cholestasis/hypoxia

We report 18 premature infants (gestational age: 31.1 weeks +/- 2.6 [mean +/- SD] (range: 28-36]) with necrotizing enterocolitis (NEC) who developed total parenteral nutrition (TPN) associated cholestasis. Liver function tests were performed at the start of TPN (D1) and repeated once a week.

An increase of toxic bile acids such as glycochenodeoxycholic acid occurs during warm ischemia reperfusion causing cholestasis and damage in hepatocytes and intrahepatic biliary epithelial cells. We aim to test antiapoptosis effects of ursodeoxycholyl lysophosphatidylethanolamide under cholestatic

Hypoxia inducible factor-1α (HIF-1α), regulated in development and DNA damage response-1 (REDD1), and mammalian target of rapamycin (mTOR) play distinct roles in response to hypoxia. The aim of this study was to evaluate whether the HIF-1α-REDD1-mTOR-mediated hypoxic stress response also operates

OBJECTIVE Hypoxia-inducible factor-2α (HIF-2α) has been reported to play an important role in a host of pathophysiological processes, including cellular survival. This study explores the role of HIF-2α in cholestasis-mediated hepatocyte apoptosis. METHODS Hypoxia-inducible factor-2α expression was

OBJECTIVE To investigate the mechanism and the related factors of fetal hypoxia in intrahepatic cholestasis of pregnancy (ICP). METHODS Cord blood total bile acids(TBA), hypoxanthine (HX), and endothelin (ET) concentrations were measured in 30 newborns of mothers with ICP and 30 infants of normal

The expression of vascular endothelial growth factor (VEGF) under hypoxia in the placenta with intrahepatic cholestasis of pregnancy (ICP) was observed, and mechanisms of ICP fetal distress were discussed. METHODS Different culturing times were established in hypoxia incubator, and protein

OBJECTIVE Owing to the molecular mechanisms unexplored yet to fetal hypoxia signaling in the intrahepatic cholestasis of pregnancy (ICP), and therefore we intend to investigate the significant expression of the hypoxia-inducible transcription factor-1alpha (HIF-1alpha) in placenta of pregnant women

BACKGROUND Intrahepatic cholestasis of pregnancy (ICP) is a liver disorder unique to pregnancy that is associated with increased rates of fetal distress and demise. While acute hypoxia is believed to cause the pathophysiology of ICP, direct molecular evidence for this is lacking. Here, we analyzed

We studied, retrospectively, 92 children who were first seen with neonatal cholestasis and who were followed up until liver test results normalized. Among the 92 children, 81 displayed factors responsible for chronic and/or acute perinatal distress. Onset of jaundice was recorded at a mean age of 7

Intrahepatic cholestasis of pregnancy (ICP) is an unique complication in pregnancy, which usually manifests in the second or third trimester, and mainly harms the fetus. Its pathogenesis is not yet clear, and placental pathological changes are insufficient to explain the clinical phenomenon.Recent

BACKGROUND Intrahepatic cholestasis of pregnancy is a cholestatic disorder with an increased risk for adverse perinatal outcome. The mechanism underlying intrauterine demise is poorly understood. METHODS A nulliparous woman with gestational age of 36 plus 6 weeks presented with suspected

An epidemiological study was conducted to estimate the proportion of infants on total parenteral nutrition (TPN) who developed cholestasis and to identify risk factors associated with the development of this disease. Data were abstracted from medical records of 624 infants less than or equal to 30

The etiology of intrahepatic cholestasis of pregnancy includes genetic and environmental factors. Bile acids elevation in maternal and fetal blood is the main fact of its physiopathology, causing maternal itching and high perinatal morbidity and mortality. High levels of maternal blood bile acids

The sensitivity of meconium stain in amniotic fluid for prediction of fetal well-being in intrahepatic cholestasis of pregnancy(ICP) was evaluated. The study consisted of an ICP group(n = 30), and a control group (n = 30) and the umbilical arterial pH value(< 7.2) was used as a standard. The