Objective: To compare composite adverse outcome rate of infants <32 weeks gestational age (GA) who were born after preterm premature rupture of membranes (PPROM) at previable gestation to those born without PPROM.Study Design: Retrospective review of prospective collected data for infants discharged between 2004 and 2007 was conducted. Cases were infants with >7 days of PPROM that occurred before 24 weeks. Matched cohort consisted of infants born without PPROM (matched for GA, sex and admission date). Composite adverse outcome was assessed considering death or any of the following three severe morbidities (severe neurological injury, severe retinopathy of prematurity or chronic lung disease).Result: The 29 cases had higher mean severity of illness score compared with 74 matched infants. Mean duration of ROM was 45 vs 2 days and mean GA at the ROM was 21 vs 27 weeks, respectively. Logistic regression confirmed significantly higher risk of composite adverse outcome rates for cases (69 vs 47%; P ¼ 0.02, adjusted odds ratio 4.0, 95% CI 1.2, 13.6). Conclusion:The survival rate for infants born at <32 weeks following PPROM at previable age has improved significantly; however, these infants had a higher rate of adverse composite neonatal outcome.

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Adenosine is a neuromodulator with its level increasing up to 100-fold during ischemic events, and attenuates the excitotoxic neuronal injury. Adenosine is produced both intracellularly and extracellularly, and nucleoside transport proteins transfer adenosine across plasma membranes. Adenosine levels and receptor-mediated effects of adenosine are regulated by intracellular ATP consumption, cellular release of ATP, metabolism of extracellular ATP (and other adenine nucleotides), adenosine influx, adenosine efflux and adenosine metabolism. Recent studies have used genetically modified mice to investigate the relative contributions of intra-and extracellular pathways for adenosine formation. The importance of cortical or hippocampal neurons as a source or a sink of adenosine under basal and hypoxic/ischemic conditions was addressed through the use of transgenic mice expressing human equilibrative nucleoside transporter 1 (hENT1) under the control of a promoter for neuron-specific enolase. From these studies, we conclude that ATP consumption within neurons is the primary source of adenosine in neuronal cultures, but not in hippocampal slices or in vivo mice exposed to ischemic conditions.