VAT is as safe as conventional thyroidectomy and is characterized by a less painful postoperative course and by better cosmetic results and postoperative outcome.

No abstract

Preterm newborns developing retinopathy of prematurity (ROP) and bronchopulmonary dysplasia (BPD) show persistently low levels of insulin-like growth factor-I (IGF-I) in sera. They also present higher free IGF-I concentrations in epithelial lining fluids (ELFs) and lung tissues. Pregnancy-associated plasma protein-A (PAPP-A) is a metalloproteinase that dissociates three binding proteins from the active form of IGF-I, namely free IGF-I. The present study analyzes the ELF concentrations of free IGF-I, PAPP-A, and their ratios in preterm newborns developing or not BPD, defined as O2 dependence at 36 wk postmenstrual age. Bronchoalveolar lavage fluids of 41 infants (34 without and 7 with BPD) were analyzed on the 2nd and 4th day after birth. Infants developing BPD showed increased ELF free IGF-I and decreased PAPP-A concentrations on both days 2 and 4 compared with newborns without BPD. A nonsignificant trend between these 2 days was observed for free IGF-I (increasing) and PAPP-A (decreasing). On the same days, the free IGF-I-to-PAPP-A ratio was always significantly higher in patients developing BPD. These differences were more significant than those of IGF-I or PAPP-A when individually evaluated. A multivariate analysis confirmed the significance for free IGF-I on day 4, whereas the ratio was confirmed on both days 2 and 4. The same ratio was significantly correlated with some indexes of disease severity, such as hours of oxygen administration, days of hospitalization, and ROP severity scores. Finally, the ratio between ELF free IGF-I and PAPP-A appears to be a useful marker for lung injury of premature newborns.

This study shows that proteomic techniques can be applied to investigate the involvement of proteolytic enzymes on the airways of mechanically ventilated premature infants.

No abstract

Insulin-like growth factor-I (IGF-I) is involved in regulating the TH-lITH-2 balance, favoring the development of the TH-2 compartment which enhances fibrosis, one of the main characteristics of Chronic Lung Disease (CLD) in premature newborns. Limited data is available concerning a possible association between early epithelial lining fluid (ELF) concentrations ofIGF-I (total and free forms), IGF-binding protein-3 (IGFBP-3), b2-microglobulin (B2M) and subsequent development of CLD in preterm neonates. If neutropenic, preterm neonates are frequently treated with recombinant human Granulocyte Colony Stimulating Factor (rhG-CSF). The objective of the study was to correlate ELF concentrations of IGF-I and B2M during the first week of life both in non-neutropenic and in rhG-CSF-treated neutropenic preterm neonates, with subsequent development in CLD. Thirty preterm neonates with Respiratory Distress Syndrome (6 with neutropenia) were studied. Eleven out of 24 non-neutropenic preterm infants (46%) and all of the six neutropenic subjects (IOOo/~) developed CLD. With the exception of first day values, there was a clear similarity in the behaviors of assayed molecules between non-neutropenic and neutropenic patients developing CLD. Non-neutropenic patients without CLD showed significantly lower values of free IGF-I and B2M both on days 1 and 3. Total IGF-I and cell counts were different only on the 3rd day. Conclusions: I) the mechanisms leading to CLD might be mediated by high levels of IGF-family molecules soon after birth 2) B2M could be a marker of increased bronchoalveolar lavage fluid cellularity with potential inflammatory properties 3) G-CSF treatment induces an increased synthesis of IGF-I moleculesby cells recruited in the lung, with possible enhancement of the fibrogenic mechanisms. Chronic lung disease (CLD) in very low birth weight infants is a major health concern facing neonatologists because of its morbidity and high mortality risk (1-2). The pathogenesis of CLD is still unclear, although several risk factors have been described (3-6). Great importance has recently been attributedto pulmonary inflammation(1-3) and several pro-inflammatory and anti-inflammatory/fibrogenic cytokines in bronchoalveolar lavage fluid (BALF) have been indicated as possible triggers of pulmonary fibrosis (1-3, 5), one of the main characteristics of CLD (I). In adult lung fibrosis, an

Among hypertensive older adults, ACE inhibitors use is associated with higher IGFBP-3 levels.

Patency of the ductus arteriosus (PDA) and bronchopulmonary dysplasia (BPD) development represent severe affections for premature newborns, therefore the research of early markers for these two conditions is really important. The aim of this study is to analyze epithelial lining fluid (ELF) Neutrophil-gelatinase-associated lipocalin (NGAL) levels for prediction of lung injury or possible involvement ofthis molecule in PDA. Only scarce and contrasting results have previously been published in this field. In contrast, this molecule, included in a large macromolecular complex together with matrix metalloproteinase-9 (MMP-9), is considered an acceptable marker of infectious/inflammatory processes, cancer monitoring and induction of apoptotic pathway. NGAL was detected in 28 pre-term newborns by means of a commercially available kit in bronchoalveolar lavage fluid (BALF). The results have been corrected to ELF levels, by the urea method, to eliminate bias due to BALF collection. ELF NGAL levels were found significantly increased both in infants developing BPD or in those affected by PDA. By means of multivariate logistic regression analysis the significances were confirmed after adjusting for possible interfering variables such as gestational age and concomitant presence of both PDA and BPD. Our results stress the involvement of NGAL in the mechanisms leading to BPD and also suggest a possible association with PDA, which is often linked to prematurity and BPD development, probably due to the involvement of inflammatory and angiogenetic processes in both pathologies.Neutrophil-gelatinase-associated lipocalin (NGAL) is a 25-kDa protein associated with neutrophil ge1atinase, a molecular complex of 220-kDa, (namely matrix metallo-protein-9, MMP-9) including a homodimer of the gelatinase component (92-kDa) and the NGAL protein (l). NGAL is present in monocyte/macrophage cell lineage, in hepatocyte, epithelial and immune cells. It has been shown to increase in inflammatory and neoplastic diseases and has been proposed as a kidney injury marker (2). The NGAL functions mainly depend on its binding activity, directed against various molecules, such as N-formylated tripeptides, fatty acids, leukotriene B4 and platelet activating factor (3) as well as plasma matrix metallo-protein MMP-9 (4). In particular, when bound to MMP-9, NGAL may modulate