Oxidative Stress and Inflammatory Markers of Cordocentesis Blood in Response to Fetal Anemia

Background: Hypothetically, fetal anemic hypoxia causes cellular damage with an increase in oxidative stress levels. This study, using hemoglobin (Hb) Bart’s disease as a study model, aims to compare the levels of oxidative stress and inflammatory markers as well as fetal hemodynamics in anemic fetuses with those of non-anemic fetuses.

Materials and methods: Forty pregnancies at risk of fetal Hb Bart’s disease scheduled for cordocentesis at 18 to 22 weeks were recruited into the study. Fetal blood was collected to measure the levels of 8-Isoprostane (8-Isop), tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), and hemoglobin as well as for hemoglobin typing.

Results: There was no significant difference in cord blood 8-Isop, TNF-α, and IL-10 levels between the Hb Bart’s disease group and the unaffected group, whereas several hemodynamic parameters, such as cardiac output, cardiac size, cardiac performance, middle cerebral artery – peak systolic velocity, etc., were significantly changed in the fetal Hb Bart’s group. In the subgroup analysis, the level of serum 8-Isop in the severe anemia group tended to increase, though not significantly, compared with the nonanemic group (275.3±141.8 vs. 203.9±49.2 pg/mL; p=0.079).

Conclusion: In response to anemia, fetuses might have a high capacity of hemodynamic adaptation without significant cellular damage, though a trend of an increase in oxidative stress marker was found in severe fetal anemia. Theoretically, intrauterine blood transfusion for fetal anemia during adaptive compensation may result in no residual insults.