We read with great interest the article, and we intend to address the interpretation of the secondary neonatal outcomes discussed in the article, “OPtimal TIming of antenatal COrticosteroid administration in pregnancies complicated by early-onset fetal growth REstriction: results of a large multicenter cohort study (the OPTICORE study),” by Mette van de Meent et al, that compares two antenatal corticosteroid (CCS) timing strategies in pregnancies complicated by early-onset fetal growth restriction (FGR).
We would like to comment on the interpretation of the secondary neonatal outcomes, particularly the markedly higher rate of necrotizing enterocolitis (NEC) (stage ≥2A) (strategy A: 3.7% vs strategy B: 7.6%; adjusted odds ratio 2.18 [1.29–3.69]) observed in offspring managed according to timing strategy B, in which CCS were administered only after the detection of absent or reversed end-diastolic flow (AEDF/REDF) in the umbilical artery.
In the discussion, the authors suggest that differences in NEC rates may be related to different management strategies implemented in the different centers rather than to CCS timing itself. However, we noted that the analysis did not explicitly account for the degree of placental and fetal hemodynamic deterioration at the time of CCS administration or delivery.
There is substantial physiological and clinical evidence indicating that severe placental insufficiency and advanced Doppler abnormalities are associated with chronic fetal hypoxemia, redistribution of cardiac output away from the splanchnic circulation, and impaired intestinal perfusion and maturation. ,, These mechanisms have been consistently implicated in the pathogenesis of NEC and may predispose growth-restricted neonates with AEDF/REDF to a higher NEC risk, independent of gestational age, birthweight, or timing of CCS administration.
From this perspective, we wonder whether the higher NEC rate observed in timing strategy B could be at least partly explained by the greater severity of placental disease and fetal compromise, rather than by the CCS timing strategy per se. We would like to know whether the authors considered additional analyses adjusting for markers of disease severity, such as umbilical artery Doppler stage, duration of AEDF/REDF exposure, or composite FGR stage at diagnosis or delivery.
Clarifying this aspect could help distinguish whether NEC risk in early-onset FGR is primarily driven by hemodynamic disease severity versus therapeutic timing and may have important implications for clinical interpretation and future study design.
We appreciate the authors’ contribution and would welcome their thoughts on this matter.
The authors report no conflict of interest.
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