Abstract
Preeclampsia (PreE) is the de novo development of hypertension and proteinuria after 20 weeks of gestation affecting 3-8% of pregnancies, and has a link to alterations of feto-placental stress that pass to the offspring causing detrimental effects. We aimed at comparing the clinical outcomes and chemokines from the maternal and cord blood between patients with and without PreE. We recruited 20 normal pregnant (NP) and PreE patients in an IRB approved prospective cohort at our institution. We evaluated maternal age, body mass index (BMI), blood pressure (BP), and gestational age (GA) at delivery along with measured serum levels of six chemokines in maternal-fetal paired samples using ELISA test. The markers are; Human CCL4/MIP-1beta, Human CXCL10/IP-10, Eotaxin/CCL11, RANTES (CCL5), Human MCP1, Human M-CSF. Maternal: The systolic blood pressure (SBP) and diastolic blood pressure (DBP) were higher in PreE (SBP 162 ± 17; DBP 97 ± 12) compared to NP (SBP 121 ± 3; DBP 75 ± 9; p <0.05). GA at delivery in weeks was lower in PreE (35.1 ± 3.8) compared to NP (39.2 ± 0.3; p <0.05), as well as birth weight in PrE (2556 ± 977) compared to NP (3385 ± 328; p <0.011) indicating a link to intrauterine growth restriction (IUGR). We did not find a difference in maternal BMI between the two groups. Biomarkers: For all six chemokines CCL4, CXCL10, CCL11, CCL5, MCP1, and M-CSF, maternal and fetal cord serum chemokines levels differ between subjects with and without PreE (p < 0.001). There is also a difference between the maternal and fetal levels for the six chemokines (<0.01). The fetal levels were compared to associated maternal levels for each of the six chemokines using t test and Mann-Whitney U test. Women with PreE had higher BP, preterm deliveries, and fetal IUGR. However, in this cohort the women were of similar age, size, and parity prior to the onset of pregnancy. The six chemokines in the samples from maternal and fetal circulation are greater in the PreE group, and each of the six chemokines samples from the fetuses had values greater than maternal samples which could implicate placental cells as the source. PreE alters the intrauterine environment and activates the detrimental signaling that is transferred to the fetus resulting in the aforementioned complications.
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