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Preterm premature rupture of membranes chorionic amniotic inflammation grade and neonatal lung development in the relationship of state.doc

Preterm premature rupture of membranes chorionic amniotic inflammation grade and neonatal lung development in the relationship of state.doc

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Preterm premature rupture of membranes chorionic amniotic inflammation grade and neonatal lung development in the relationship of state

 PAGE \* MERGEFORMAT 11 Preterm premature rupture of membranes chorionic amniotic inflammation grade and neonatal lung development in the relationship of state [Abstract] Objective: To study the preterm premature rupture of membranes (PPROM) in histologic chorioamnionitis (HCA) status of the baby would affect the development of the lungs. Programs: the continuous production of 287 preterm children (during pregnancy ≤ 32 +6 weeks) placental samples for histological analysis, divided into 4 groups: meningitis in a premature rupture of membranes plush wool; there was no rupture of the membranes chorioamnionitis; no chorioamnionitis with premature rupture of membranes; no premature rupture of membranes without chorioamnionitis. Results: 287 intensive care unit confirmed in preterm children, 68/287 (23.6%) histologic chorioamnionitis, 16/68 (23.5%) complicated with fetal inflammatory response , 74/287 (25.7%), the preterm premature rupture of membranes. chorioamnionitis (HCA) and multiple vaginal delivery (P lt;0.0001), low gestational age (P lt;0.0001) and fetal low birth weight (P lt;0.01) between the close. chorioamnionitis (HCA) although no effect on the baby’s lung maturity, but it is an important risk factor for chronic lung disease. Chorioamnionitis (HCA) and the baby is preterm premature rupture of membranes inflammatory response (PPROM) is an important risk factor. In contrast, preterm premature rupture of membranes (PPROM) with histological chorioamnionitis (HCA) did not show respiratory distress syndrome (RDS) protection, or chronic lung disease caused by subtypes (CLD) of risk. Multivariate analysis showed that the mother source of HCA (P = 0.04), gestational age (P lt;0.0001) and HCA combined with the gestational age effect (P = 0.04) for the development of chronic lung disease were significant independent effect, and the source of this effect and fetal HCA, HCA the interaction of gestational age and gestational age of PPROM or PPROM independent int

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