Ukrainian Journal Health of Woman. 2022. 1(158): 18-24; doi 10.15574/HW.2022.158.18
Lemish N. Y.
SHEI «Uzhgorod National University», Ukraine

For citation: Lemish NY. (2022). Somatic and reproductive history of pregnant, with complications from group of great obstetrical syndromes. Ukrainian Journal Health of Woman. 1(158): 18-24; doi 10.15574/HW.2022.158.18
Article received: Nov 18, 2021. Accepted for publication: Mar 08, 2022.

Purpose – to conduct retrospective clinical and statistical analyses of somatic, reproductive history of mowen, with complications from the group of great obstetrical syndromes (GOS).
Materials and methods. We conducted retrospective clinical and statistical analyses of somatic and reproductive history of 239 pregnant women (I^st – main group), who had coplications from the group of GOS, who were subdivided into 3 groups: Ia group (n=103) pregnant with severe preeclampsia, Ib group (n=67) pregnant with placenta insufficiency, with clinical manifestation by intrauterine growth retardation syndrome (IUGR); Ic group (n=69) pregnant with preterm delivery with gestational term 22-34 weeks. Control group (CG) was formed by 56 practically healthy pregnant with favourable reproductive history and non complicated course of current pregnancy. Statistical analyses was conducted by using standart programs Microsoft Excel 5.0 and Statistica 6.0.
Results. We stated, that in I group the incidence of complicated heredity of cardiovascular pathology was significantly higher: 69 (28.8%) in I group (χ²=5.46, р=0.03, OR=2.79, CI 95% 1.14-6.79), in CG this factor was diagnosed only in 4 (7.1%) of patients. In subgroup Ib (patients with IUGR of 2-3 stage) the incidence of abortions and miscarriages in history was higher: in subgroup Ib these parameters were 0.83 (1.37) and 0.32 (0.59) correponding, and in CG – 0.19 (0.85) and 0.07 (0.42) corresponding (р<0.05). The most reasonable difference compated to CG were diagnosed in patients from Ic subgroup (patients with spontaneous preterm deliveries). The highest incidence of patiens with obesity was diagnosed in subgroups Ia and Ic – 18 (17.5%) and 16 (23.2%), the difference compared to CG clinically significant (р<0.01). A high incidence of anemia was noted in pregnant, especially among the ones with pregnancy complications – in I group anemia was diagnosed in more that half of patients – in 179 (74.8%), in CG – every third – in 18 (32.1%) (χ²=21.48, р<0.01, OR=2.95, CI 95% 1.85-4.71). The data in CG are approximately the same as the incidence of this pathology in population of pregnant women of Ukraine. Diseases, characterized by elevated blood pressure in group I were diagnosed several times higher, compared to CG – 41 (17.1%) compared to 5 (8.9%) (χ²=11.1, р<0.01, OR=6.08, CI 95% 1.84-20.1). In subgroup Ia the incidence of patients with this pathology was the highest – 25.2% (n=26) (χ²=20.78, р<0.01, OR=11.03, CI 95% 3.21-37.9).
Results. Peculierities of somatic and reproductive history of pregnant were gisgnosed in pregnant, who had complications grom GOS group that may be high risk factors of significant increase of obstetrical and perinatal complications from materal and fetal side. The usage of routine treatment and prophylactic measures were not effective enough, that is quite convincing reason for making up a new approach for decreasing the incidence and severity of GOS in these patients, and their prophylaxis is a relevant problem of modern obstetrics.
The research was conducted according to principles of Declaration of Helsinki. Protocol of research was proved by local ethical committee, mentioned in institution’s work. A informed sonsennt was collected in order to carry out the research.
No conflict of interests was declared by the author.
Key words: retrospective analys, clinical and statistical analyses, somatic history, reproductive history, great obstetrical syndromes.

REFERENСЕS

1. Brosens I, Pijnenborg R, Vercruysse L, Romero R. (2011). The «Great obstetrical syndromes» are associated with disorders of deep placentation. Am J Obstet Gynecol. 204 (3): 193-201. https://doi.org/10.1016/j.ajog.2010.08.009; PMid:21094932 PMCid:PMC3369813

2. Chaiworapongsa T, Romero R, Gotsch F et al. (2008). Low maternal concentrations of soluble vascular endothelial growth factor receptor-2 in preeclampsia and small for gestational age. J Matern Fetal Neonatal Med. 21 (1): 41-52. https://doi.org/10.1080/14767050701831397; PMid:18175243 PMCid:PMC7062305

