Bile acid stress in the mother and baby unit

Howard, Philip J.; Murphy, G. M.

doi:10.1097/00042737-200303000-00016

Cited by 16 publications

(9 citation statements)

References 59 publications

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“…These compounds cross the placenta mostly in the fetomaternal direction. The impaired maternal clearance produced by ICP can limit the passage of BA from fetus to maternal circulation thereby inducing a further elevation of BA levels in the fetal circulation, 3,12,13 and high BA levels in the neonates could easily pass to the alveoli.…”

Section: Discussionmentioning

confidence: 99%

Intrahepatic Cholestasis of Pregnancy and Neonatal Respiratory Distress Syndrome

Zecca

Luca²,

Marras³

et al. 2006

Pediatrics

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Section: Discussionmentioning

confidence: 99%

Intrahepatic Cholestasis of Pregnancy and Neonatal Respiratory Distress Syndrome

Zecca

Luca²,

Marras³

et al. 2006

Pediatrics

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“…SULT2A1 sulfonates the gonadal hormone precursor DHEA and provides the starting material for estrogen biosynthesis in the placenta (Barker et al, 1994). In addition, since SULT2A1 catalyzes the sulfonation of toxic monohydroxy bile acids (Kitada et al, 2003), its continuous expression during fetal and postnatal life may be essential to avoid bile acid stress and the emergence of intrahepatic cholestasis, a life-threatening event in the developing human (Howard and Murphy, 2003).…”

Section: Discussionmentioning

confidence: 99%

Developmental Expression of Aryl, Estrogen, and Hydroxysteroid Sulfotransferases in Pre- and Postnatal Human Liver

Duanmu

Weckle

Koukouritaki

et al. 2005

J Pharmacol Exp Ther

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Aryl-(SULT1A1), estrogen-(SULT1E1), and hydroxysteroid-(SULT2A1) sulfotransferases (SULTs) are active determinants of xenobiotic detoxication and hormone metabolism in the adult human liver. To investigate the role of these conjugating enzymes in the developing human liver, the ontogeny of immunoreactive SULT1A1, SULT1E1, and SULT2A1 expression was characterized in a series of 235 pre-and postnatal human liver cytosols ranging in age from early gestation to a postnatal age of 18 years. Interindividual variability in expression levels was apparent for all three SULTs in pre-and postnatal liver samples. Expression of the three SULTs displayed distinctly different developmental profiles. Semiquantitative Western blot analyses indicated that SULT1A1 and SULT2A1 immunoreactive protein levels were readily detectable in the majority of developmental human liver cytosols throughout the prenatal period. Whereas SULT1A1 expression did not differ significantly among the various developmental stages, SULT2A1 expression increased during the third trimester of gestation and continued to increase during postnatal life. By contrast, SULT1E1, a cardinal estrogen-inactivating enzyme, achieved the highest levels of expression during the earliest periods of gestation in prenatal male livers, indicating a requisite role for estrogen inactivation in the developing male. The present analysis suggests that divergent regulatory mechanisms are responsible for the differential patterns of hepatic SULT1A1, SULT1E1, and SULT2A1 immunoreactive protein levels that occur during pre-and postnatal human development, and implicates a major role for sulfotransferase expression in the developing fetus.

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“…Healthy pregnant women have higher total BA levels than non-pregnant women and levels up to 11.0 μmol/l are considered as normal in late gestation [40]. In ICP, abnormal BA profiles have been found in maternal serum, fetal circulation and meconium [41] and serum BA composition in women with ICP generally shows a shift towards a hydrophobic pattern, with higher levels of lithocolic acid and free bile acids [42]. Glantz et al showed that the probability of fetal complications increased by 1 -2% per additional μmol of maternal BA [1].…”

Section: Symptoms and Diagnosismentioning

confidence: 99%

Intrahepatic Cholestasis of Pregnancy and Bile Acids Induced Lung Injury in Newborn Infants

Zecca¹,

Luca²,

Marras³

et al. 2007

CPR

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Intrahepatic cholestasis of pregnancy (ICP) is a clinical syndrome of unknown pathophysiology, occurring during the second half of pregnancy and persisting until delivery. The incidence of ICP varies from 0.1% to 1.5% of pregnancies in Europe, North America and Australia and from 9.2% to 15.6% in South American countries such as Bolivia and Chile. This syndrome has been associated with increased foetal distress, intrauterine death, premature delivery, perinatal mortality and, more recently, with the occurrence of respiratory distress syndrome in the newborn infant. Bile acids (BA) are supposed to be the main mediators for these complications because ICP seriously impairs the placental clearance of foetal BA leading to a dangerous accumulation of these compounds within the foetus and the newborn. Cholestatic pregnancies have to be considered high risk ones, recent reports showing that BA can interfere with surfactant metabolism and are particularly harmful for the developing lung.This review summarizes existing literature data on this topic with particular emphasis on bile acids-induced lung injury. The authors discuss possible mechanisms of lung damage and highlight future research perspectives in this field.

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Bile acid stress in the mother and baby unit

Cited by 16 publications

References 59 publications

Intrahepatic Cholestasis of Pregnancy and Neonatal Respiratory Distress Syndrome

Intrahepatic Cholestasis of Pregnancy and Neonatal Respiratory Distress Syndrome

Developmental Expression of Aryl, Estrogen, and Hydroxysteroid Sulfotransferases in Pre- and Postnatal Human Liver

Intrahepatic Cholestasis of Pregnancy and Bile Acids Induced Lung Injury in Newborn Infants

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