Molecular genetic predictors of congenital infection in fetal growth restriction pregnancy
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Aim: to estimate the rate of early-onset and late-onset fetal growth restriction (FGR) in stillbirth, identify features of placentaassociated complications and determine respective risk factors of stillbirth (especially at early gestational age).Materials and Methods. There were retrospectively studied 61 stillbirth cases in 2016–2019 that occurred in the III level obstetric hospitals: 32 early (23–31 weeks of gestation) and late (32–39 weeks) cases; 156 live births with 8–10 Apgar scores delivered at 36–41 weeks of gestation used as controls. Quantitative parameters were compared using the mean values and standard deviation; nominal parameters were analyzed using odds ratio (OR) and adjusted OR (aOR) with 95 % confidence interval (CI).Results. More than half of stillbirths are associated with FGR with almost 60 % of early-onset phenotype of this pathology. Both in stillbirths and live births, 2/3 of FGR have extremely low weight (OR = 1.8; 95 % CI = 0.6–6.9); 1/3 of growth restricted fetuses were detected shortly before delivery (OR = 1.3; 95 % CI = 0.7–2.4); 1/4 of pregnancies complicated by placental insufficiency are not associated with FGR (OR = 1.4; 95 % CI = 0.7–2.7). Risk factors of stillbirth in pregnancy complicated by FGR are the early-onset growth restriction phenotype (aOR = 3.2; 95 % CI = 1.0–10.3), maternal age over 28 years (aOR = 6.0; 95 % CI = 1.2–29.4), miscarriages and multiple induced abortions (aOR = 3.6; 95 % CI = 1.1–11.2), non-compliance in regular clinics visiting and correction of threatening conditions (aOR = 10.9; 95 % CI = 1.3–91.6), toxoplasma infection (aOR = 6.0; 95 % CI = 1.5–24.5). Early stillbirth with FGR is associated with an older mother's age (aOR = 5.8; 95 % CI = 1.0–34.4), greater parity (aOR = 3.3; 95 % CI = 1.0–10.4), uterine diseases including endometrial polyps, endometriosis, cervix cervicitis, cervix dysplasia (aOR = 4.0; 95 % CI = 0.9–17.2), diabetes mellitus (aOR = 3.1; 95 % CI = 0.8–13.2) and preeclampsia.Conclusion. The rate of early-onset FGR in stillbirth comprises almost 60 % that is twice higher than in live birth, with the rate of late-onset phenotype being less than 30 %. In late stillbirths the early-onset phenotype also prevails. There are no prominent features for stillbirths with FGR compared to previously known risk factors regardless of hypotrophy. Early vs. late stillbirth with FGR is more associated with gynecological pathologies as well as with diabetes mellitus and preeclampsia.
Aim: to estimate the rate of early-onset and late-onset fetal growth restriction (FGR) in stillbirth, identify features of placentaassociated complications and determine respective risk factors of stillbirth (especially at early gestational age).Materials and Methods. There were retrospectively studied 61 stillbirth cases in 2016–2019 that occurred in the III level obstetric hospitals: 32 early (23–31 weeks of gestation) and late (32–39 weeks) cases; 156 live births with 8–10 Apgar scores delivered at 36–41 weeks of gestation used as controls. Quantitative parameters were compared using the mean values and standard deviation; nominal parameters were analyzed using odds ratio (OR) and adjusted OR (aOR) with 95 % confidence interval (CI).Results. More than half of stillbirths are associated with FGR with almost 60 % of early-onset phenotype of this pathology. Both in stillbirths and live births, 2/3 of FGR have extremely low weight (OR = 1.8; 95 % CI = 0.6–6.9); 1/3 of growth restricted fetuses were detected shortly before delivery (OR = 1.3; 95 % CI = 0.7–2.4); 1/4 of pregnancies complicated by placental insufficiency are not associated with FGR (OR = 1.4; 95 % CI = 0.7–2.7). Risk factors of stillbirth in pregnancy complicated by FGR are the early-onset growth restriction phenotype (aOR = 3.2; 95 % CI = 1.0–10.3), maternal age over 28 years (aOR = 6.0; 95 % CI = 1.2–29.4), miscarriages and multiple induced abortions (aOR = 3.6; 95 % CI = 1.1–11.2), non-compliance in regular clinics visiting and correction of threatening conditions (aOR = 10.9; 95 % CI = 1.3–91.6), toxoplasma infection (aOR = 6.0; 95 % CI = 1.5–24.5). Early stillbirth with FGR is associated with an older mother's age (aOR = 5.8; 95 % CI = 1.0–34.4), greater parity (aOR = 3.3; 95 % CI = 1.0–10.4), uterine diseases including endometrial polyps, endometriosis, cervix cervicitis, cervix dysplasia (aOR = 4.0; 95 % CI = 0.9–17.2), diabetes mellitus (aOR = 3.1; 95 % CI = 0.8–13.2) and preeclampsia.Conclusion. The rate of early-onset FGR in stillbirth comprises almost 60 % that is twice higher than in live birth, with the rate of late-onset phenotype being less than 30 %. In late stillbirths the early-onset phenotype also prevails. There are no prominent features for stillbirths with FGR compared to previously known risk factors regardless of hypotrophy. Early vs. late stillbirth with FGR is more associated with gynecological pathologies as well as with diabetes mellitus and preeclampsia.
