• Modern possibilities of pre-eclampsia prediction and prevention

Modern possibilities of pre-eclampsia prediction and prevention

HEALTH OF WOMAN.2016.7(113):44–48; doi 10.15574/HW.2016.113.44 
 

Modern possibilities of pre-eclampsia prediction and prevention


Lakhno I. V.

Kharkiv medical Academy of postgraduate education


Prediction of pre-eclampsia (PE) remains a very important problem of modern obstetrics.


The objective: study forecasting capabilities and PE drug prevention.


Patients and methods. Totally 292 pregnant women and 154 pre-eclamptic patients were enrolled in the study. The traditional combination of biochemical and biophysical tests for the selection of high risk for PE patients were used (PI in the uterine arteries> 2.25; PAPP-A <0.69 MoM; b-hCG>3.0 MoM; AFP>2.5 MoM). Patients of group II were divided into subgroup II A and II subgroup B. This was done to evaluate the complex medical prophylaxis (CMP) of PE, which was administered in the II B subgroup.


Results. The prospective study showed the following diagnostic value of a positive result in the screening for PE in subgroup II A. OR was 16.5. The sensitivity of this method was 87,1%, specificity – 71.0%, PPV – 75.0%, NPV – 84.6%, IA – 79.0%. The additional usage of the sympathovagal balance in the position on the right side and active orthostasis increased the predictive value of screening for PE in 4.5 times. The sensitivity of the method was 90.3% and specificity – 84.3%. PPV was 84.8%. NPV had a maximal value – 100.0%. IA – 92.3%. The proposed method of CMP decreased the odds of PE in 8.3 times.


Conclusion. This study led to the development of pathogenetically reasonable screening protocol included biochemical and biophysical tests, as well as an effective method of PE prevention.


Key words: preeclampsia, screening, drug prevention.


REFERENCES

1. Daneva AM, Hadћi-Lega M, Stefanovic M. 2016. Correlation of the system of cytokines in moderate and severe preeclampsia. Clin Exp Obstet Gynecol. 43;2:220–224. PMid:27132414

2. D’Angelo A, Valsecchi L. 2016. ATIII-Early Preeclampsia Study Group (ATIII-EPAS) High dose antithrombin supplementation in early preeclampsia: A randomized, double blind, placebo-controlled study. Thromb Res. 140:7–13. http://dx.doi.org/10.1016/j.thromres.2016.01.024; PMid:27046798

3. Elliot MG. 2016. Oxidative stress and the evolutionary origins of preeclampsia. J Reprod Immunol. 114:75–80. http://dx.doi.org/10.1016/j.jri.2016.02.003; PMid:26995772

4. Friedman AM, Cleary KL. 2014. Prediction and prevention of ischemic placental disease. Semin Perinatol. 38;3:177–182. http://dx.doi.org/10.1053/j.semperi.2014.03.002; PMid:24836830

5. Hladunewich M, Karumanchi SA, Lafayette R. 2007. Pathophysiology of the Clinical Manifestations of Preeclampsia. Clin J Am Soc Nephrol. 2:543–549. http://dx.doi.org/10.2215/CJN.03761106; PMid:17699462

6. Maeda K. 2014. Preeclampsia is caused by continuous sympathetic center excitation due to an enlarged pregnant uterus. J. Perinat. Med. 42;2:233–237. http://dx.doi.org/10.1515/jpm-2013-0096

7. McGregor L, Bellangeon M, Chignier E et al. 1999. Effect of a micronized purified flavonoid fraction on in vivo platelet functions in the rat. Thromb Res. 94;4:235–240. http://dx.doi.org/10.1016/S0049-3848(98)00216-3

8. McMaster-Fay RA. 2008. Pre-eclampsia – a disease of oxidative stress resulting from the catabolism of DNA (primarily fetal) to uric acid by xanthine oxidase in the maternal liver: A hypothesis. Bioscience Hypotheses. 1:35–43. http://dx.doi.org/10.1016/j.bihy.2008.01.002

9. Milchev N, Markova D, Dimitrova E. 2008. Use of phlebodia in pregnant women with feto-placental insufficiency (preeclampsia). Akush. Ginekol. 47;1:7–9.

10. Roberge S, Nicolaides KH, Demers S et al. 2013. Prevention of perinatal death and adverse perinatal outcome using low-dose aspirin: a meta-analysis. Ultrasound Obstet Gynecol. 41:491–499. http://dx.doi.org/10.1002/uog.12421; PMid:23362106

11. Rosser ML, Katz NT. 2013. Preeclampsia: an obstetrician’s perspective. Adv Chronic Kidney Dis. 20;3:287–296. http://dx.doi.org/10.1053/j.ackd.2013.02.005; PMid:23928395

12. Sugerman HJ. 2011. Hypothesis: preeclampsia is a venous disease secondary to an increased intra-abdominal pressure. Med Hypotheses. 77;5:841–849. http://dx.doi.org/10.1016/j.mehy.2011.07.051; PMid:21862236

13. Tamбs P, Ifi Zs, Szilбgyi A. 2007. Discordant clinical characteristics suggest different pathogenesis of praeeclampsia. J Perinat Med. 35(2):278.

14. Turgut A, Ozler A, Goruk NY et al. 2015. Serum levels of the adipokines, free fatty acids, and oxidative stress markers in obese and non-obese preeclamptic patients. Clin Exp Obstet Gynecol. 42;4:473–479. PMid:26411214

15. Uzan J, Carbonnel M, Piconne O et al. 2011. Pre-eclampsia: pathophysiology, diagnosis, and management. Vasc Health Risk Manag. 7:467–474. PMid:21822394 PMCid:PMC3148420