فهرست نشریات علمی دسترسی آزاد ایران

Introduction: The predominant etiologic theory of preeclampsia is that reduced uteroplacental perfusion is the unique pathogenic process in the development of preeclampsia. Maternal and fetal erythroblast counts are elevated in the peripheral blood of pregnant women with preeclampsia. The purpose of this study was to examine whether this elevation actually occurs before the clinical onset of the disorder. Results: Significantly higher quantities of erythroblasts (mean 2.46?1.23 vs. 0.44?0.55; p=0.009) were detected in blood samples obtained from women who later acquired preeclampsia (n=50) than in blood samples from the control Cohort (n=549). Intrauterine growth restriction was accompany by a similar rise in erythroblast count (mean NRBC 0.82?0.8 in preeclamptic group vs. 0.59?0.85 in normotensive group; p=0.009). Mean gestational age was less in preeclamptic group (37.58?1.45 vs. 39.07?0.94, p=0.009).On the basis of 1.5 erythroblast as point of convergence there was sensitivity =61.45, specificity=93.02,NPV=98.16, accuracy=91.65 Conclusion: Because a large proportion of the erythroblasts in maternal blood are fetal origin, our data suggest that fetal-maternal cell traffic is affected early in pregnancies that are later complicated by preeclampsia.