Pre-eclampsia is a major cause of maternal and perinatal mortality and morbidity worldwide, but remains unclear about the underlying disease mechanisms. Pre-eclampsia is currently believed to be a two-stage disease. The first stage involves shallow cytotrophoblast invasion of maternal spiral arteriole, resulting in placental insufficiency. The hypoxic placenta release soluble factors, cytokines, and trophoblastic debris into maternal circulation, which induce systemic endothelial damage and dysfunction. This cause the second stage of the disease: maternal syndrome. Epidemiological research has consistently demonstrated a familial predisposition to pre-eclampsia. Intensive research efforts have been made to discover susceptibility genes that will inform our understanding of the pathophysiology of pre-eclampsia and that may provide direction for therapeutic or preventative strategies. In this review, we summarize the current understanding of the role of genetic factors in the pathophysiology of pre-eclampsia and explain the molecular approach to search for genetic clues in pre-eclampsia.
Arterioles ; Cytokines ; Perinatal Mortality ; Placenta ; Placental Insufficiency ; Pre-Eclampsia ; Trophoblasts

Fetal growth restriction (FGR) occurs due to various reasons and is associated with increased fetal and neonatal mortality and morbidity. FGR has been defined as having birth weight less than the 10th centile. The first clinically relevant step is the detection of true FGR, pathological small fetuses, associated with signs of abnormal placental insufficiency and poorer perinatal outcome. The role of obstetric management is to identify growth restricted fetuses at risk of chronic hypoxia in uterus, to monitor their wellbeing, and to deliver when the adverse outcome is imminent. The purpose of this document is to review the FGR with diagnosis, antenatal surveillance tools, and guidance for management and timing of delivery.
Anoxia ; Birth Weight ; Fetal Development* ; Fetus ; Humans ; Infant ; Infant Mortality ; Placental Insufficiency ; Prenatal Diagnosis ; Uterus

OBJECTIVE: The purpose of this study was to investigate the prenatal hypoxic effect on the fetal brain development. METHODS: We used the guinea pig chronic placental insufficiency model to investigate the effect of hypoxia on fetal brain development. We ligated unilateral uterine artery at 30-32 days of gestation (dg : with term defined as -67 dg). At 50 dg, 60 dg, fetuses were sacrificed and assigned to either the growth-restricted (GR) or control (no ligation) group. After fixation, dissection, and sectioning of cerebral tissue from these animals, immunohistochemistry was performed with NeuN antibody, which is a mature neuronal marker in the cerebral cortex. RESULTS: The number of NeuN-immunoreactive (IR) cells in the cerebral cortex did not differ between the GR and control groups at 50 dg. However, the number of NeuN-IR cells was lesser in GR fetuses than in controls at 60 dg (p<0.05). CONCLUSION: These findings show that chronic prenatal hypoxia affect the number of neuron in the cerebral cortex of guinea pig fetus at 60 dg. The approach used in this study is helpful for extending our understanding of neurogenesis in the cerebral cortex, and the findings may be useful for elucidating the brain injury caused by prenatal hypoxia.
Animals ; Anoxia* ; Brain ; Brain Injuries ; Cerebral Cortex ; Fetus ; Guinea Pigs ; Immunohistochemistry ; Neurogenesis ; Neurons* ; Placental Insufficiency ; Pregnancy ; Uterine Artery

We experienced Hyperviscosity syndrome in 5 newborn infants during 6 months period from August 1980 to January 1981. Diagnosis was made on the basis of characteristic clinical symp-toms along with polythemia. The following results were obtained. Sex in 5 affected infants showed male in 2 and female in 3. And gestational age showed preterm in 3 and full term in 2 cases. Predisposing factors were intertwin transfusion in 1, placental insufficiency with maternal to-xemia in 2(one of which was accompained with interwin transfusion) and small for gestational age in 1. Signs and symptoms associated with hyperviscosity syndrome were cyanosis in 3, dyspnea in 2, lethargy in 2, plethora in 1, hypocalcemia in 4, hypoglycemia in 2 and hyperbilirubinemia in 2 cases. Partial exchange transfusion was done in all cases, resulting in improvement of polycythem-ia and clinical condition, except 1 expired case.
Causality ; Cyanosis ; Diagnosis ; Dyspnea ; Female ; Gestational Age ; Humans ; Hyperbilirubinemia ; Hypocalcemia ; Hypoglycemia ; Infant ; Infant, Newborn* ; Lethargy ; Male ; Placental Insufficiency ; Polycythemia

