Altered frequency and reduced PD-1 expression combined together with the elevated perforin content of MAIT cells insinuate their potential roles in the pathogenesis of early-onset pre-eclampsia.

The heart-rate stability suggests that the change of cardiac output was due to a decrease in blood volume. These data suggest that diuretics could be useful in the management of late-onset pre-eclampsia, indicating that an increase in water retention could play a role in the development of late-onset pre-eclampsia.

Parameters of l-arginine metabolism do not discriminate the early-onset from late-onset pre-eclampsia. Our study provided indirect evidences for the redirection of l-arginine-NOS to the l-arginine-arginase pathway.

Obesity might not influence the fetal electrocardiogram during labor as an independent risk factor for adverse pregnancy outcomes. Studies with larger cohort sizes are needed to confirm our findings.

Objective: Homogenous pathogenesis of preeclampsia has been challenged. We examined the clinical characteristics of preeclamptic patients with discordant fetal growth which is one of the controversial issues in preeclampsia. Methods: Clinical index values including central hemodynamics of third-trimester preeclamptic patients with distinct fetal birth weights (group A: birth weight ≥ 50th percentile; n = 23 and group B: birth weight < 50th percentile; n = 14) were compared. Results: Pregnant women of group A were characteristically obese and edematous, but no fetal complications were observed. Patients of group B were younger, onset of preeclampsia was earlier, proteinuria was more severe, and fetal compromise was frequent. A marked difference between the two groups was noticed in central hemodynamics as the mean of CO (cardiac output) was 8.5 and 5.6 l/min in group A and B, respectively (p < 0.001). CO of less than 7.45 l/min was found to be associated with fetal birth weight below 50th percentile (OR = 15.6; 95% CI: 3.2 and 45.8, p = 0.001). Conclusions: Augmented CO in pregnancy may ensure efficient placental blood supply, but it may cause hypertension with subsequent moderate proteinuria. This condition, however, seems to be different from the "classical" preeclampsia.