摘要
AIM: To investigate the association between total bile acid(TBA) level during intrahepatic cholestasis of pregnancy(ICP) and fetal lung surfactant alteration. METHODS: We recruited 42 ICP and 32 normal pregnancy women in this study. The maternal blood, fetal blood and amniotic fluid TBA level were detected using a circulating enzymatic method. Umbilical blood pulmonary surfactant protein A(SP-A) was evaluated with enzyme-linked immunosorbent assay. High performance liquid chromatography was used for the determination of phosphatidyl choline(PC), phosphatidyl inositol(PI), lysolecithin(LPC) and sphingomyelin(SM). Amniotic fluid lamellar body was counted with a fully automatic blood cell counter. Fetal lung area and fetal body weight were calculated from data obtained with an iu22 color supersonic diagnostic set. Clinical information of a nonstress test, amniotic fluid properties and neonatal Apgar score, and birth weight were recorded for review. RESULTS: The TBA level in maternal blood, fetal blood and amniotic fluid in the ICP group were significantly higher than that in the control group(maternal blood: 34.11 ± 6.75 mmol/L vs 4.55 ± 1.72 mmol/L, P < 0.05; fetal blood: 11.9 ± 2.23 mmol/L vs 3.52 ± 1.56 mmol/L, P < 0.05; amniotic fluid: 3.89 ± 1.99 mmol/L vs 1.43 ± 1.14 mmol/L, P < 0.05). Amniotic fluid PC and PI in the ICP group were significantly lower than that in the control group(PC: 65.71 ± 7.23 μg/m L vs 69.70 ± 6.68 μg/m L, P < 0.05; PI: 3.87 ± 0.65 μg/m L vs 4.28 ± 0.74 μg/m L, P < 0.05). PC/LPC ratio of the ICP group was lower than that of the control group(14.40 ± 3.14 vs 16.90 ± 2.52, P < 0.05). Amniotic LB in the ICP group was significantly lower than that of the control group((74.13 ± 4.37) × 109/L vs(103.0 ± 26.82) × 109/L, P < 0.05). Fetal umbilical blood SP-A level in the ICP group was significantly higher than that of the control group(30.26 ± 7.01 ng/m L vs 22.63 ± 7.42 ng/m L, P < 0.05). Fetal lung area/body weight ratio of the ICP group was significantly lower than that of the control group(5.76 ± 0.63 cm2/kg vs 6.89 ± 0.48 cm2/kg, P < 0.05). In the ICP group, umbilical cord blood TBA concentration was positively correlated to the maternal blood TBA concentration(r = 0.746, P < 0.05) and umbilical blood SP-A(r = 0.422, P < 0.05), but it was negatively correlated to the amniotic fluid lamellar corpuscle(r = 0.810, P < 0.05) and fetal lung area/body weight ratio(r = 0.769, P < 0.05). Furthermore, umbilical blood TBA showed a negative correlation to PC, SM and PI(r pc = 0.536, r sm = 0.438, r pi = 0.387 respectively, P < 0.05). The neonatal asphyxia, neonatal respiratory distress syndrome, fetal distress and perinatal death rates in the ICP group are higher than that of theCONCLUSION: ICP has higher TBA in maternal and fetal blood and amniotic fluid. The high concentration of TBA may affect fetal pulmonary surfactant production and fetal lung maturation.
AIM： To investigate the association between total bile acid （TBA） level during intrahepatic cholestasis of preg-nancy （ICP） and fetal lung surfactant alteration. METHODS： We recruited 42 ICP and 32 normal preg-nancy women in this study. The maternal blood, fetal blood and amniotic fluid TBA level were detected us-ing a circulating enzymatic method. Umbilical blood pulmonary surfactant protein A （SP-A） was evaluated with enzyme-linked immunosorbent assay. High per-formance liquid chromatography was used for the determination of phosphatidyl choline （PC）, phospha-tidyl inositol （PI）, lysolecithin （LPC） and sphingomyelin（SM）. Amniotic fluid lamellar body was counted with a fully automatic blood cell counter. Fetal lung area and fetal body weight were calculated from data obtained with an iu22 color supersonic diagnostic set. Clinical information of a nonstress test, amniotic fluid proper-ties and neonatal Apgar score, and birth weight were recorded for review. RESULTS： The TBA level in maternal blood, fetal blood and amniotic fluid in the ICP group were significantly higher than that in the control group （maternal blood： 34.11 ± 6.75 mmol/L vs 4.55 ± 1.72 mmol/L, P 〈 0.05; fetal blood： 11.9 ± 2.23 mmol/L vs 3.52 ± 1.56 mmol/L, P 〈 0.05; amniotic fluid： 3.89 ± 1.99 mmol/L vs 1.43 ± 1.14 mmol/L, P 〈 0.05）. Amniotic fluid PC and PI inthe ICP group were significantly lower than that in the control group （PC： 65.71 ± 7.23 μg/mL vs 69.70 ± 6.68 μg/mL, P 〈 0.05; PI： 3.87 ± 0.65 μg/mL vs 4.28 ± 0.74 μg/mL, P 〈 0.05）. PC/LPC ratio of the ICP group was lower than that of the control group （14.40 ± 3.14 vs 16.90 ± 2.52, P 〈 0.05）. Amniotic LB in the ICP group was significantly lower than that of the control group （（74.13 ± 4.37） × 109/L vs （103.0 ± 26.82） × 109/L, P 〈 0.05）. Fetal umbilical blood SP-A level in the ICP group was significantly higher than that of the control group （30.26 ± 7.01 ng/mL vs 22.63 ± 7.42 ng/mL, P 〈 0.05）. Fetal lung area/body weight ratio of the ICP group was significantly lower than that of the control group （5.76 ± 0.63 cm2/kg vs 6.89 ± 0.48 cm2/kg, P 〈 0.05）. In the ICP group, umbilical cord blood TBA concentration was positively correlated to the mater-nal blood TBA concentration （ r = 0.746, P 〈 0.05） andumbilical blood SP-A （ r = 0.422, P 〈 0.05）, but it was negatively correlated to the amniotic fluid lamellar cor-puscle （ r = 0.810, P 〈 0.05） and fetal lung area/body weight ratio （ r = 0.769, P 〈 0.05）. Furthermore, um-bilical blood TBA showed a negative correlation to PC, SM and PI （ rpc = 0.536, r sm = 0.438, rpi = 0.387 respec-tively, P 〈 0.05）. The neonatal asphyxia, neonatal re-spiratory distress syndrome, fetal distress and perinatal death rates in the ICP group are higher than that of theCONCLUSION： ICP has higher TBA in maternal and fetal blood and amniotic fluid. The high concentration of TBA may affect fetal pulmonary surfactant produc-tion and fetal lung maturation.
