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IntroductionBronchopulmonary dysplasia (BPD) is a syndrome of respiratory distress caused by chronic lung parenchymal injury, occurring especially in preterm infants (1). BPD remains a serious problem in very low birthweight (VLBW) infants despite the use of antenatal steroids and postnatal surfactant therapy to decrease the incidence and severity of respiratory distress syndrome (RDS) (2,3). BPD has a complex and multifactorial etiology, including oxygen toxicity, preterm delivery, hypoxia/hyperoxia, infection, and inflammation (4).Many studies have suggested that lung inflammation is a major contributor to the pathogenesis of BPD (5,6). Various parameters of lung inflammation may be used to show lung inflammation. However, most of them such as N-terminal propeptide of type 3 collagen, SP-A, anti-SP-A immune complexes, nitrotyrosine, soluble E-selectin, intercellular adhesion molecule-1, allantoin, and aldehydes are not specific for lung disease or are complicated to measure (6). Krebs yon den Lundgen-6 (KL-6) is a mucinlike high-molecular weight glycoprotein that is classified into cluster 9 (MUC1) of lung tumor and differentiation antigens. It is preferentially expressed by alveolar type 2 cells and stimulates lung fibrosis through its action as a fibroblast chemotactic factor (7).There are many studies suggesting plasma KL-6 is increased in adult patients with various types of interstitial pneumonia, characterized by type 2 alveolar hyperplasia and fibrosis (8-11). KL-6 has also shown to be as a useful marker for increased alveolar vascular permeability associated with lung injury. However, plasma KL-6 levels are not elevated in noninterstitial lung diseases such as bacterial pneumonia, bronchial asthma, and pulmonary emphysema (9). Similar pathological changes seen in interstitial pneumonia in the lung are also predominant in BPD (7,12,13). Plasma KL-6 can be a clinically useful early marker for BPD. However, there are few data on the predictive characteristics of KL-6. Therefore, in the present study, we aimed to evaluate the predictive values of KL-6 in BPD within the first days of life. Materials and methods Study populationAll eligible preterm infants between May 2014 and April 2015 were prospectively enrolled in this study, specifically neonates with birthweight ≤1500 g and gestational age ≤32 Background/aim: It has been suggested that plasma KL-6 increases in premature infants with bronchopulmonary dysplasia (BPD). We aimed to evaluate the predictive values of KL-6 in BPD. Materials and methods:The study was performed in preterm neonates with birthweight ≤1500 g and gestational age ≤32 weeks. Plasma KL-6 levels were measured on postnatal days 1, 7, and 14.Results: BPD was identified in eight of the 28 study infants. On postnatal days 1 and 7, plasma KL-6 levels were similar in infants with BPD [on

Objective Urinary tract infection (UTI) is a disease that can cause significant complications in the neonatal period. The thiol-disulfide homeostasis is one of the important antioxidant defense mechanisms. The purpose of this study is to show the relationship between UTI and thiol-disulfide homeostasis in newborns. Study Design In this prospective study, 40 newborns with UTI and 40 healthy controls were included. Thiol-disulfide tests (disulfide, native thiol, and total thiol levels) and septic screening tests were performed before and after antibiotherapy in UTI group. The control group was selected from healthy newborns who applied to the outpatient clinic. Results The C-reactive protein and interleukin-6 levels were higher, while native thiol and native thiol/total thiol ratio were significantly lower in pretreatment group compared with post-treatment and control group. Also, the levels of disulfide, ischemia modified albumin, disulfide/native thiol ratio, and disulfide/total thiol ratio were higher in pretreatment group compared with post-treatment group. Conclusion The thiol-disulfide homeostasis is an important indicator of oxidative stress during infections. It is valuable to be detected with small amounts of serum in newborns. These molecules can be used to support the diagnosis of UTI in the newborn. Further studies are needed to define the role of thiol-disulfide homeostasis in the UTI of newborn. Key Points