Preeclampsia is a leading cause of death and disability in mothers and infants. It's cause remains unknown. The only effective treatment is delivery. Preeclampsia is currently believed to be a 2-stage disease. The first stage is characterized by shallow cytotrophoblast invasion of maternal spiral arteriole, resulting in placental insufficiency. There are no maternal signs and symptoms during this stage. The hypoxic placenta release soluble factors into maternal circulation, which induce systemic endothelial dysfunction. This cause the second stage of the disease: the maternal syndrome. During this stage, the clinical signs of preeclampsia, are manifested. We review the evidence that an imbalance of circulating angiogenic factors, the prevention and treatment of preeclampsia including antioxidants for the prevention of preeclampsia, the expectant management and antihypertensive medications to treat mild and severe hypertension in women preeclampsia.
Angiogenesis Inducing Agents ; Antioxidants ; Arterioles ; Cause of Death ; Female ; Humans ; Hypertension ; Infant ; Mothers ; Placenta ; Placental Insufficiency ; Pre-Eclampsia* ; Trophoblasts

Small-for-gestational-age (SGA) is associated with poor perinatal outcomes. The term SGA is descriptive and means that the fetal size and weight at birth are less than expected (in general, 10th percentile using standard curves for gestational age) regardless of the cause. It was estimated that about 50~70% of fetuses born weighing less than the 10th percentile for gestational age are constitutionally small, with fetal growth appropriate for parental size and ethnicity; these are usually associated with normal placental function and have a normal outcome. Fetal growth restriction (FGR) describes a decrease in the fetal growth rate that prevents an infant from obtaining the complete genetic growth potential. It is common with placental dysfunction occurring in about 3% of pregnancies despite advances in obstetric care. In human pregnancies, placental insufficiency is the leading cause of FGR and is usually due to poor utero-placental blood flow and placental infarcts. The reduction of placental supply of nutrients to the fetus has been associated with several adaptive changes taking place in both the placenta and fetus. Adaptive changes can be followed by pathology leading to fetal death, and therefore staging of the disease is fundamental to timing delivery. Thus, it is responsible for the obstetricians to distinguish SGA from intrauterine growth restriction, correct the causes if possible, and if not, accurately stage the disease progress so as to deliver at the most suitable time. In this review, the management of fetal growth restrictions is summarized based on the diagnosis, etiologic factors, antenatal surveillance, and their possible therapeutic approaches.
Constitution and Bylaws ; Fetal Death ; Fetal Development ; Fetus ; Gestational Age ; Humans ; Hypogonadism ; Infant ; Mitochondrial Diseases ; Ophthalmoplegia ; Parents ; Parturition ; Placenta ; Placental Insufficiency ; Pregnancy

Impetigo herpetiformis (IH) is an extremely rare pustular disorder and potentially life-threatening condition for both mother and fetus. Intrauterine growth retardation, fetal abnormalities, and even fetal/neonatal death can occur with worsening maternal disease and are probably related to placental insufficiency. Maternal risk is linked to fluid and electrolyte abnormalities, in particular, hypocalcemia- induced convulsions and sepsis. Therefore, early recognition is crucial to reduce both maternal and fetal morbidities, and a patient with IH may require emergency caesarean delivery. Here, we report a case of a 34-year-old pregnant woman with IH who underwent successful urgent general anesthesia for caesarean section.
Adult ; Anesthesia ; Anesthesia, General ; Cesarean Section* ; Emergencies ; Female ; Fetal Growth Retardation ; Fetus ; Humans ; Impetigo* ; Mothers ; Placental Insufficiency ; Pregnancy ; Pregnant Women ; Psoriasis ; Seizures ; Sepsis

BACKGROUND: Abnormal umbilical artery Doppler velocimetry is one of the important findings of intrauterine growth restriction (IUGR) and IUGR is associated with high perinatal morbidity and mortality. In addition, this abnormal Doppler velocimetry is correlated with placental insufficiency. The aim of this study was to determine the pathologic differences in the placentas from IUGR pregnancies with and without the absent or reversed end diastolic velocity (AREDV). METHODS: Among the cases that had undergone prenatal follow-up in our institute, a retrospective slide review was conducted for 18 cases of IUGR with AREDV and 17 cases with IUGR that had normal end-diastolic flow of the umbilical artery. RESULTS: The birth weight and the other clinical parameters were not different among the two groups. Grossly, the placental weight percentiles were significantly smaller in AREDV group when they were adjusted according to gestational age. Histologically, chronic deciduitis, mural hypertrophy of the decidual arteries, an intimal fibrin cushion of the large fetal vessels, increased syncytial knots, villous agglutinations, avascular villi, villous stromal-vascular karyorrhexis, and acute atherosis were more frequently found in the AREDV group and their presence showed statistical significance. CONCLUSIONS: These findings suggest that pathologic abnormalities due to fetal and maternal vasculopathies in the placenta may be the cornerstone for inducing AREDV in the umbilical artery.
Arteries ; Birth Weight ; Fetal Growth Retardation ; Fibrin ; Follow-Up Studies ; Gestational Age ; Hypertrophy ; Placenta ; Placental Insufficiency ; Pregnancy ; Retrospective Studies ; Rheology ; Umbilical Arteries

