scholarly journals Obeticholic Acid Protects against Lipopolysaccharide-Induced Fetal Death and Intrauterine Growth Restriction through Its Anti-Inflammatory Activity

2016 ◽  
Vol 197 (12) ◽  
pp. 4762-4770 ◽  
Author(s):  
Yuan-Hua Chen ◽  
Xiao-Guang Hu ◽  
Yan Zhou ◽  
Zhen Yu ◽  
Lin Fu ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Fetal Death ◽  
Growth Restriction ◽  
Inflammatory Activity ◽  
Obeticholic Acid ◽  
Intrauterine Growth ◽  
Anti Inflammatory

scholarly journals Intrauterine Growth Restriction: Cytokine Profiles of Trophoblast Antigen-Stimulated Maternal Lymphocytes

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Raj Raghupathy ◽  
Majedah Al-Azemi ◽  
Fawaz Azizieh
Keyword(s):  
Inflammatory Cytokines ◽  
Peripheral Blood ◽  
Intrauterine Growth Restriction ◽  
Mononuclear Cells ◽  
Normal Pregnancy ◽  
Placental Insufficiency ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Anti Inflammatory ◽  
Ifnγ And Tnfα

Intrauterine growth restriction (IUGR) is an important perinatal syndrome that poses several serious short- and long-term effects. We studied cytokine production by maternal peripheral blood lymphocytes stimulated by trophoblast antigens. 36 women with a diagnosis of IUGR and 22 healthy women with normal fetal growth were inducted. Peripheral blood mononuclear cells were stimulated with trophoblast antigens and levels of the proinflammatory cytokines IL-6, IL-8, IL-12, IL-23, IFNγ, and TNFα and the anti-inflammatory cytokines IL-4, IL-10, and IL-13 were measured in culture supernatants by ELISA. IL-8 was produced at higher levels by blood cells of the IUGR group than normal pregnant women, while IL-13 was produced at lower levels. IL-8, IFNγ, and TNFα were higher in IUGR with placental insufficiency than in normal pregnancy. IL-12 levels were higher and IL-10 levels were lower in IUGR with placental insufficiency than in IUGR without placental insufficiency. We suggest that a stronger pro-inflammatory bias exists in IUGR as compared to normal pregnancy and in IUGR with placental insufficiency when compared to IUGR without placental insufficiency. Several ratios of proinflammatory to anti-inflammatory cytokines also support the existence of an inflammatory bias in IUGR.

scholarly journals Maternal and perinatal outcomes of hyperthyroidsm in pregnancy at Dr. Cipto Mangunkusumo Hospital, Jakarta, period of January 2015 - December 2016

2021 ◽  
Vol 29 (1) ◽  
pp. 36
Author(s):  
Fita Maulina ◽  
M Adya F F Dilmy ◽  
Ali Sungkar
Keyword(s):  
Pregnant Women ◽  
Preterm Delivery ◽  
Intrauterine Growth Restriction ◽  
Fetal Death ◽  
Perinatal Outcomes ◽  
Growth Restriction ◽  
Intrauterine Fetal Death ◽  
Adequate Treatment ◽  
Intrauterine Growth ◽  
In Pregnancy

Objectives: To report maternal and perinatal outcomes of hyperthyroidsm in pregnancy.Case Report: There were 3622 cases of delivering pregnant women during the period of the study. From this number, the prevalence of pregnant women with hyperthyroid was 0.2 %. We reported 9 cases of hyperthyroid in pregnancy. The number of pregnancy complication and outcome on pregnant women with hyperthyroidism were preterm labor (44%) and preeclampsia (22%), both were found in group of mother who did taking antihyperthyroid therapy. In those who did not take antihyperthyroid therapy 11% had spontaneous abortion and 11% had preterm delivery. Fetal complications were intrauterine growth restriction (11%) and intrauterine fetal death (23%), both of these complication were on the group who did not take antihyperthyroid. On the contrary, 44% babies were born with normal birthweight in group who took antihyperthyroid.Conclusion: There were differences noted between the group that took adequate treatment and the group that did not take antihyperthyroid. The incidence of intrauterine growth restriction and intrauterine fetal death were high in group that did not took antihyperthyroid therapy but the incidence of preterm delivery as the maternal complication was high in group that did take the antihyperthyroid therapy.  

scholarly journals Obeticholic Acid Protects against Gestational Cholestasis-Induced Fetal Intrauterine Growth Restriction in Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
Wei Chen ◽  
Xing-Xing Gao ◽  
Li Ma ◽  
Zhi-Bing Liu ◽  
Li Li ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Glutathione Depletion ◽  
Common Disease ◽  
Obeticholic Acid ◽  
Antioxidant Genes ◽  
Crown Rump Length ◽  
Intrauterine Growth ◽  
Nadph Oxidase 4 ◽  
Pregnant Mice