3. Di Renzo GC. (2008). The role of an «anti-angiogenic state» in complications of pregnancy. J Matern Fetal Neonatal Med. 21 (1): 3-7. https://doi.org/10.1080/14767050701855081; PMid:18175240

4. Di Renzo GC. (2009). The Great Obstetrical Syndromes. The Journal of Maternal-Fetal & Neonatal Medicine. 22 (8): 633-635. https://doi.org/10.1080/14767050902866804; PMid:19736613

5. Erez O, Romero R, Hoppensteadt D et al. (2008). Tissue factor and its natural inhibitor in preeclampsia and SGA. J Matern Fetal Neonatal Med. 21 (12): 855-869. https://doi.org/10.1080/14767050802361872; PMid:19065458 PMCid:PMC3171292

6. Espinoza J, Chaiworapongsa T, Romero R et al. (2007). Unexplained fetal death: another anti- angiogenic state. J Matern Fetal Neonatal Med. 20 (7): 495-507. https://doi.org/10.1080/14767050701413022; PMid:17674262 PMCid:PMC7062303

7. Espinoza J, Romero R, Nien JK et al. (2007). Identification of patients at risk for early onset and/or severe preeclampsia with the use of uterine artery Doppler velocimetry and placental growth factor. Am J Obstet Gynecol. 196 (4): 326.e1-e13. https://doi.org/10.1016/j.ajog.2006.11.002; PMid:17403407 PMCid:PMC2190731

8. Gabbay-Benziv R, Baschat A. (2015). Gestational diabetes as one of the «great obstetrical syndromes» – the maternal, placental, and fetal dialog. Best Practice & Research Clinical Obstetrics & Gynaecology. 28 (2): 150-155. https://doi.org/10.1016/j.bpobgyn.2014.04.025; PMid:25225057

9. Glants S. (1998). Mediko-biologicheskaya statistika. Per. s angl. Moskva: Praktika: 459.

10. Gordon A, Jeffery HE. (2008). Classification and description of stillbirths in New South Wales, 2002-2004. Med J Aust. 188 (11): 645-648. https://doi.org/10.5694/j.1326-5377.2008.tb01822.x; PMid:18513173

11. HAPO Study Cooperative Research Group. (2009). Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study: associations with neonatal anthropometrics. Diabetes. 58 (2): 453-459. https://doi.org/10.2337/db08-1112; PMid:19011170 PMCid:PMC2628620

12. Kim YM, Bujold E, Chaiworapongsa T et al. (2013). Failure of physiologic transformation of the spiral arteries in patients with preterm labor and intact membranes. Am J Obstet Gynecol. 189 (4): 1063-1069. https://doi.org/10.1067/S0002-9378(03)00838-X

13. Kim YM, Chaiworapongsa T, Gomez R et al. (2012). Failure of physiologic transformation of the spiral arteries in the placental bed in preterm premature rupture of membranes. Am J Obstet Gynecol. 187 (5): 1137-1142. https://doi.org/10.1067/mob.2002.127720; PMid:12439491

14. Korteweg FJ, Gordijn SJ, Timmer A et al. (2008). A placental cause of intra-uterine fetal death depends on the perinatal mortality classification system used. Placenta. 29 (1): 71-80. https://doi.org/10.1016/j.placenta.2007.07.003; PMid:17963842

15. Kusanovic JP, Romero R, Hassan SS et al. (2007). Maternal serum soluble CD30 is increased in normal pregnancy, but decreased in preeclampsia and small for gestational age pregnancies. J Matern Fetal Neonatal Med. 20 (12): 867-878. https://doi.org/10.1080/14767050701482993; PMid:17853188 PMCid:PMC2276339

16. Lang TA, Sesik M. (2011). Kak opisyivat statistiku v meditsine. Rukovodstvo dlya avtorov, redaktorov i retsenzentov. Moskva: Prakticheskaya Meditsina: 480.

17. Metzger BE, Lowe LP, Dyer AR et al. (2008). Hyperglycemia and adverse pregnancy outcomes. N Engl J Med. 358 (19): 1991-2002. https://doi.org/10.1056/NEJMoa0707943; PMid:18463375

18. Mintser AP. (2010). Statisticheskie metodyi issledovaniya v klinicheskoy meditsine. Prakticheskaya meditsina. 3: 41-45.

