Introduction
In pregnancy, a combination of hormonal changes and mechanical effects of the enlarging uterus may result in pulmonary changes including rhinitis of pregnancy, sleep-disordered breathing, and small airway closure 1. Sickle cell disease (SCD), the commonest genetic disease in the world, affects multiple organ systems including the respiratory system 2. Specifically, SCD is associated with reduced lung growth, airway hyperresponsiveness, pulmonary hypertension, and acute chest syndrome (ACS)2–5. The combined effects of pulmonary changes in pregnancy and SCD may result in substantial reductions in maternal pulmonary reserves 1,6, with resultant uteroplacental dysfunction and reduced fetal oxygenation 1,6,7.
In a systematic review and meta-analysis, we demonstrated that pregnant women living with SCD have increased risk of maternal and perinatal morbidity and mortality 8. In contrast to poor maternal outcomes 8–10, the biological basis of the poor perinatal outcomes is not clear, although factors such maternal body mass index (BMI) and SCD phenotype have been implicated11,12. One potential modifiable risk factor is the role of abnormal pulmonary function in pregnant women with SCD on the outcome of the fetus. In a prospective cohort study of pregnant women with SCD, we tested the hypothesis that impaired pulmonary function during pregnancy, assessed by a moderate to severe reduction in baseline forced expiratory volume in one second (FEV1), is associated with increased risk of adverse perinatal outcomes in pregnant women with SCD.