OBJECTIVE: During pregnancy, the impaired placental perfusion causes complications such as preeclampsia, intrauterine growth restriction and fetal death in utero. In order to investigate the maternal and fetal response to the impaired placental perfusion, the author induced the impaired placental perfusion by the ligation of the rat uterine artery and investigated its effect on the expression of VEGF (vascular endothelial growth factor) in the placenta and serum VEGF level. METHODS: The rats on day 15 of gestation were used for the experiment. They were divided into two groups. The control group consists of the 20 rats that underwent laparotomy without uterine artery ligation. The experimental group consists of the 20 rats that underwent laparotomy and the uterine artery ligation by silk on day 15 of gestation. On day 16, 17, 18 and 19 of gestation, the placental tissues were obtained. The mRNA expressions of the VEGF in the placenta were measured by the relative RT-PCR in the control and experimental group. The localization and intensity of immunohistochemical staining of VEGF in placenta were determined in both groups and the maternal serum levels of VEGF were also measured in both groups. RESULTS: The mRNA expressions of VEGF120 and VEGF164 were significantly increased 48 hours after the ligation (day 17 of gestation) but the mRNA expression of VEGF188 was not changed after the ligation. There was no difference in the location and intensity of immunohistochemical staining of VEGF in the placenta between control and experimental groups. The serum VEGF levels of control group were 9 times as high as those of non-pregnant rats. The significant increases of the serum VEGF levels were noted 48 and 72 hours after the ligation (day 17 and 18 of gestation) but the significant increase was not noted 96 hours after the ligation (day 19 of gestation) as compared to control group. CONCLUSION: This study demonstrated firstly that the experimentally induced reduction of placental perfusion increased expressions of VEGF in the placenta and maternal serum. The results support that the measurement of maternal serum VEGF levels in pregnancy may help the diagnosis of placental insufficiency.
Animals ; Diagnosis ; Fetal Death ; Laparotomy ; Ligation* ; Perfusion ; Placenta ; Placental Insufficiency ; Pre-Eclampsia ; Pregnancy ; Rats* ; RNA, Messenger ; Silk ; Uterine Artery* ; Vascular Endothelial Growth Factor A*

OBJECTIVE: During pregnancy, the impaired placental perfusion causes complications such as preeclampsia, intrauterine growth restriction and fetal death in utero. In order to investigate the maternal and fetal response to the impaired placental perfusion, the author induced the impaired placental perfusion by the ligation of the rat uterine artery and investigated its effect on the expression of VEGF (vascular endothelial growth factor) in the placenta and serum VEGF level. METHODS: The rats on day 15 of gestation were used for the experiment. They were divided into two groups. The control group consists of the 20 rats that underwent laparotomy without uterine artery ligation. The experimental group consists of the 20 rats that underwent laparotomy and the uterine artery ligation by silk on day 15 of gestation. On day 16, 17, 18 and 19 of gestation, the placental tissues were obtained. The mRNA expressions of the VEGF in the placenta were measured by the relative RT-PCR in the control and experimental group. The localization and intensity of immunohistochemical staining of VEGF in placenta were determined in both groups and the maternal serum levels of VEGF were also measured in both groups. RESULTS: The mRNA expressions of VEGF120 and VEGF164 were significantly increased 48 hours after the ligation (day 17 of gestation) but the mRNA expression of VEGF188 was not changed after the ligation. There was no difference in the location and intensity of immunohistochemical staining of VEGF in the placenta between control and experimental groups. The serum VEGF levels of control group were 9 times as high as those of non-pregnant rats. The significant increases of the serum VEGF levels were noted 48 and 72 hours after the ligation (day 17 and 18 of gestation) but the significant increase was not noted 96 hours after the ligation (day 19 of gestation) as compared to control group. CONCLUSION: This study demonstrated firstly that the experimentally induced reduction of placental perfusion increased expressions of VEGF in the placenta and maternal serum. The results support that the measurement of maternal serum VEGF levels in pregnancy may help the diagnosis of placental insufficiency.
Animals ; Diagnosis ; Fetal Death ; Laparotomy ; Ligation* ; Perfusion ; Placenta ; Placental Insufficiency ; Pre-Eclampsia ; Pregnancy ; Rats* ; RNA, Messenger ; Silk ; Uterine Artery* ; Vascular Endothelial Growth Factor A*