The role of serum N-terminal pro-brain natriuretic peptide in transient tachypnea of the newborn.

BACKGROUND AND OBJECTIVES

Transient tachypnea of the newborn (TTN), also known as wet lung disease, is a common cause of respiratory distress in the newborn. It has been demonstrated that, in alveolar type II cell cultures of the rat, receptors affected by the natriuretic peptides are expressed and that atrial natriuretic peptide (ANP) reduced amiloride-sensitive Na+ transport in these cells with a pattern similar to that in renal tubules, thereby inhibiting Na+ re-absorption in a concentration-dependent manner. Brain natriuretic peptide (BNP) is known to act on these receptors and it is suggested that it may be involved in fluid absorption by the lungs. The present study aimed to investigate the role of BNP in the pathogenesis of transient tachypnea of the newborn.

PATIENTS AND RESULTS

Serum NT-proBNP (N-terminal-proBNP) level measurements of 43 infants diagnosed with transient tachypnea of the newborn were compared to those of 29 healthy neonates. There were no statistically significant differences in NT-proBNP level between the study group and the control group.

CONCLUSIONS

NT-proBNP has no role in the pathophysiology of transient tachypnea of the newborn. Other factors which may potentially be involved in this etiology should be investigated.