Résumé
Background: Intrauterine fetal death (IUFD) is the tragic event contributing to high perinatal mortality in developing countries. So many risk factors have been seen associated with IUFD that can be prevented with better antenatal care and timely detection at the earliest so that the prevalence can be decreased. This study was done to identify the risk factors associated with IUFD.Methods: This is a retrospective study from done from March 2017 to March 2018 at skims maternity hospital. IUFD was defined as fetal death beyond 20 weeks of gestation. Records were analyzed and data was compiled.Results: In our study there were total of 2500 deliveries out of which 70 were IUFD. Incidence was 28 per 1000 live births. It was found more common in the age group of 20-29 year (65.71%) %). Preeclampsia was the risk factor in 17.14% of cases , followed by abruption in 11.42% followed by placenta previa in 7.14% of cases. However, 20% of the cases had unidentified risk factor.Conclusions: Present study was an effort to compile common risk factors associated with IUFD at tertiary centre of Kashmir.
Résumé
OBJECTIVE To investigate the effect of sodium ferulate (SF) on lipopolysaccharide (LPS)-induced preterm delivery and intra-uterine fetal death (IUFD). METHODS Pregnant Kunming mice were subcutaneously pretreated with SF (25 or 50 mg · kg-1) from gestational day (GD) 10 to GD 15 and with the single injection of LPS (150μg·kg-1, ip) on GD15.5. The incidence of preterm delivery and IUFD was observed. HE staining was used for uterine and placental histological evaluation. The levels of thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) as well as the activities of glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) were detected in the maternal liver, placenta, and fetal liver using commercial kits. Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) levels in amniotic fluid were evaluated by enzyme linked immunosorbent assay. RESULTS For LPS group, the incidence of preterm was 47.8%, delivery time was (17.5 ± 1.3) d, and the pups′survival rate was only 42.6%. Compared with LPS-treated group, SF 50 mg · kg-1 group showed a lower incidence of preterm (14.3%, P<0.01), longer gestational days (18.4 ± 0.5, P<0.05), and a higher pups′survival rate (75.6%, P<0.01). SF 50 mg · kg-1 restored the LPS-induced GSH both in the maternal and fatal liver (a tendency without statistical significance), GST activity〔(163±82) kU·g-1 protein vs (95±90) kU·g-1 protein, P<0.01)〕in the placenta, TBARS content〔(2.5±0.4)μmol·g-1 protein vs (3.1±0.6)μmol·g-1 protein, P<0.01〕in the fetal liver, and TNF-αlevel〔(11±8) ng·L-1 vs (20±8) ng·L-1, P<0.01〕in the amniotic fluid. SF also attenuated LPS-induced placental congestion and neutrophil infiltra?tion in the uterus. CONCLUSION SF may protect against LPS-induced preterm delivery and IUFD, and anti-oxidation as well as anti-inflammation may contribute to these effects.
Résumé
Aim To investigate the effect of N-acetylcysteine (NAC) pretreatment/posttreatment on lipopolysaccharide (LPS)-induced intra-uterine fetal death (IUFD) and intra-uterine growth retardation (IUGR) in mice.Methods In the first experiment,all pregnant mice except controls received an intraperitoneal (75 ?g?kg-1) injection of LPS on gd 15~17.In LPS+NAC groups,the pregnant mice were treated with NAC before and/or after LPS. The saline-and NAC-treated pregnant mice served as controls. The dams were sacrificed on gd 18. In the second experiment,all pregnant mice except controls received an intraperitoneal (75 ?g?kg-1) injection of LPS on gd 15. In LPS+NAC groups,the pregnant mice were treated with NAC before and/or after LPS. The saline-and NAC-treated pregnant mice served as controls. The dams were sacrificed at 1.5 h or 6 h after LPS.Results pretreatment with NAC significantly alleviated LPS-induced fetal mortality and reversed LPS-induced growth development retardation.Correspondingly,pretreatment with NAC significantly attenuated LPS-induced elevation in TNF-? concentration in maternal serum and amniotic fluid and lipid peroxidation in maternal and fetal livers. By contrast to pretreatment,posttreatment with NAC had no effect on LPS-induced TNF-? production and lipid peroxidation,and did not protect against LPS-induced IUFD and IUGR and in fact aggravated LPS-induced preterm labor.Conclusion Pretreatment with NAC attenuates LPS-induced IUFD and IUGR,whereas posttreatment with NAC aggravates LPS-induced preterm labor.