• Perinatal complication prognosis in pregnant with obesity and metabolic syndrome 

Perinatal complication prognosis in pregnant with obesity and metabolic syndrome 

HEALTH OF WOMAN. 2016.4(110):163–167; doi 10.15574/HW.2016.110.163 
 

Perinatal complication prognosis in pregnant with obesity and metabolic syndrome 
 

Dyndar O. A., Benyuk V. O., Nykoniuk T. R.

A.A. Bogomolets National Medical University, Kiev


The objective: the prediction of perinatal complications in pregnant women with obesity and metabolic syndrome by examining the state of the fetoplacental complex and the factors of angiogenesis.


Patients and methods. А survey of 238 pregnant women, of whom 185 with obesity and metabolic syndrome (MS), 53 – with normal body weight. We have studied the content in the peripheral blood of hormones, placental proteins, as well as indicators of endothelial dysfunction in the third trimester of pregnancy by conducting the radioimmunoassay and enzyme immunoassay.


Results. The Presence of overweight and obesity of the First degree has virtually no effect on the functional state of the fetoplacental complex. In pregnant women with II-III degree of obesity and MS changes endocrinological indicators of fetoplacental complex are subcompensated character, as evidenced by the decrease in the level of E2 is 1.3–1.6 times, PG, PL, CG, PRL 86%, while increasing To 1.2–1.6 times in comparison with the control group. Placental dysfunction with sub – and decompensated nature of the flow, in pregnant women with MS and obesity II–III degree, manifested by increased б-FP 1.6–2 times, PAMG 1.5–2.1 times, AMGF 1.3–1.9 times, SSBG 1,2–1,5 times and a decrease in SP1 in 1.3–1.5 times, respectively. In pregnant women with obesity II–III degree and MS is endothelial dysfunction characterized by reduced production of vascular endothelial growth factor is 2.3–2.5 times, placental growth factor 2.2–2.3 times increase in soluble receptor of vascular endothelial growth factor in 3.0–3.3 times in comparison with the control group.


Conclusion. We conducted comprehensive studies show that the prognosis for pregnant women with obesity II–III degree and MS has adverse consequences in terms of the development of perinatal complications. Diagnostic, therapeutic, and preventive activities aimed at the dynamic reducing body weight, improving metabolic processes in pregnant women, it is advisable to carry out the program pregravidarnaya training.


Key words: pregnancy, obesity, metabolic syndrome, angiogenesis.


REFERENCES

1. Alfirevic Z, Devane D, Gyte GM. 2013. Continuous cardiotocography (CTG) as a form of electronic fetal monitoring for fetal assessment during labour. Cochrane Database Syst rev (5) CD006066. http://dx.doi.org/10.1002/14651858.cd006066.pub2

2. National institute for health and care excellence. Intrapartum care: care of healthy women and their babies during child-birth. NICE clinical guideline 190. (Manchester): NICE; 2014.

3. George Saade. 2015. Fetal ECG analysis of the ST segment as an adjunct to intrapartum fetal heart rate monitoring: a randomized clinical trial. American Journal of Obstetrics and Gynecology. Suppl. S2.

4. Kuzin AI. 2011. Metabolic syndrome: clinical and population aspects:120.

5. Lipatov IS, Melnikov VA, Tezikov YuV. 2008. Assessment of severity of placental insufficiency in pregnant women. Russian Bulletin of the obstetrician-gynecologist. 8(5):38-43.

6. Filippov OS, Kazantsev AA. 2003. The Prognostic significance of various methods of diagnostics of fetoplacental insufficiency. Problems of reproduction 3:44-49.

7. Milovanov AP. 2005. Pathology of the system mother-placenta-fetus:230.

8. Tischer E, Mitchell R, Hartman T. 2011. The human gene for vascular endothelial growth factor. Multiple protein forms are encoded through alternative exon splicing. The Journal of Biological Chemistry 266(18):11947–54.

9. Muller YA, Li B, Christinger HW, Wells JA. 2012. Vascular endothelial growth factor: crystal structure and functional mapping of the kinase domain receptor binding site. Proceedings of the National Academy of Sciences of the United States of America 94(14):7192–7. http://dx.doi.org/10.1073/pnas.94.14.7192

10. Dolgov VV, Men'shikov VV. 2012. Clinical laboratory diagnostics. National leadership. In 2 vols, 2:928.

11. Andraweera PH, Dekker GA, Roberts CT. 2012. The vascular endothelial growth factor family in adverse pregnancy outcomes. Human Reproduction Update 18(4):436–457. http://dx.doi.org/10.1093/humupd/dms011; PMid:22495259

12. Ferrara N, Gerber HP. 2012. The role of vascular endothelial growth factor in angiogenesis. Acta Haematol. 106(4):148–56. http://dx.doi.org/10.1159/000046610

13. Eremina V, Quaggin SE. 2014. The role of VEGF-A in glomerular development and function. Curr. Opin. Nephrol. Hypertens 13(1):9–15. http://dx.doi.org/10.1097/00041552-200401000-00002

14. Ribatti D. 2012. The crucial role of vascular permeability factor/vascular endothelial growth factor in angiogenesis: a historical review. Br. J. Haematol. 128(3):303–9. http://dx.doi.org/10.1111/j.1365-2141.2004.05291.x; PMid:15667531

15. Tong JP, Yao YF. 2014. Contribution of VEGF and PEDF to choroidal angiogenesis: a need for balanced expressions. Clin. Biochem. 39(3):267–74. http://dx.doi.org/10.1016/j.clinbiochem.2005.11.013; PMid:16409998

16. Matsumoto T, Mugishima H. 2011. Signal transduction via vascular endothelial growth factor (VEGF) receptors and their roles in atherogenesis. J. Atheroscler. Thromb. 13(3):130–5. http://dx.doi.org/10.5551/jat.13.130