Intrauterine growth retardation may permanently influence the endocrine system by affecting its programming during development. The aim of this study was to evaluate thyroid and adrenal function together with insulin sensitivity in a group of children born small for gestational age (SGA). Forty SGA children (mean age, 6.7 ؎ 1.7 yr) and 35 children born appropriate for gestational age (mean age, 6.5 ؎ 2.2 yr) were selected for the study. TSH, free T 4 , free T 3 (fT 3 ), rT 3 , antithyroid antibodies, cortisol, and dehydroepiandrosterone sulfate (DHEAS) were assessed. Insulin sensitivity was evaluated with the quantitative insulin sensitivity check index (QUICKI). A thyroid ultrasound was also performed in the SGA children. We found that TSH was significantly higher in SGA than in children born appropriate for gestational age [2.9 ؎ 1.1 vs. 1.7 ؎ 0.7 U/ml (mIU/liter); P < 0.001]; furthermore, eight SGA children (20%), seven born preterm and one at term, had TSH levels above the upper limit of normality. fT 3 was also higher in SGA children (4.2 ؎ 0.4 vs. 3.6 ؎ 0.6 pg/ml; 6.4 ؎ 0.6 vs. 5.5 ؎ 0.9 pmol/liter; P < 0.0001), whereas no difference was found for free T 4 , rT 3 , and the fT 3 /rT 3 ratio. Urinary iodine was normal, and antithyroid antibodies were absent. Thyroid ultrasound showed a normal echographic pattern with a normal volume in SGA children. Serum cortisol was similar in both groups, whereas DHEAS was significantly lower in SGA subjects (43 ؎ 18 vs. 65 ؎ 50 g/dl; 1.1 ؎ 0.4 vs. 1.7 ؎ 1.3 mol/liter; P < 0.05). There was no difference in insulin sensitivity between the two groups. Birth length and birth weight were the main determinants of TSH and DHEAS serum levels, respectively.In conclusion, functional thyroid and adrenal changes have been found in children who suffered from intrauterine growth retardation. A larger survey with an appropriate follow-up is, however, required to confirm these findings and to assess their natural evolution. (J Clin Endocrinol Metab 89: 6320 -6324, 2004) R ECENT STUDIES HAVE provided unequivocal evidence of the role played by events occurring in prenatal life in modulating the future development of adult diseases. Intrauterine growth retardation is frequently associated with a higher systolic blood pressure (1, 2), increased cardiovascular mortality (3), elevated plasma cortisol (4), glucose intolerance, hyperinsulinism, type 2 diabetes (5, 6), premature pubarche, and ovarian hyperandrogenism (7-9). Given the significant alterations that thyroid and adrenal glands show in case of severe illness (10 -15) or metabolic derangement (16, 17), we decided to study a group of children born small for gestational age (SGA) to investigate whether fetal growth restriction could induce permanent changes in thyroid and adrenal function. Subjects and MethodsWe studied 40 children (29 female, 11 male) born SGA who, at the time of the investigation, were 6.7 Ϯ 1.7 (2.2-11.5) years old. SGA was defined as weight and length at birth below the 10th centile, according to Lubchenko et al. (18...

Objective: The aim was to investigate the effects of two different GH dosage regimens on growth, bone geometry and bone strength. Subjects and methods: Final height; parentally adjusted final height; the metacarpal index (MI) SDS, the inner and outer diameters; and the total cross-sectional area (CSA), cortical CSA, medullary CSA and bone strength (Bending Breaking Resistance Index (BBRI)) were evaluated at the metacarpal site in two cohorts of GH-deficient children, treated with two different doses of GH. Group 1 (38 patients) was treated with 0.16 mg/kg body weight per week of GH and group 2 (37 patients) with 0.3 mg/kg per week. Results: At the end of treatment, with group 1 vs group 2, height SDS was 20.84^1.07 vs 2 0.46^0.76, and parentally adjusted height SDS was 0.14^1.08 vs 0.27^0.82. Parentally adjusted relative height gain was 1.14^0.89 vs 2.14^0.72 SDS (P , 0.0001). MI SDS was 0.58^1.31 vs 2 0.42^1.54 (P , 0.005). MI SDS gain was 0.07^1.41 vs 20.35^1.85. There was no difference between groups in the outer and inner diameter, in the total and cortical CSAs, whereas medullary CSA was higher in group 2 (P , 0.05). BBRI was 10.02^5.37 vs 11.52^5.49 cm 3 , and BBRI gain was 3.33^5.06 vs 6.88^6.65 (P ¼ 0.01). P values were assessed using student's t-test. Conclusion: Higher GH doses result in a greater height gain and improved bone strength.European Journal of Endocrinology 154 479-482

Acylated ghrelin has been originally described for its potent GH-releasing activity mediated by the activation of the GH secretagogue receptor type 1a. More recently, ghrelin has been reported to exert several other GH-independent biological actions, among which in the modulation of metabolic functions. Glucocorticoids are well known to exert important metabolic functions but also to modulate GH secretion, although through mechanisms that have not been fully clarified so far. Interestingly, the existence of a feedback link between glucocorticoids and ghrelin system has already been reported. The aim of our study was to evaluate the acute GH and ghrelin responses to dexamethasone (DEX) administration in children with idiopathic short stature (ISS) or isolated idiopathic GH deficiency (GHD). Eight children with ISS (age: 9.5+/-1.2 yr) and 7 with GHD (12.1+/-1.4 yr) underwent iv DEX administration (0.3 mg/body surface area at 0 min). IGF-I, GH, and ghrelin levels were assayed at baseline and every 30 min from 120 up to 240 min after DEX. Compared to baseline levels DEX decreased ghrelin in ISS at 120 min and 240 min (p<0.04). On the other hand DEX did not modify ghrelin levels in GHD. After DEX, ghrelin was reduced in ISS compared to GHD (p<0.02). DEX increased GH in ISS but not in GHD (peak: 11.1+/-1.2 vs 7.6+/-0.9 microg/l). Basal, as well as after-DEX ghrelin levels negatively correlated with IGF-I in GHD (p<0.03) and with height SD score (HSDS) in ISS (p<0.02). Acute DEX administration is able to decrease ghrelin in ISS, but not in GHD children. Both basal and after-DEX ghrelin levels negatively correlate with IGF-I and HSDS. All these data suggest the existence of a feedback link among ghrelin, glucocorticoids and the GH/IGF-I axis.