Conclusion
in preeclamptic women, obesity seems to act as an additive factor of placental damage by means of the dysregulation of hypotensive mechanisms.
Material and methods
the research material was blood serum and oral mucosa swabs, obtained from 168 patients. Pregnant women were divided into the following: a control group (C)-67 women; a gestational hypertension group (GH)-35 patients; a preeclampsia with obesity group (PE + O) (pre-gravid BMI > 30)-23 patients. The rest were lean preeclamptic women (PE)-66 patients-(pre-gravid BMI < 25 in 43 women).
Methods
the research material was blood serum and oral mucosa swabs, obtained from 168 patients. Pregnant women were divided into the following: a control group (C)-67 women; a gestational hypertension group (GH)-35 patients; a preeclampsia with obesity group (PE + O) (pre-gravid BMI > 30)-23 patients. The rest were lean preeclamptic women (PE)-66 patients-(pre-gravid BMI < 25 in 43 women).
Results
the cffDNA was observed in 1.50% of women in the C group, in 2.45% in the GH group, but in 18.18% of lean patients with preeclampsia. The cffDNA was detected in 58% of obese pregnant women with PE. The greater the placental hypoxia was in preeclampsia, the less efficient the hypotensive mechanisms, according to an analysis of the studied adipokines. The prosalusin concentration was significantly lower in the PE group with cffDNA than in the PE group without it (p = 0.008). Apelin was higher in the PE group with cffDNA (p = 0.006) compared to other groups. The same results were also observed in the subgroup with obesity.