Central apnoea and endogenous prostaglandins in neonates

Abstract

Aim: Central apnoeas without an identifiable precipitating cause frequently occur in the neonatal period. Serious apnoeas should be treated with ventilation‐enhancing methylxanthines. Drugs such as opioids or prostaglandins (PGE2) are known to induce apnoea. PGE2 is an endogenous hormone that plays an important role in the regulation of neural activity and a relationship between PGE2 and central apnoeas has been postulated. Methods: In order to test the hypothesis that the incidence of central apnoeas in preterm infants is related to endogenous PGE concentration, we measured the urinary concentration of PGE2 and PGE‐M and determined the number of central apnoeas >10s/12h in overnight polygraphy in 18 preterm infants with apnoeas, bradycardias and desaturations, and 18 normal controls. Results: We found 80.6 (SE 6.9) central apnoeas in the study group, and 52.9 (SE 4.1) in the control group (p= 0.002). Urinary PGE2 concentration was 25.9 (SE 6.1)ng/h/1.73m2 in the control, 31.2 (SE 15.8) ng/h/1.73m2 in the study group (p= n.s.), PGE‐M concentration was 486 (SE 35) ng/h/1.73m2 in the control and 1132 (SE 131) ng/h/1.73m2 in the study group (p < 0.0001). There was a significant correlation between the number of central apnoeas and the PGE‐M concentration in the study group (r= 0.68, p < 0.0001). Conclusion: Our results suggest a relationship between PGE and the respiratory system and open potential therapeutic options for the treatment of central apnoeas in neonates.