RT Journal Article SR Electronic T1 Pregnancy complications and respiratory outcomes in very preterm infants JF European Respiratory Journal JO Eur Respir J FD European Respiratory Society SP P4652 VO 40 IS Suppl 56 A1 Luigi Gagliardi A1 Franca Rusconi A1 Monica Da Frè A1 Giorgio Mello A1 Virgilio Carnielli A1 Domenico Di Lallo A1 Francesco Macagno A1 Silvana Miniaci A1 Carlo Corchia A1 Marina Cuttini YR 2012 UL http://erj.ersjournals.com/content/40/Suppl_56/P4652.abstract AB Very preterm infants have a high mortality and morbidity, due to a combination of immaturity per se, and of the underlying pathology causing preterm birth. The role of prenatal infection on increasing the risk of bronchopulmonary dysplasia (BPD) is still unsettled.Aim: To test the hypothesis that infection/inflammation disorders (I) (prelabor premature rupture of membranes, spontaneous preterm labor, infection and hemorrage) and hypertensive disorders (H) (maternal hypertension and intrauterine growth restriction) are differently associated to in-hospital mortality and BPD.Methods: A population-based prospective cohort of 2085 singleton infants 23 to 31 weeks gestational age (GA) born in 6 Italian regions in 2003-2005 (ACTION study), was analyzed.Infants born of mothers with H (31%) were contrasted with those born after I (63%) with respect to mortality and BPD. Multivariable logistic analyses (generalized estimating equations) were used.Results: Mortality was 14.3%, with 48.7 % of deaths occurring in the first 5 days of life, largely due to respiratory causes. Infants born after H had more respiratory distress syndrome than the I group (odds ratio (OR)= 1.41, 95% confidence interval (CI): 1.1-1.8, adjusted for GA, sex and antenatal steroids). 12.8 % of neonates had BPD. After adjustment for GA, H disorders had a higher risk of mortality (OR=1.4; 95% CI:1.0, 2.0) and of BPD (OR=2.5; CI: 1.8, 3.6). Further adjustment for maternal age, education, citizenship, and antenatal steroids did not change results.Conclusions: Our results support the hypothesis that pathogenetic mechanisms involving the regulation of lung/airways size and vessels are more important than I in the development of BPD.