EP06.43: Fetal anemia causes placental and maternal cellular damage: a lesson from fetal hemoglobin Bart's disease
Year: 2024
Type: conference-abstract
Abstract: To compare oxidative stress levels and mitochondrial function in the placenta and maternal peripheral blood mononuclear cell (PMBCs) between anemic fetuses (using fetal Hb Bart's disease as a study model) and non-anemic fetuses. A cross-sectional study was conducted on pregnancies affected by Hb Bart's disease and non-anemic fetuses between16 and 22 weeks of gestation. Placental tissue and maternal blood for PBMCs were collected after pregnancy termination for determination of oxidative stress and mitochondrial function. A total of 18 pregnancies affected by Hb Bart's disease and 12 non-anemic fetuses were enrolled. Placental thickness was significantly greater (p-value < 0.001) in the affected pregnancies, whereas all Doppler indices of uteroplacental blood flow were comparable. Mitochondrial dysfunction was significantly increased (p-value < 0.001) in the placenta of the affected fetuses. In the mothers of affected fetuses, there was an increase in mitochondrial oxidative stress levels with a significant increase in mitochondrial dysfunction in isolated PBMCs (p-value < 0.001). In the presence of normal uteroplacental Doppler studies, fetal anemia can induce a significant increase in oxidative stress and mitochondrial dysfunction in the placentas and mothers. The findings support that the placenta can be a source of oxidative stress agents which are released into systemic circulation prior to development of maternal adverse outcomes, and may explain pathophysiology of subsequent pre-eclampsia in late gestation, as commonly seen in pregnancies affected by fetal Hb Bart's disease, if pregnancy is not terminated.
DOI: 10.1002/uog.28215
Institution: Chiang Mai University
Language: English
Subfield: Obstetrics and Gynecology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W4402358251