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Red cell distribution width as a predictor for bronchopulmonary dysplasia in premature infants.

ABSTRACT: Bronchopulmonary dysplasia (BPD) is the most common morbidity complicating preterm birth. Red blood cell distribution width (RDW), a measure of the variation red blood cell size, could reflect oxidative stress and chronic inflammation in many diseases such as cardiovascular, pulmonary, and other diseases. The objectives of the present study were to evaluate perinatal factors affecting RDW and to validate whether RDW could be a potential biomarker for BPD. A total of 176 preterm infants born at < 30 weeks were included in this study. They were categorized into BPD (n = 85) and non-BPD (n = 91) infants. RDW at birth and 14 days and 28 days of life (DOL 14, DOL 28) were measured. Clinical data were obtained from all subjects at Fukushima Medical University (Fukushima, Japan). The mean RDW at birth, DOL 14 and DOL 28 were 16.1%, 18.6%, 20.1%, respectively. Small for gestational age (SGA), chorioamnionitis (CAM), hypertensive disorders of pregnancy (HDP), gestational age and birth weight were significantly associated with RDW at birth. SGA, BPD and red blood cell (RBC) transfusion before DOL 14 were associated with RDW at DOL 14. BPD and RBC transfusion before DOL 14 were associated with RDW at DOL 28. Compared with non-BPD infants, mean RDW at birth DOL 14 (21.1% vs. 17.6%, P < 0.001) and DOL 28 (22.2% vs. 18.2%, P < 0.001) were significantly higher in BPD infants. Multivariate analysis revealed that RDW at DOL 28 was significantly higher in BPD infants (P = 0.001, odds ratio 1.63; 95% CI 1.22-2.19). Receiver operating characteristic analysis for RDW at DOL 28 in infants with and without BPD yielded an area under the curve of 0.87 (95% CI 0.78-0.91, P < 0.001). RDW at DOL 28 with mild BPD (18.3% vs. 21.2%, P < 0.001), moderate BPD (18.3% vs. 21.2%, P < 0.001), and severe BPD (18.3% vs. 23.9%, P < 0.001) were significantly higher than those with non-BPD, respectively. Furthermore, there are significant differences of RDW at DOL 28 between mild, moderate, and severe BPD. In summary, we conclude that RDW at DOL 28 could serve as a biomarker for predicting BPD and its severity. The mechanism by which RDW at DOL 28 is associated with the pathogenesis of BPD needs further elucidation.

SUBMITTER: Go H

PROVIDER: S-EPMC8012706 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundA previous study showed that the lungs are involved in the biogenesis of platelets (PLTs). Thus, the present study aimed to investigate the association between bronchopulmonary dysplasia (BPD), a chronic lung disease, and PLT parameters in very premature infants.MethodsThe study subjects were premature infants with a gestational age of ≤ 30 weeks and birth weight of ≤ 1500 g in a preterm birth cohort study recruited between January 1, 2015, and August 31, 2019. BPD was defined as the need for oxygen supplementation more than 28 days after birth. The PLT count, mean platelet volume (MPV), platelet distribution width (PDW), and plateletcrit (PCT) level were compared between BPD and non-BPD infants. A generalized estimating equation model was used to adjust for confounding factors. A forward stepwise logistic regression model was used to calculate the adjusted odds ratio (OR) for thrombocytopenia in the BPD group. Receiver operating characteristic curve analysis was performed to assess the predictive value of PLT count combined with gestational age (GA) and birth weight (BW) for BPD.ResultsThe final study subjects were 134 very premature infants, namely, 64 infants with BPD and 70 infants without BPD. The BPD infants had lower PLT counts (F = 4.44, P = 0.03) and PCT levels (F = 12.54, P = 0.00) than the non-BPD infants. However, the MPV (F = 14.25, P = 0.00) and PDW (F = 15.04, P = 0.00) were higher in the BPD group. After adjusting for potential confounding factors, the BPD infants had a higher risk of thrombocytopenia than the non-BPD infants (adjusted aOR 2.88, 95% CI 1.01-8.15), and the risk of BPD was increased in very premature infants with a PLT count ≤ 177*109/L (OR 4.74, 95% CI 1.93-11.62) at the end of the second week. In the multivariate predictive model, it was showed that the AUC area (0.85), sensitivity (0.88), specificity (0.70) and Youden index (0.58) are improved using PLT counts ≤ 177*109/L combined with GA and BW.ConclusionsAbnormal PLT parameters were observed in BPD infants, and a PLT count ≤ 177*109/L was a potential risk factor for the development of BPD in very premature infants.

Project description:Premature infants are at high risk for developing bronchopulmonary dysplasia (BPD), characterized by chronic inflammation and inhibition of lung development, which we have recently identified as being modulated by microRNAs (miRNAs) and alterations in the airway microbiome. Exosomes and exosomal miRNAs may regulate cell differentiation and tissue and organ development. We discovered that tracheal aspirates from infants with severe BPD had increased numbers of, but smaller, exosomes compared with term controls. Similarly, bronchoalveolar lavage fluid from hyperoxia-exposed mice (an animal model of BPD) and supernatants from hyperoxia-exposed human bronchial epithelial cells (in vitro model of BPD) had increased exosomes compared with air controls. Next, in a prospective cohort study of tracheal aspirates obtained at birth from extremely preterm infants, utilizing independent discovery and validation cohorts, we identified unbiased exosomal miRNA signatures predictive of severe BPD. The strongest signal of reduced miR-876-3p in BPD-susceptible compared with BPD-resistant infants was confirmed in the animal model and in vitro models of BPD. In addition, based on our recent discovery of increased Proteobacteria in the airway microbiome being associated with BPD, we developed potentially novel in vivo and in vitro models for BPD combining Proteobacterial LPS and hyperoxia exposure. Addition of LPS led to a larger reduction in exosomal miR 876-3p in both hyperoxia and normoxia compared with hyperoxia alone, thus indicating a potential mechanism by which alterations in microbiota can suppress miR 876-3p. Gain of function of miR 876-3p improved the alveolar architecture in the in vivo BPD model, demonstrating a causal link between miR 876-3p and BPD. In summary, we provide evidence for the strong predictive biomarker potential of miR 876-3p in severe BPD. We also provide insights on the pathogenesis of neonatal lung disease, as modulated by hyperoxia and microbial product-induced changes in exosomal miRNA 876-3p, which could be targeted for future therapeutic development.

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Red cell distribution width as a predictor for bronchopulmonary dysplasia in premature infants.

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