BACKGROUND: Despite recent advances in preterm newborns healthcare, perinatal pathologies and disabilities are increasing. Oxidative stress (OS) is determinant for the onset of an unbalance between free radicals (FRs) production and antioxidant systems which plays a key role in pathogenesis of pathologies such as retinopathy of prematurity (ROP), bronchopulmonary dysplasia (BPD), necrotizing enterocolitis (NEC), intraventricular hemorrhage (IVH), grouped as 'free radical-related diseases' (FRD). AIM: This study tests the hypothesis that OS markers levels in cord blood may predict the onset of FRD pathologies. PATIENTS AND METHODS: 168 preterm newborns of GA: 24-32weeks (28.09+/-1.99); and BW: 470-2480 gr (1358.11+/-454.09) were consecutively recruited. Markers of potential OS risk (non-protein bound iron, NPBI; basal superoxide anion, BSA; under stimulation superoxide anion, USSA) and markers of OS-related damage (total hydroperoxides, TH; advanced oxidation protein products, AOPP) were assessed in cord blood. Associations between FRD onset and OS markers were checked through inferential analysis (univariate logistic regression). RESULTS: The development of FRD was significantly associated to high cord blood levels of TH, AOPP and NPBI (respectively p=0.000, OR=1.025, 95%CI=1.013-1.038; p=0.014, OR=1.092, 95%CI=1.018-1.172; p=0.007, OR=1.26995%CI=1.066-1.511). CONCLUSIONS: Elevated levels of TH, AOPP and, above all, NPBI, in cord blood are associated with increased risk for FRD. OS markers allow the early identification of infants at risk for FRD because of perinatal oxidant exposure. This can be useful in devising strategies to prevent or ameliorate perinatal outcome.

Perrone, S., Tataranno, M.L., Negro, S., Longini, M., Marzocchi, B., Proietti, F., et al. (2010). Early identification of the risk for free radical-related diseases in preterm newborns. EARLY HUMAN DEVELOPMENT, 86(4), 241-244 [10.1016/j.earlhumdev.2010.03.008].

Early identification of the risk for free radical-related diseases in preterm newborns

TATARANNO, M. L.;LONGINI, M.;MARZOCCHI, B.;PROIETTI, F.;IACOPONI, F.;CAPITANI, S.;BUONOCORE, G.
2010-01-01

Abstract

BACKGROUND: Despite recent advances in preterm newborns healthcare, perinatal pathologies and disabilities are increasing. Oxidative stress (OS) is determinant for the onset of an unbalance between free radicals (FRs) production and antioxidant systems which plays a key role in pathogenesis of pathologies such as retinopathy of prematurity (ROP), bronchopulmonary dysplasia (BPD), necrotizing enterocolitis (NEC), intraventricular hemorrhage (IVH), grouped as 'free radical-related diseases' (FRD). AIM: This study tests the hypothesis that OS markers levels in cord blood may predict the onset of FRD pathologies. PATIENTS AND METHODS: 168 preterm newborns of GA: 24-32weeks (28.09+/-1.99); and BW: 470-2480 gr (1358.11+/-454.09) were consecutively recruited. Markers of potential OS risk (non-protein bound iron, NPBI; basal superoxide anion, BSA; under stimulation superoxide anion, USSA) and markers of OS-related damage (total hydroperoxides, TH; advanced oxidation protein products, AOPP) were assessed in cord blood. Associations between FRD onset and OS markers were checked through inferential analysis (univariate logistic regression). RESULTS: The development of FRD was significantly associated to high cord blood levels of TH, AOPP and NPBI (respectively p=0.000, OR=1.025, 95%CI=1.013-1.038; p=0.014, OR=1.092, 95%CI=1.018-1.172; p=0.007, OR=1.26995%CI=1.066-1.511). CONCLUSIONS: Elevated levels of TH, AOPP and, above all, NPBI, in cord blood are associated with increased risk for FRD. OS markers allow the early identification of infants at risk for FRD because of perinatal oxidant exposure. This can be useful in devising strategies to prevent or ameliorate perinatal outcome.
2010
Perrone, S., Tataranno, M.L., Negro, S., Longini, M., Marzocchi, B., Proietti, F., et al. (2010). Early identification of the risk for free radical-related diseases in preterm newborns. EARLY HUMAN DEVELOPMENT, 86(4), 241-244 [10.1016/j.earlhumdev.2010.03.008].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/22321
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