Journal
MEDICAL SCIENCE MONITOR
Volume 17, Issue 5, Pages CR265-CR271Publisher
INT SCIENTIFIC LITERATURE, INC
DOI: 10.12659/MSM.881766
Keywords
cortisol; dehydroepiandrosterone sulfate; intrahepatic cholestasis of pregnancy; fetal death; cholic acid; human; rat
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Funding
- National Key Basic Research Plan of China (973 Plan) [2010CB529500]
- National High Technology Research and Development Program (863 program) [054119512]
- Chinese Ministry of Health [2007-353]
- National Science & Technology Key Program of the Eleventh Fiveyear Plan of China [2006BAI05A05]
- Science and Technology Commission of Shanghai [064909006]
- National Health Ministry Clinical Medicine Key program, National Science Fund of China [30872777]
- Shanghai Leading Academic Discipline Project [B117]
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Background: Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-associated liver disease of unknown etiology. The aim of this study was to investigate the change in maternal and fetal adrenal function in clinical and experimental ICP. Material/Methods: The maternal and fetal serum levels of cortisol and dehydroepiandrosterone sulfate (DHEAS) were determined in 14 women with ICP and in pregnant rats with estrogen-induced intrahepatic cholestasis. Results: In women with ICP, the fetal serum cortisol and DHEAS levels were significantly higher than those in women with normal pregnancy, after correcting the impact of gestational age at delivery. The relationship between fetal cortisol and maternal cholic acid levels was bidirectional; the fetal cortisol tended to increase in mild ICP, while it decreased in severe ICP. In pregnant rats with estrogen-induced cholestasis, the fetal cortisol level was significantly lower in the group with oxytocin injection, compared with the group without oxytocin injection (191.92 +/- 18.86 vs. 272.71 +/- 31.83 ng/ml, P<0.05). In contrast, the fetal cortisol concentration was increased after oxytocin injection in normal control rats. Conclusions: The data indicate that fetal stress-responsive system is stimulated in mild ICP, but it is suppressed in severe ICP, which might contribute to the occurrence of unpredictable sudden fetal death. Further studies are warranted to explore the role of impaired fetal adrenal function in the pathogenesis of ICP and the clinical implications.
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