Placenta · 2026
Placental abnormalities of malperfusion, inflammation, and meconium are associated with neonatal pulmonary vascular disease.
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Tsoi Stephanie M, Gasper Cynthia, Maltepe Emin, Chidboy Megan A, Ozarslan Nida, Blauvelt Christine A, Buarpung Sirirak, Cheung Shannon, Steurer Martina, Keller Roberta L, Fineman Jeffrey R, Gaw Stephanie L
Аннотация
OBJECTIVES: The primary objective was to elucidate whether placental histopathology representative of intrauterine insults during pulmonary vascular development are associated with a diagnosis of persistent pulmonary hypertension of the newborn (PPHN). The secondary objective was to compare placental histopathologic lesions across PPHN etiologies.
STUDY DESIGN: We conducted a case-control study of mother-infant dyads ≥35 weeks gestation who delivered at a tertiary care center between 2020 and 2025. Cases were infants diagnosed with PPHN and treated with inhaled nitric oxide; unaffected controls were infants without congenital anomalies. Placentas underwent blinded histopathologic review using standardized criteria. Multivariate logistic regression modeling was used to control for confounding maternal and infant factors.
RESULTS: 106 placentas were analyzed (53 PPHN, 53 controls). Placental lesions were significantly more common in PPHN placentas, including fetal vascular malperfusion (30.2% vs 9.4%, p < 0.01), placental inflammation (66.0% vs 37.7%, p < 0.01), chronic presence of meconium (43.4% vs 15.2%, p < 0.01), and chorangiosis (7.6% vs 0%, p = 0.04). In adjusted analyses compared to controls, among 41 placentas with fetal development etiologies (e.g. congenital anomalies) of PPHN, fetal vascular malperfusion, placental inflammation and fetal inflammatory response were more common. Among 12 placentas with typical causes of PPHN (e.g. meconium aspiration syndrome), placental inflammation, maternal and fetal inflammatory responses, and meconium were more common.
CONCLUSIONS: PPHN placentas demonstrate lesions of malperfusion, inflammation, and chronic meconium, suggesting a complex interplay between intrauterine hypoxia and inflammation as a potential mechanism for the abnormal pulmonary vascular development and function seen in PPHN.
STUDY DESIGN: We conducted a case-control study of mother-infant dyads ≥35 weeks gestation who delivered at a tertiary care center between 2020 and 2025. Cases were infants diagnosed with PPHN and treated with inhaled nitric oxide; unaffected controls were infants without congenital anomalies. Placentas underwent blinded histopathologic review using standardized criteria. Multivariate logistic regression modeling was used to control for confounding maternal and infant factors.
RESULTS: 106 placentas were analyzed (53 PPHN, 53 controls). Placental lesions were significantly more common in PPHN placentas, including fetal vascular malperfusion (30.2% vs 9.4%, p < 0.01), placental inflammation (66.0% vs 37.7%, p < 0.01), chronic presence of meconium (43.4% vs 15.2%, p < 0.01), and chorangiosis (7.6% vs 0%, p = 0.04). In adjusted analyses compared to controls, among 41 placentas with fetal development etiologies (e.g. congenital anomalies) of PPHN, fetal vascular malperfusion, placental inflammation and fetal inflammatory response were more common. Among 12 placentas with typical causes of PPHN (e.g. meconium aspiration syndrome), placental inflammation, maternal and fetal inflammatory responses, and meconium were more common.
CONCLUSIONS: PPHN placentas demonstrate lesions of malperfusion, inflammation, and chronic meconium, suggesting a complex interplay between intrauterine hypoxia and inflammation as a potential mechanism for the abnormal pulmonary vascular development and function seen in PPHN.