Fetal growth restriction is associated with an increased risk of developing insulin resistance and type 2 diabetes in adulthood. In addition, 10-20% of children born small for gestational age (SGA) do not achieve a normal final height. The purpose of this study was to investigate insulin sensitivity and endocrine status in SGA children, compared with that in children born appropriate for gestational age (AGA). Furthermore, within the SGA group, we aimed to relate postnatal growth to anthropometric, biochemical, and endocrine parameters. Eighty-two SGA children (with a mean age of 8.6 +/- 3.5 yr) and 53 short-AGA children (with a mean age of 9.3 +/- 3.3 yr) were studied. A case-control study was carried out in 26 SGA and 26 short-AGA subjects. For each SGA subject, we selected a short-AGA child matched for sex, age (within 1 yr), pubertal status, body mass index (within 0.5 kg/m(2)), and height (within 0.25 z-score). Children's statures were corrected for their midparental height, and SGA children were subdivided into 2 groups: catch-up growth (CG) group (children with corrected height with at least 0 z-score); and non-CG (NCG) group (subjects with corrected height with less than 0 z-score). Comparing SGA with short-AGA subjects, no significant differences in fasting insulin, fasting glucose/insulin ratio, homeostasis assessment model for insulin resistance, and homeostasis assessment model-beta-cell values were observed. SGA children showed significantly reduced levels of glucose (4.4 +/- 0.6 vs. 4.9 +/- 0.6 mM, P < 0.0001), total cholesterol (160.1 +/- 28.8 vs. 171.8 +/- 28.5 mg/dl, P = 0.02), and high-density-lipoprotein cholesterol (53.3 +/- 12.1 vs. 58 +/- 11.4 mg/dl, P = 0.02). The analysis of the subjects selected for the case-control study confirmed that SGA children did not have significant differences in the indices of insulin sensitivity but showed significantly lower glucose levels (4.4 +/- 0.7 vs. 4.9 +/- 0.4 mM, P < 0.005). Subdividing the SGA group into CG (n = 25) and NCG (n = 57) children, we found that NCG children showed significantly higher levels of TSH (2.5 +/- 1.3 vs. 1.9 +/- 0.6 mU/liter, P = 0.002). Our data indicate that SGA children do not have altered insulin sensitivity when compared with auxologically identical AGA subjects but show a significant reduction of glucose concentrations. Whether the lower glucose levels are attributable to an early phase of augmented insulin sensitivity, as previously reported in animal models, has to be established. The finding of higher TSH concentrations in SGA children with blunted CG suggests that intrauterine reprogramming might involve thyroid function, which, in turn, might affect postnatal growth and cholesterol metabolism, eventually increasing the risk of cardiovascular disease.

