Authors’ Reply


We appreciate the opportunity to reply to Drs Been and Zimmermann1 to correct a misinterpretation of the data and to comment on how an adjustment for important confounders, i.e. gestational age, would affect the association between chorioamnionitis and respiratory distress syndrome (RDS) in the reported cohort.

In this study, we focused on chorioamnion inflammation as a potential clinical risk factor for fetal lung inflammation and maturation in the setting of preterm premature rupture of membranes (PPROM), given the current standards of antenatal steroids and surfactant use. Our histopathological findings confirmed a pathogenetic role of chorioamnionitis in PPROM, the frequent coexistence of the two, as well as the relationship between chorioamnionitis occurrence and chronic lung damage. Conversely, histological chorioamnionitis (HCA) per se or in the setting of PPROM failed to reveal any protection against RDS. These findings are not surprising given that, although several studies have suggested that PPROM confers protection against RDS, a large review did not confirm this protective effect.2

However, because both HCA and PPROM in the presence of HCA were associated with a greater frequency of lower gestational age, and the recorded cohort may be dissimilar in certain important ways (i.e. women who had clinical chorioamnionitis and developed PPROM, women with PPROM tocolysed for up to 48 hours who developed histological and/or clinical chorioamnionitis, women treated with antibiotics or with ritodrine), such information might have been important for the data analysis.

We feel that a multicentre study with multiple clinical measures taken from preterm neonates with different fetal and maternal HCA scores would allow the verification of the assumption underlying this analysis and the investigation of other important confounders, including gestational age. Furthermore, there might be sufficient power to detect the unanticipated PPROM disparity in the effect of HCA on RDS incidence.


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