19. Ness RB, Sibai BM. (2006). Shared and disparate components of the pathophysiologies of fetal growth restriction and preeclampsia. Am J Obstet Gynecol. 195 (1): 40-49. https://doi.org/10.1016/j.ajog.2005.07.049; PMid:16813742

20. Redman CW, Sargent IL. (2015). Latest advances in understanding preeclampsia. Science. 308 (5728): 1592-1594. https://doi.org/10.1126/science.1111726; PMid:15947178

21. Roberts JM, Gammill HS. (2015). Preeclampsia: recent insights. Hypertension. 46 (6): 1243-1249. https://doi.org/10.1161/01.HYP.0000188408.49896.c5; PMid:16230510

22. Romero R, Espinoza J, Gotsch F et al. (2006). The use of high-dimensional biology (genomics, transcriptomics, proteomics, and metabolomics) to understand the preterm parturition syndrome. BJOG. 113 (3): 118-135. https://doi.org/10.1111/j.1471-0528.2006.01150.x; PMid:17206980 PMCid:PMC7062297

23. Romero R, Espinoza J, Mazor M, Chaiworapongsa T. (2004). The preterm parturition syndrome. In: Critchely H, Bennett P, Thornton S, editors. Preterm Birth. London: RCOG Press: 28-60.

24. Romero R, Mazor M, Munoz H et al. (1994). The preterm labor syndrome. Ann N Y Acad Sci. 734: 414-429. https://doi.org/10.1111/j.1749-6632.1994.tb21771.x; PMid:7978942

25. Romero R, Nien JK, Espinoza J et al. (2008). A longitudinal study of angiogenic (placental growth factor) and anti-angiogenic (soluble endoglin and soluble vascular endothelial growth factor receptor-1) factors in normal preg- nancy and patients destined to develop preeclampsia and deliver a small for gestational age neonate. J Matern Fetal Neonatal Med. 21 (1): 9-23. https://doi.org/10.1080/14767050701830480; PMid:18175241 PMCid:PMC2587364

26. Romero R. (2009). Prenatal medicine: The child is the father of the man. J Matern Fetal Neonatal Med. 22 (8): 636-639. https://doi.org/10.1080/14767050902784171; PMid:19736614

27. Sibai B, Dekker G, Kupferminc M. (2015). Preeclampsia. Lancet. 365 (9461): 785-799. https://doi.org/10.1016/S0140-6736(05)71003-5

28. Sibai BM. (2004). Preeclampsia: an inflammatory syndrome? Am J Obstet Gynecol. 191 (4): 1061-1062. https://doi.org/10.1016/j.ajog.2004.03.042; PMid:15507921

29. Soto E, Romero R, Kusanovic JP et al. (2012). Late-Onset Preeclampsia Is Associated with an Imbalance of Angiogenic and Anti-Angiogenic Factors in Patients with and without Placental Lesions Consistent with Maternal Underperfusion. The Journal of Maternal-Fetal & Neonatal Medicine. 25: 498-507. https://doi.org/10.3109/14767058.2011.591461; PMid:21867402 PMCid:PMC3401571

30. Stella CL, Sibai BM. (2016). Preeclampsia: Diagnosis and management of the atypical presentation. J Matern Fetal Neonatal Med. 19 (7): 381-386. https://doi.org/10.1080/14767050600678337; PMid:16923692

31. Strauss JF, Romero R, Gomez-Lopez N et al. (2018). Spontaneous preterm birth: advances toward the discovery of genetic predisposition . Am J Obstet Gynecol. 218 (3): 294-314. https://doi.org/10.1016/j.ajog.2017.12.009; PMid:29248470 PMCid:PMC5834399

32. Tsahilova SG, Akulenko LV, Kuznetsov VM. (2017). Geneticheskie prediktoryi preeklampsii (obzor literaturyi). Problemyi reproduktsii. 1: 110-114. https://doi.org/10.17116/repro2017231110-114

33. Uzunm A, Schuster J, McGonnigal B et al. (2016). Targeted sequencing and meta-analysis of preterm birth. PLoS One. 11 (5): 194-199. https://doi.org/10.1371/journal.pone.0155021; PMid:27163930 PMCid:PMC4862658

34. Varli IH, Petersson K, Bottinga R et al. (2008). The Stockholm classification of stillbirth. Acta Obstet Gynecol Scand. 87 (11): 1202-1212. https://doi.org/10.1080/00016340802460271; PMid:18951207

35. Yogev Y, Langer O. (2008). Pregnancy outcome in obese and morbidly obese gestational diabetic women. Eur J Obstet Gynecol Reprod Biol. 137 (1): 21-26. https://doi.org/10.1016/j.ejogrb.2007.03.022; PMid:17517462