目的　探讨妊娠肝内胆汁淤积症（ICP)的围生结局。方法　对近10年在我院产前检查并住院治疗分娩的1210例ICP病例资料进行回顾性分析。结果　ICP先兆早产率19.0%（230 /1210），88.7%（204 /230）发生于32周后，先兆早产住院病例发生死胎占所有ICP 死胎的4617%（7 /15)；ICP早产率24.0%（290 /1210），96.2%（279 /290)分布于34周以后，89.7%（260 /290)为胎儿异常行剖宫产；羊水胎粪污染率23.2%（281 /1210），41.3%（116 /281)发生于临产前，羊水胎粪污染对新生儿窒息（新生儿1 min Apgar评分≤7分)预测率为25%（70 /281）；新生儿窒息发生率7.1%（86 /1210）；围生儿病死率22.5‰（27 /1210），其中死胎占56%（15 /27），死胎平均孕周36.5周±1.2周，80%（12 /15)发生于妊娠35周后，所作胎心监护均无异常发现，95%（19 /20)的死胎、死产突然发生于先兆早产、偶然宫缩或临产初期；剖宫产率85.9% （1039 /1210），胎儿生长受限（FGR)发生率0.9%（11 /1210），产后出血率1.4%（17 /1210），8.1%（101 /1210）ICP患者合并子痫前期。结论ICP胎儿无明显FGR表现，子痫前期及产后出血发生率与一般孕妇人群相似；常规胎儿监护手段难以预测ICP死胎；积极防治先兆早产，重视先兆早产、偶然宫缩、产前羊水胎粪污染或临产初期时的胎儿监护，把握终止妊娠时机（34～37周），是降低ICP围生儿病死率的重要手段。

对ICP临床流行病学及病因假说、病理、临床表现、妊娠结局、诊断、产科处理等方面进行全面描述，为临床诊治提供参考和指导。

Objective: Intrahepatic cholestasis of pregnancy (ICP) is the most common pregnancy-specific liver disorders. Although various biological effects of corticotrophin-releasing hormone (CRH) has in pregnancy have been reported, its activities in patients with ICP are lacking. Here we evaluated CRH and its receptor (CRH-R1) expression in placenta and serum in control and ICP patients, to assess their potential activities in the ICP pathogenesis. Methods and materials: Placental tissues were obtained from the control and ICP patients (10 cases for each group) between 37 and 39 gestational weeks. Immunohistochemistry, Western Blotting and realtime PCR analysis were used to detect the CRH and CRH-R1 expression in placenta. Meanwhile, maternal serums were analyzed for detecting CRH in the control and ICP patients (80 cases for each group) in 34e37 gestational weeks. All data were observed and recorded for comparing and analyzing in control and ICP patients. Results: CRH staining was found in syncytiotrophoblast and feto-placental vascular endothelium cells of placenta, whereas CRH-R1 staining was found in syncytiotrophoblast by using immunohistochemical analysis. The CRH expression level in ICP placenta was significantly lower than those results in controls (P < 0.01). For CRH-R1, CRH mRNA and CRH-R1 mRNA expressions, no statistical differences were found between control and ICP groups (all P > 0.05). Serum CRH levels increased in both control and ICP groups, but the growth rate was limited in ICP group, especially in late pregnancy (P < 0.05). Conclusions: The down-regulation of CRH in ICP placentas and the limited growth rate of CRH in the maternal serum of ICP patients might impair the blood flow regulation of the utero-placental-fetal unit, which might result in poor fetoplacental vascular perfusion and adverse pregnancy outcomes. CRH might play a significant role in the pathogenesis of ICP and provide a new approach to further investigate the etiology of ICP.