Objective Early decrease in fetal haemoglobin (HbF) is an indicator of loss of endogenous blood components that might have predictive value for development of bronchopulmonary dysplasia (BPD). The link between HbF and BPD has not been evaluated.
Design Retrospective observational study.
Setting Tertiary level neonatal intensive care unit, referral centre for Southern Sweden.
Patients 452 very preterm infants (<30 gestational weeks) born 2009–2015.
Interventions Regular clinical practice.
Main outcome measures Mean HbF, haemoglobin (Hb) and partial oxygen pressure (PaO2) levels calculated from 11 861 arterial blood gas analyses postnatal week 1. Relationship between HbF (%) and BPD (requirement of supplemental oxygen at 36 weeks’ postmenstrual age) and the modifying influence of PaO2 (kPa) and total Hb (g/L) was evaluated.
Results The mean gestational age (GA) at birth was 26.4 weeks, and 213 (56%) infants developed BPD. A 10% increase in HbF was associated with a decreased prevalence of BPD, OR 0.64 (95% CI 0.49 to 0.83; p<0.001). This association remained when adjusting for mean PaO2 and Hb. Infants with an HbF in the lowest quartile had an OR of 27.1 (95% CI 11.6 to 63.4; p<0.001) for development of BPD as compared with those in the highest quartile. The area under the curve for HbF levels and development of BPD in the full statistical model was 0.871.
Conclusions Early rapid postnatal decline in HbF levels was associated with development of BPD in very preterm infants. The association between HbF and BPD was not mediated by increased oxygen exposure. The potential benefit of minimising loss of endogenous blood components on BPD outcome will be investigated in a multicentre randomised trial.
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Contributors All authors made substantial contributions to the conception and design, acquisition of data and/or analysis and interpretation of data in this study. WH, DL and TM performed the statistical analysis, drafted the initial manuscript and designed the figures. All authors contributed to the writing of the article and revising it critically for important intellectual content and approved the final version for publication.
Funding This study was funded by the Swedish Research Council (2016-01131, 2017-02112), ALF Government grants to Lund University and Skåne University Hospital and the Skåne Council Foundation for research.
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval This study was approved by the regional ethical review board in Lund, approval number: D:nr 197/2006 (decision 2006-06-01), and D:nr 2009/190 (decision 2009-06-11).
Provenance and peer review Not commissioned; externally peer reviewed.
Data availability statement Deidentified data will be available on reasonable request.
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