Pulmonary overcirculation secondary to a hemodynamically significant patent ductus arteriosus (hsPDA) increases endothelial shear stress, triggering the release of endogenous nitric oxide (NO). Since NO rapidly oxidizes hemoglobin to methemoglobin (MetHb), we hypothesized that preterm infants with hsPDA would exhibit elevated serum MetHb levels. This study aimed to investigate the association between peak MetHb levels and hsPDA requiring treatment. This retrospective cohort study included preterm infants ( 3.4% demonstrated significant predictive value (AUC = 0.74). Synchronized analysis at physical ductal closure confirmed a significant drop in MetHb levels (p < 0.001), indicating dynamic reversibility. Severe hsPDA is associated with a significant, transient elevation in serum methemoglobin levels during the first week of life. While this observational data cannot establish causality, the ‘oxidative spike’ may reflect the systemic spillover of endothelium-derived nitric oxide released in response to pulmonary overcirculation. With further prospective validation, monitoring MetHb trends could serve as an accessible adjunctive marker to aid in evaluating the hemodynamic burden of a patent ductus arteriosus.
Karakurt et al. (Thu,) studied this question.