Adenosine is produced in the inflammed and damaged lung where it plays roles in the regulation of inflammation and tissue remodeling. Adenosine deaminase (ADA) is an enzyme responsible for the degradation of adenosine. Our aim was to compare the levels of ADA between infants with and without respiratory distress syndrome (RDS) and to determine the relationship between plasma ADA levels and bronchopulmonary dysplasia (BPD). One-hundred and twenty-five premature infants who were admitted to our neonatal intensive care unit were included in the study. Eighty-one of these infants with RDS were study group and the other 44 infants without RDS served as controls. Blood collection was made in the first day of life at the end of 24th-h and was used for laboratory testing. In the RDS group, mean ADA level was 25.5 (± 4.5) U/l, and in controls it was 26.3 (± 5.7) U/l. There was no statistically significant difference (p = 0.326) in these groups although there was a statistically difference of ADA levels between BPD (34.5 ± 5.2 U/l) and non-BPD (24.6 ± 4.1) patients (p = 0.001). There was also a positive relationship between ADA levels and severity of BPD (r = + 0.845, p = 0.01). Perinatal inflammation is the key mechanism of BPD. ADA level in early postnatal life is elevated in infants with BPD and may be related with perinatal inflammation.