Gestational cholestasis is a common disease and is associated with adverse pregnancy outcomes. However, there are still no effective treatments. We investigated the effects of obeticholic acid (OCA) on fetal intrauterine growth restriction (IUGR) during 17α-ethynylestradiol- (E2-) induced gestational cholestasis in mice. All pregnant mice except controls were subcutaneously injected with E2 (0.625 mg/kg) daily from gestational day (GD) 13 to GD17. Some pregnant mice were orally administered with OCA (5 mg/kg) daily from GD12 to GD17. As expected, OCA activated placental, maternal, and fetal hepatic FXR signaling. Additionally, exposure with E2 during late pregnancy induced cholestasis, whereas OCA alleviated E2-induced cholestasis. Gestational cholestasis caused reduction of fetal weight and crown-rump length and elevated the incidence of IUGR. OCA decreased the incidence of IUGR during cholestasis. Interestingly, OCA attenuated reduction of blood sinusoid area in placental labyrinth layer and inhibited downregulation of placental sodium-coupled neutral amino acid transporter- (SNAT-) 2 during cholestasis. Additional experiment found that OCA attenuated glutathione depletion and lipid peroxidation in placenta and fetal liver and placental protein nitration during cholestasis. Moreover, OCA inhibited the upregulation of placental NADPH oxidase-4 and antioxidant genes during cholestasis. OCA activated antioxidant Nrf2 signaling during cholestasis. Overall, we demonstrated that OCA treatment protected against gestational cholestasis-induced placental dysfunction and IUGR through suppressing placental oxidative stress and maintaining bile acid homeostasis.

Alpha hemoglobin stabilizing protein (AHSP) in hemolysis elevated liver enzyme and low platelet (HELLP) syndrome, intrauterine growth restriction (IUGR) and fetal death

2005 ◽  
Vol preprint (2007) ◽  
pp. 1
Author(s):  
Monica Emanuelli ◽  
Davide Sartini ◽  
Valentina Rossi ◽  
Alessandra Corradetti ◽  
Beatrice Landi ◽  
...  
Keyword(s):  
Liver Enzyme ◽  
Intrauterine Growth Restriction ◽  
Hellp Syndrome ◽  
Fetal Death ◽  
Elevated Liver Enzyme ◽  
Growth Restriction ◽  
Intrauterine Growth

Role of the alpha hemoglobin-stabilizing protein in HELLP syndrome, intrauterine growth restriction and fetal death

2006 ◽  
Vol 195 (6) ◽  
pp. S164
Author(s):  
Monica Emanuelli ◽  
Beatrice Landi ◽  
Francesca Pierella ◽  
Alessandra Corradetti ◽  
Claudia Regina Vianna ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Hellp Syndrome ◽  
Fetal Death ◽  
Growth Restriction ◽  
Intrauterine Growth

Pathological features of the sequence in pregnant women with delayed fetal growth

2019 ◽  
pp. 50-54
Author(s):  
V.O. Golyanovskiy ◽  
◽  
Ye.O. Didyk ◽  
Keyword(s):  
Pregnant Women ◽  
Intrauterine Growth Restriction ◽  
Normal Development ◽  
Intrauterine Infection ◽  
Normal Pregnancy ◽  
Growth Restriction ◽  
Control Group ◽  
Intrauterine Growth ◽  
Increased Risk ◽  
Infection And Inflammation

Pregnant women with intrauterine growth restriction (IUGR) have an increased risk of adverse perinatal and long-term complications compared with the birth of children with normal body weight. Thus, IUGR is one of the main challenges for the global health system, especially in poor and developing countries. Morpho-functional studies of the placentas help in determining the causes of IUGR, and therefore, timely prevent complications in pregnant women with IUGR. The objective: The purpose of this study is to investigate various morphometric and pathomorphological changes in the placenta, including inflammatory, in cases of IUGR, and to establish a correlation of these results with the etiology and complications for the fetus. Materials and methods. In the current study, 54 placentas of the fetuses with IUGR (the main group) were compared with 50 placentas of the fetuses with normal development (control group). The criteria for the inclusion of IUGR were gestational age more than 30 weeks and all fetuses with a weight less than 10th percentile for this period of pregnancy. The placenta material was studied pathomorphologically with laboratory screening for infection and inflammation. Similarly, the results were determined for placentas of the fetuses with normal development compared to placentas with IUGR. Results. The placenta study showed the presence of calcification in the case of IUGR, as well as in the case of prolonged pregnancy. However, calcification of the placenta in the case of IUGR was more progressive compared with placenta in the normal pregnancy. In addition, the presence of intrauterine infection and inflammation was observed, which could also lead to an adverse outcome for the further progression of pregnancy with IUGR. Conclusion. A comparative macro- and microscopic pathomorphological study of the placentas in the two groups has shown a significant increase in the pathological changes in all the anatomical structures of the fetuses with IUGR. Key words: Intrauterine growth restriction (IUGR), fetal weight, pathomorphological changes of the placenta.

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