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.