Intrauterine growth retardation (IUGR) is one of the major causes of short stature in childhood. Although postnatal catch-up growth occurs in the majority of IUGR children, approximately 20% of them remain permanently short. The mechanisms that allow catch-up growth or, on the contrary, prevent IUGR children from achieving a normal height are still unknown. Our aim was to investigate whether intrauterine reprogramming of hypothalamic-pituitary-adrenal axis may be involved in postnatal growth retardation of IUGR children through a modulation of the function of the IGF system. Anthropometry, IGF system assessment, cortisol measurement, and lipid profile evaluation were performed in 49 IUGR children. Children were subdivided into two groups according to their actual height corrected for midparental height: CG (catch-up growth) group, 19 children with corrected height Ն0 z-score; and NCG (noncatch-up growth) group, 30 subjects with corrected height Ͻ0 z-score. CG children showed significantly higher birth weight (p Ͻ 0.005) and body mass index (p Ͻ 0.05). No significant differences in IGF-I, IGF-II, IGF binding protein (IGFBP)-1, IGFBP-3, soluble IGF-II receptor levels (IGF2R), IGF-II/IGF2R ratio, and relative amounts of IGFBP-3 circulating forms were found between CG and NCG children. None of the IGF system-related variables correlated with anthropometric indices. NCG children showed significantly higher concentrations of cortisol (p Ͻ 0.005) and cortisol levels resulted inversely to birth weight (r ϭ Ϫ0.34, p Ͻ 0.05), birth length (r ϭ Ϫ0.36, p Ͻ 0.05), and corrected height (r ϭ Ϫ0.44, p Ͻ 0.01). Whereas total and HDL cholesterol concentrations were not significantly different in the two groups, LDL cholesterol levels were significantly higher in NCG children (p Ͻ 0.05), and five of 49 showed LDL cholesterol concentrations Ͼ3.4 mM (130 mg/dL). LDL cholesterol was inversely related to birth weight (r ϭ Ϫ0.31, p Ͻ 0.05), corrected stature (r ϭ Ϫ0.32, p Ͻ 0.05), and actual height (r ϭ Ϫ0.31, p Ͻ 0.05) and directly related to the levels of IGF2R (r ϭ 0.44, p Ͻ 0.01). Reanalysis of 15 of 30 IUGR newborns in whom we previously reported an inverse relationship between cord blood cortisol levels and first trimester length gain (r ϭ Ϫ0.54, p Ͻ 0.005) showed that the relative amount of the IGFBP-3 18-kD fragment was related inversely to cortisol (r ϭ Ϫ0.67, p Ͻ 0.01) and directly to early postnatal growth (r ϭ 0.65, p Ͻ 0.05). Our results suggest that catch-up growth in IUGR children might be affected by intrauterine reprogramming of hypothalamicpituitary-adrenal axis, which may result in a permanent modification of the neuroendocrine response to stress: children with increased cortisol secretion may be at higher risk of growth failure. During the neonatal period cortisol might act by limiting IGFBP-3 proteolysis and, therefore, reducing IGF bioavailability. ABSTRACT94

We evaluated severe acute respiratory syndrome coronavirus 2 RNA clearance in 22 children. The estimation of positivity at day 14 was 52% for nasopharyngeal swab and 31% for stool samples. These data underline the significance of nasopharyngeal and stoolsample for detecting infected children. Additional studies are needed for transmissibility.

Background Lately, one of the major clinical and public health issues has been represented by Coronavirus disease of 2019 (COVID-19) during pregnancy and the risk of transmission of the infection from mother to child. Debate on perinatal management and postnatal care is still ongoing, principally questioning the option of the joint management of mother and child after birth and the safety of breastfeeding. According to the available reports, neonatal COVID-19 appears to have a horizontal transmission and seems to be paucisymptomatic or asymptomatic, compared to older age groups. The aim of this work is to describe a cluster of neonatal COVID-19 and discuss our experience, with reference to current evidence on postnatal care and perinatal management. Methods This is a retrospective observational case series of five mother-child dyads, who attended the Labor and Delivery Unit of a first-level hospital in Italy, in March 2020. Descriptive statistics for continuous variables consisted of number of observations, mean and the range of the minimum and maximum values. Results Five women and four neonates tested positive for Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). In one case, the mother-child dyad was separated and the neonate remained negative on two consecutive tests. Two positive neonates developed symptoms, with a predominant involvement of the gastrointestinal tract. Blood tests were unremarkable, except for a single patient who developed mild neutropenia. No complications occurred. Conclusions We agree that the decision on whether or not to separate a positive/suspected mother from her child should be made on an individual basis, taking into account the parent’s will, clinical condition, hospital logistics and the local epidemiological situation. In conformity with literature, in our study, affected neonates were asymptomatic or paucisymptomatic. Despite these reassuring findings, a few cases of severe presentation in the neonatal population have been reported. Therefore, we agree on encouraging clinicians to monitor the neonates with a suspected or confirmed infection.

Children born small for gestational age (SGA) are at high risk of permanent short stature, with approximately 10% continuing to have stature below the third centile throughout childhood and adolescence and into adulthood. The mechanisms involved in catch-up growth, and those that prevent catch-up growth, are still unknown. To date, no reliable anthropometric or endocrine parameter predictive of postnatal catch-up growth has been identified. However, subtle abnormalities in the growth hormone-insulin-like growth factor axis, the hypothalamic-pituitary-adrenal axis and thyroid function have been described, and a mechanism involving intrauterine programming of hypothalamic-pituitary function has been proposed.