moreira-Andrés, Karen Papapietro, Francisco J Cañizo, Javier Rejas, Luisa Larrodera, and Federico G Hawkins

Moreira-Andrés MN, Papapietro K, Cañizo FJ, Rejas J, Larrodera L, Hawkins FG. Correlations between bone mineral density, insulin-like growth factor I and auxological variables. Eur J Endocrinol 1995; 132:573–9. ISSN 0804–4643

Recent studies have shown growth-related changes in spinal bone mineral density (BMD) in children; however, there is less information available on the relationship between BMD and insulin-like growth factor I (IGF-I). The aim of this study was to relate the BMD of the spine and radius with serum IGF-I levels and auxological variables in normally growing children. We used dual X-ray absorptiometry to measure the BMD in the lumbar spine (L1–L4) and distal radius of 121 children (69 boys, 52 girls) aged 3–18 years whose growth velocity was normal. Lumbar and radial BMD increased with age (p < 0.001) and puberty (p < 0.001) and was highly correlated to age, weight, height, body surface and bone age (r = 0.70–0.89 and p < 0.001 for all variables). Partial correlation, with age held constant, was weaker but still significant for most auxological variables. Serum IGF-I concentrations increased slowly during childhood and markedly during early stages of puberty, and correlated with lumbar and radial BMD (r = 0.55 and 0.45, respectively; p < 0.001) and with the auxological variables (p < 0.001). When age was held constant, IGF-I levels still correlated significantly with the auxological variables and with BMD, except in the case of radial BMD in boys. By multiple regression analysis IGF-I, unlike auxological variables, did not reach significance in the ability to predict BMD. Therefore, in healthy children, serum IGF-I levels show a weaker relationship to BMD than do auxological variables.

MN Moreira-Andrés, Servicio de Endocrinología, Hospital 12 de Octubre, Carretera de Andalucia km. 5,4, 28041 Madrid, Spain

Restricted access

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


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.

Restricted access

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