Abstract
Probiotic supplementation reduces the risk of necrotizing enterocolitis (NEC) and late-onset sepsis (LOS) in preterm infants, but it remains to be determined whether this reduction translates into a reduction of other complications. We conducted a systematic review and meta-analysis to evaluate the possible role of probiotics in altering the risk of bronchopulmonary dysplasia (BPD). Fifteen randomized controlled trials (4782 infants; probiotics: 2406) were included. None of the included studies assessed BPD as the primary outcome. Meta-analysis confirmed a significant reduction of NEC (risk ratio (RR) 0.52, 95% confidence interval (CI) 0.33 to 0.81, p = 0.004; random effects model), and an almost significant reduction of LOS (RR 0.82, 95% CI 0.65 to 1.03, p = 0.084). In contrast, meta-analysis could not demonstrate a significant effect of probiotics on BPD, defined either as oxygen dependency at 28 days of life (RR 1.01, 95% CI 0.91 to 1.11, p = 0.900, 6 studies) or at 36 weeks of postmenstrual age (RR 1.07, 95% CI 0.96 to 1.20, p = 0.203, 12 studies). Meta-regression did not show any significant association between the RR for NEC or LOS and the RR for BPD. In conclusion, our results suggest that NEC and LOS prevention by probiotics does not affect the risk of developing BPD in preterm infants.
Highlights
Bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity, is considered one of the major complications of premature birth [1,2,3,4]
The pathogenesis of bronchopulmonary dysplasia (BPD) is initiated by the arrest in alveolar and lung vascular development, due to premature birth, and sustained by inflammatory events that play a paramount role in the progression of BPD [3,4,8,9]
All the included studies reported data on necrotizing enterocolitis (NEC) (Table 3) and, when pooled, we observed that probiotics significantly reduced the risk of developing NEC (RR 0.52, 95% CI 0.33–0.81, p = 0.004, Table 4)
Summary
Bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity, is considered one of the major complications of premature birth [1,2,3,4]. The incidence of BPD is inversely proportional to gestational age, with rates reaching up to 60–90% in extremely preterm infants (22–25 weeks gestation). Infants suffering from BPD are at increased risk of death and long-term pulmonary and neurodevelopmental morbidities [5,6,7]. The pathogenesis of BPD is initiated by the arrest in alveolar and lung vascular development, due to premature birth, and sustained by inflammatory events that play a paramount role in the progression of BPD [3,4,8,9]. The initiation of the inflammatory response can already occur in utero, in the setting of chorioamnionitis [3,4,10,11] Postnatal stimuli, such as the ex-utero higher oxygen partial pressures, the need for oxygen administration or mechanical ventilation, and the occurrence of postnatal infections (including late onset sepsis (LOS) and necrotizing enterocolitis
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