Vitamin d deficiency with high parathyroid hormone levels is related to late onset SEPSIS among preterm infants.

Preterm infants (PTs) are at greater risk for vitamin D deficiency, which relates to the possibility of a higher incidence of comorbidities. Our goal was twofold, 1) to monitor vitamin D, calcium, phosphorus, parathyroid hormone (PTH), matrix metalloproteinase-8 (MMP-8) serum levels at three-time points during hospitalization, and 2) to assess the association between 25-hydroxyvitamin D (25OHD) levels and outcomes in PTs. METHODS: We carried out a follow-up on 50 Caucasian PTs ≤ 32 weeks of gestational age (GA) and/or ≤ 1500 g birth weight at 28 days and at 4 months. PTs were divided into two subgroups for tests of association with clinical outcomes based on vitamin D deficient infants 25(OH) D cord blood levels: ≤ 20 ng/ml). At an initial stage, 25(OH) D levels were determined in maternal/preterm blood samples and were compared to full term delivery infants. RESULTS: There were no differences in 25(OH) D serum levels at birth when comparing PTs to term infants, or regarding maternal levels. A strong positive correlation was detected between maternal and neonatal 25(OH) D serum levels among PTs and term infants (r: 0.466; p < 0.001). Neonates with vitamin D deficiency did not present a higher incidence of comorbidities. PTs were classified in two subgroups based on vitamin D and PTH (group 1: vitamin D < 20 ng/mL and PTH > 60 pg/mL; group 2: vitamin D > 20 and PTH < 60 pg/mL). The PTs in group 1 showed a higher incidence of LOS (RR: 2; 95% CI: 1.31-3.55). No relationship was observed between MMP-8 serum levels and the incidence of sepsis. CONCLUSIONS: This study did not find any evidence of an increase in preterm birth risk related to vitamin D level at birth. Vitamin D deficiency by itself is not associated with a higher incidence of comorbidities. However, the binomial vitamin D-PTH must be taken into consideration.

Short-Term Evaluation of Left Ventricular Mass and Function in Children With Growth Hormone Deficiency After Replacement Treatment.

Background: Our study was designed to assess the effects of GHD on nutritional and metabolic parameters, brain natriuretic peptide (BNP) levels, and left ventricular mass (LVM) in prepubertal children and after short-term GH replacement therapy. Materials and Methods: This prospective study enrolled 81 children. We compared 40 GHD children (16 males and 24 females) to 41 healthy children (control group) (18 males and 23 females). All subjects were at Tanner Stage I (aged 7-11 years). At the baseline, a blood sample was drawn and echocardiographic images were obtained. These tests were repeated on the GHD subjects after 6 months of GH replacement therapy. Body surface, weight, size, blood pressure, heart rate, glucose, insulin, HOMA-IR, HOMA-ß, QUICKI, cholesterol, HDLc, LDLc, triglycerides, IGF1, and IGFBP3 were measured. Indexed LVM, diastolic and systolic diameter (dD-sD), diastolic and systolic LV function, isovolumic relaxation time, right ventricle function, and BNP levels were obtained through echocardiography. These parameters were correlated to growth factors. Data were analyzed using Student's t-test or U-Mann-Whitney-test and Pearson's correlation, considering p < 0.05 to be significant. Results: Indexed LVM was smaller in GHD patients than in controls, whereas diastolic and systolic functions, BNP, metabolic, and nutritional profiles were similar. After treatment, nutritional and metabolic profiles significantly improved, though diastolic and systolic functions did not seem to have changed. There was a significant increase in LVM. Indexed LVM was similar to that of controls. Significant correlations were obtained between LVM-IGF1 and sD-IGFBP3. Conclusions: GHD in childhood is associated with a lower indexed LVM. In the short-term, GH increases the indexed LVM, while maintaining normal systolic and diastolic functions, BNP, and an improved lipid profile.

Morbility, clinical data and proteomic analysis of IUGR and AGA newborns at different gestational ages.

The data are related to the proteomic analysis of 43 newborns with intrauterine growth retardation (IUGR) and 45 newborns with appropriate weight for gestational age (AGA) carried out by separation via 2DE and analyzed by MS-TOF/TOF. All newborns were separated into three gestational age groups, "Very Preterm" 29-32 weeks, "Moderate Preterm" 33-36 weeks, and, "Term" ≥37weeks. From each newborn, blood was drawn three times from birth to 1 month life. High-abundant serum proteins were depleted, and the minority ones were separated by 2DE and analyzed for significant expression differences. The data reflect analytic and clinic variables analyzed globally and categorized by gestational age in relation to IUGR and the optimization of conditions for 2-DE separation. The data from this study are related to the research article entitled "Alterations of Protein Expression in Serum of Infants with Intrauterine Growth Restriction and Different Gestational Ages" (M.D. Ruis-González, M.D. Cañete, J.L. Gómez-Chaparro, N. Abril, R. Cañete, J. López-Barea, 2015) [1]. The present dataset of serum IUGR newborn proteome can be used as a reference for any study involving intrauterine growth restriction during the first month of life.

Recruiting of somatotroph cells after combined somatostatin, GHRH and growth hormone (GH) secretagogue stimulation in a study of pituitary GH reserve in prepuberal female rats.

Diagnostic confirmation of growth hormone (GH) deficiency in children and adults is based on stimulation tests designed to assess the pituitary reserve by measuring the amount of GH released into the bloodstream; however, the results obtained by this means cannot provide any direct indication of the amount of GH actually produced by pituitary somatotroph cells. The present paper sought to test the hypothesis that release of GH following administration of specific stimuli does not accurately reflect the somatotroph cell response, and that the amount of GH released into the bloodstream may often be greater or smaller than the amount synthesized. GH release and changes in the proportion of somatotroph cells were charted in prepuberal female Wistar rats, following administration of several different GH stimuli: GHRH (1 microg/kg), GHRP-6 (1 microg/kg), GHRELIN (1 microg/kg) and combined GHRH-based treatments, with or without SRIH pretreatment (1 microg/kg) 90 minutes earlier. Peak serum GH values were recorded 15 minutes after administration of GHRH+GHRELIN and GHRH+GHRP-6; maximum stimulation in terms of an increased proportion of somatotroph cells occurred 15 minutes after combined adminstration of GHRH + GHRELIN. SRIH pretreatment (- 90 min) inhibited GH release, with a subsequent "escape" and lack of response to stimulation which lasted at least 30 minutes except following administration of GHRH. However, combined administration of GHRH+GHRELIN maintained stimulation of the somatotroph cell population. In conclusion, the results suggest that the enhanced GH release prompted by stimulation tests used to diagnose GH deficiency in prepuberal female rats does not fully reflect somatroph cell dynamics, and that not all the GH produced and stored by somatotroph cells is released into the bloodstream.