Цель исследования. Изучение особенностей полиморфизма генов системы HLA II класса (DRB1, DQA1, DQB1) у глубоконедоношенных новорожденных с массой тела при рождении менее 1500 г, имеющих врожденную пневмонию, и определение факторов риска формирования данного заболевания. Материал и методы. Проведено комплексное обследование 103 новорожденных: в 1-ю группу вошли дети с клинико-лабораторными признаками врожденной пневмонии (n=61), во 2-ю-дети с респираторным дисстрес-синдромом и без врожденной пневмонии (n=42). Геномную ДНК выделяли из лимфоцитов венозной крови и эпителиальных клеток буккального соскоба, тестирование генов HLA II класса проводили с использованием классической полимеразной цепной реакции. Результаты. В группе детей с врожденной пневмонией выявлено увеличение частоты аллелей DRB1*04 и DRB1*15, а также генотипа DQB1 0302/0602, что может свидетельствовать о предрасполагающем к развитию данного заболевания эффекте указанных генов и служить молекулярно-генетическим предиктором формирования данного заболевания. В генотипе у недоношенных новорожденных с врожденной пневмонией достоверно реже встречались аллели DRB1*13, DQA1*0103, DQB1*0501, DRB1*13/13; DQA1*0101/0103; DQB1*0501/0602; GSTM1 +/+ GSTТ1 +/+ DRB1*13 DQA1*0501 DQB1*0301, оказывающие протективный эффект в отношении развития воспаления в легочной ткани. Статистически значимых различий по частоте низкофункциональных аллелей генов семейства глутатитон-S-трансфераз (GSTM1 и GSTT1) в ходе настоящего исследования не обнаружено. Заключение. Результаты проведенного исследования могут быть использованы для персонификации лечебно-диагностического процесса и выхаживания глубоконедоношенных новорожденных. Ключевые слова: глубоконедоношенные новорожденные, врожденная пневмония, факторы риска, генетические факторы, полиморфизм генов, гены детоксикации, главный комплекс гистосовместимости.
Objective: To evaluate lipid peroxidation (LPO) and antioxidant defense (AOD) system in full-term and preterm neonates with specific intrauterine infections (IUI). Methods: Eighty full-term and preterm newborns with specific IUI were examined; 48 of them (60%) with a severe course of IUI, and 32 (40%) with an extremely severe IUI course. The control group included 30 relatively healthy newborns, including 22 full-term and 8 late premature (born at 34-37 weeks of gestation) neonates. The state of LPO and AOD was assessed by the levels of malondialdehyde (MDA), superoxide dismutase (SOD), ascorbic (AA), and sialic (SA) acids. Enzyme-linked immunosorbent assay (ELISA) of blood serum of newborns with IUI and their mothers was carried out in paired sera, with IgG, IgM, and avidity level (%) of IUI pathogens determined. Results: Analysis of epidemiological data on TORCH infection in the examined neonates revealed diagnostic titers of cytomegalovirus infection (91.3%), herpes (70.4%), toxoplasmosis (50.1%), and chlamydia (43.4%). Comparative analysis of MDA level in the first and control groups showed a statistically significant difference (p 0.05); while its comparison between the 2nd and control group showed even higher level difference (p 0.05). The levels of SOD, AA and SA in the 1st and 2nd groups were highly significantly different from the control group (p 0.001). All these tests showed significant differences between the 1st and the 2nd group (p 0.05), except for the levels of sialic acid (p 0.05). Conclusion: In neonates with specific IUI, statistically significant changes in LPO and AOD parameters were obtained compared with the control group. Enzymatic and non-enzymatic antioxidant parameters can be diagnostically significant for early prediction of infectious processes in the body of a newborn. The revealed changes in the LPO and AOD indicators in the neonates with IUI, dictate the need for timely and adequate antioxidant therapy along with etiotropic treatment. Keywords: Homeostasis, lipid peroxidation, intrauterine infections, antioxidant defense, tricarboxylic acid cycle.
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