The Effect of Maternal and Neonatal Vitamin D Levels on Respiratory Distress Syndrome in Preterm Infants

Respiratory distress syndrome (RDS) of the newborn, also called as hyaline membrane disease, is the most common cause of respiratory distress in premature infants, correlating with structural and functional lung immaturity. The pathophysiology of RDS is complex. Immature type II alveolar cells produce less surfactant that causes an increase in alveolar surface tension and a decrease in compliance. This resultant atelectasis lead to pulmonary vascular constriction, hypoperfusion, and lung tissue ischemia. RDS and prolonged ventilation and associated systemic/lung injury may also contribute to long term oxygen dependency and may result in bronchopulmonary dysplasia (BPD). Vitamin D is a fat-soluble steroid hormone that primarily contributes to the maintenance of normal calcium homeostasis and skeletal mineralization. In addition to its classical role in bone metabolism, vitamin D deficiency has been associated with impaired pulmonary function, increased incidence of viral and bacterial infections and inflammatory lung diseases. Although exact mechanisms are not fully understood, vitamin D appears to impact on a variety of inflammatory and structural cells within the lung including macrophages, lymphocytes and epithelial cells. To our best of knowledge, no study has evaluated the effect of vitamin D levels on the severity and presence of RDS in preterm infants. Therefore, the aim of this study is to evaluate the possible role of maternal/neonatal vitamin D levels on RDS development in preterm infants. We also aim to determine the possible association between maternal/neonatal vitamin D levels and the incidence of BPD and other neonatal morbidities.