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

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

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

2008 ◽  
Vol 13 (1) ◽  
pp. 67-71 ◽  
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

Association of maternal and/or fetal factor V Leiden and G20210A prothrombin mutation with HELLP syndrome and intrauterine growth restriction

2003 ◽  
Vol 105 (3) ◽  
pp. 279-285 ◽  
Author(s):  
Dietmar SCHLEMBACH ◽  
Ernst BEINDER ◽  
Juergen ZINGSEM ◽  
Ute WUNSIEDLER ◽  
Matthias W. BECKMANN ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intrauterine Growth Restriction ◽  
Hellp Syndrome ◽  
Factor V Leiden ◽  
Growth Restriction ◽  
Control Group ◽  
Factor V ◽  
Intrauterine Growth ◽  
Prothrombin Mutation ◽  
Thrombophilic Mutations

This study was conducted to investigate the association of maternal and/or fetal factor V Leiden (FVL) and G20210A prothrombin mutation with HELLP syndrome. FVL and G20210A prothrombin mutation were determined using PCR. Sixty-three pregnant women, 36 of them diagnosed with HELLP syndrome, were included in the study. Overall, 68 children were born as a result of these pregnancies and blood sampling was possible in 28 out of 39 children from HELLP patients and 25 out of 29 children from the control women. The prevalence of a maternal FVL was elevated 2-fold in HELLP patients compared with the control women [six out of 36 (16.7%) compared with two out of 27 (7.4%); P=0.282]. None of the HELLP patients and only one woman in the control group was found to be positive for the G20210A prothrombin mutation (P=0.251). The fetal carrier frequency was four out of 28 compared with three out of 25 for FVL (P=0.811), and two out of 28 compared with one out of 25 for G20210A prothrombin mutation (P=0.629). Intrauterine growth restriction (IUGR) was significantly higher in fetuses found to be positive for a thrombophilic mutation (P=0.022). IUGR occurred in seven out of ten fetuses with a thrombophilic mutation compared with 11 out of 43 in fetuses without a mutation. The prevalence of FVL, but not of the G20210A prothrombin mutation, seems to be elevated in women with HELLP syndrome. A fetal thrombophilic mutation does not contribute significantly to the clinical features of the HELLP syndrome. Our results demonstrate a fetal contribution to IUGR. Fetal thrombophilic mutations may lead to placental microthrombosis, which consecutively could lead to a disturbed fetoplacental blood flow and thus cause growth restriction.

The Role of the Anti-Angiogenic Factor Endostatin in Intrauterine Growth Restriction

2005 ◽  
Vol 12 (3) ◽  
pp. 195-197 ◽  
Author(s):  
Ariadne Malamitsi-Puchner ◽  
Theodora Boutsikou ◽  
Emmanuel Economou ◽  
Evangelos Makrakis ◽  
Zoe Iliodromiti ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Angiogenic Factor ◽  
Intrauterine Growth

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.  

The brain development of infants with intrauterine growth restriction: role of glucocorticoids

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Ying-xue Ding ◽  
Hong Cui
Keyword(s):  
Endothelial Cells ◽  
Brain Injury ◽  
Intrauterine Growth Restriction ◽  
Growth And Development ◽  
Growth Restriction ◽  
Microvascular Endothelial Cells ◽  
Intrauterine Growth ◽  
Growth Restrictions ◽  
The Brain

Abstract Brain injury is a serious complication of intrauterine growth restriction (IUGR), but the exact mechanism remains unclear. While glucocorticoids (GCs) play an important role in intrauterine growth and development, GCs also have a damaging effect on microvascular endothelial cells. Moreover, intrauterine adverse environments lead to fetal growth restriction and the hypothalamus-pituitary-adrenal (HPA) axis resetting. In addition, chronic stress can cause a decrease in the number and volume of astrocytes in the hippocampus and glial cells play an important role in neuronal differentiation. Therefore, it is speculated that the effect of GCs on cerebral neurovascular units under chronic intrauterine stimulation is an important mechanism leading to brain injury in infants with growth restrictions.

Angiopoietin-2 in the perinatal period and the role of intrauterine growth restriction

2006 ◽  
Vol 85 (1) ◽  
pp. 45-48 ◽  
Author(s):  
Ariadne Malamitsi-Puchner ◽  
Theodora Boutsikou ◽  
Emmanuel Economou ◽  
Anastasia Tzonou ◽  
Evangelos Makrakis ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Perinatal Period ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Angiopoietin 2

scholarly journals The detrimental role of angiotensin receptor agonistic autoantibodies in intrauterine growth restriction seen in preeclampsia

2009 ◽  
Vol 206 (12) ◽  
pp. 2809-2822 ◽  
Author(s):  
Roxanna A. Irani ◽  
Yujin Zhang ◽  
Sean C. Blackwell ◽  
Cissy Chenyi Zhou ◽  
Susan M. Ramin ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Causative Factor ◽  
Growth Restriction ◽  
Hypertensive Disorder ◽  
Human Trophoblast ◽  
Fetal Circulation ◽  
Intrauterine Growth ◽  
Underlying Mechanisms ◽  
Agonistic Autoantibodies

Growth-restricted fetuses are at risk for a variety of lifelong medical conditions. Preeclampsia, a life-threatening hypertensive disorder of pregnancy, is associated with fetuses who suffer from intrauterine growth restriction (IUGR). Recently, emerging evidence indicates that preeclamptic women harbor AT1 receptor agonistic autoantibodies (AT1-AAs) that contribute to the disease features. However, the exact role of AT1-AAs in IUGR and the underlying mechanisms have not been identified. We report that these autoantibodies are present in the cord blood of women with preeclampsia and retain the ability to activate AT1 receptors. Using an autoantibody-induced animal model of preeclampsia, we show that AT1-AAs cross the mouse placenta, enter fetal circulation, and lead to small fetuses with organ growth retardation. AT1-AAs also induce apoptosis in the placentas of pregnant mice, human villous explants, and human trophoblast cells. Finally, autoantibody-induced IUGR and placental apoptosis are diminished by either losartan or an autoantibody-neutralizing peptide. Thus, these studies identify AT1-AA as a novel causative factor of preeclampsia-associated IUGR and offer two possible underlying mechanisms: a direct detrimental effect on fetal development by crossing the placenta and entering fetal circulation, and indirectly through AT1-AA–induced placental damage. Our findings highlight AT1-AAs as important therapeutic targets.

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