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Officials strive to understand infection routes and promote prevention and testing.

The aim of this study was to define the inflammatory changes occurring in the lungs of infants at risk for bronchopulmonary dysplasia (BPD) over the first 28 days of life, and to define an optimal strategy for steroids therapy in the prevention of BPD. We measured levels of interleukin-6 (IL-6) and interleukin-1 beta (IL-1beta) in tracheal aspirate (TA) samples and blood of premature infants with severe respiratory distress syndrome RDS (n = 45) on the first day of life prior to initiation of surfactant therapy and on days 5-7, 12-14, 19-21, and 26-28. Levels of IL-6 and IL-1beta were determined with a commercially available enzyme-linked immunoassay. Logistic regression analyses were performed in order to examine differences in trends in levels of IL-6 and IL-1beta between groups of infants. Infants were divided into group I (n = 30, FiO(2) < or = 0.35 at 28 days) and group II (n = 15, FiO(2) > 0.35 based on their likelihood of developing BPD at 36 weeks postconceptional age (PCA). The infants were comparable with respect to mean ( +/- SEM) birth weight (895 +/- 33 g vs. 900 +/- 40 g), gestational age (27 +/- 0.38 weeks vs. 27 +/- 0.54 weeks), and severity of respiratory illness at entry into the study (mean airway pressure: 12 +/- 1 cmH(2)O vs. 12 +/- 1 cmH(2)O, and oxygen index: 15 +/- 2 vs. 19 +/- 4) (group I vs. group II, respectively). Logistic regression analyses failed to reveal any significant differences in linear trends of levels of IL-6 and IL-1beta in TA samples between both groups of infants. No particular pattern of change in levels of IL-6 or IL-1beta could be identified among groups of infants. Levels of IL-6 and IL-1beta in TA samples on the first day of life failed to predict the need for FiO(2) > 0.35 at 28 days of age. We could not identify an increasing trend or a specific pattern of changes in postnatal levels of IL-6 or IL-1beta in TA samples of infants who were at greater risk of developing BPD at 36 weeks PCA compared to infants who were not.

Red blood cell transfusions (RBCTs) have been associated with necrotising enterocolitis (NEC) in preterm infants (PTIs). The objective of this report is to evaluate the use of regional cerebral (cRSO 2) and splanchnic (sRSO 2) tissue oximetry measured using near infrared (NIR) spectroscopy as biomarkers to evaluate the association between RBCT and NEC in a secondary analysis of a hypothesis-generating Phase I exploratory study of biomarker development. cRSO 2 and sRSO 2 were monitored in PTIs receiving RBCTs. Three time periods were defined: pre-RBCT (12 h prior to RBCT), during RBCT and post-RBCT (24 h after RBCT). Three groups were defined: absence of NEC within ±7 days of index RBCT (Group 1); NEC within 7 days prior (Group 2) and within 7 days after RBCT (Group 3). Mean hourly sRSO 2 and cRSO 2 were compared between groups across RBCT periods using the mixed effect method. Neonatal postnatal morbidities and treatments were included as covariates. Fifty-seven infants (median gestational age 27 weeks) received 147 RBCTs (Group 1 = 120, Group 2 = 19, and Group 3 = 8) during NIR spectroscopy monitoring. In the adjusted analysis, there was a significant change in sRSO 2 during the course of RBCT (p = 0.0405) with significant interaction with group (p < 0.0001) such that in Groups 1 and 2, sRSO 2 increased over RBCT periods, whereas in Group 3, sRSO 2 declined over RBCT periods. cRSO 2 increased during the course of the RBCT (p < 0.0001) with significant interaction with group (p = 0.0258). cRSO 2 and sRSO 2 increased significantly following RBCT in infants without NEC or NEC diagnosed prior to RBCT. Post-RBCT sRSO 2 decreased in infants who were subsequently diagnosed with NEC in this exploratory secondary analysis of a Phase I Biomarker study. sRSO 2 response may potentially be a biomarker to identify infants who are likely to develop NEC post-RBCT that needs to be validated in larger prospective "hypothesis-testing" randomised controlled trials.