中文摘要：

目的：观察原发性胆汁性肝硬化（primary biliary cirrhosis,PBC）患者治疗前后血清IL-6表达水平,探索其与熊去氧胆酸（Ursodeoxycholic acid,UDCA）疗效的临床相关性。方法：本研究回顾性纳入自2013年-2015年就诊于第四军医大学西京消化病医院的40例新诊断PBC患者,及40例健康对照者。收集PBC患者治疗前后的相关临床资料和血清样本,采用ELISA方法检测患者血清IL-6表达水平,并进一步分析其临床意义。结果：1）治疗前PBC患者血清IL-6表达水平明显高于健康对照者（P〈0.001）;2）PBC患者在接受UDCA治疗后的第3,6和12个月血清IL-6水平与治疗前相比明显降低（P〈0.05）,且在第3个月时下降最明显。3）无论是依据Paris I标准还是Barcelona标准,结果显示,UDCA应答者与应答不佳者相比其治疗前血清IL-6水平无统计学差异（P=0.373;P=0.409）。但UDCA应答者在治疗3个月时其血清IL-6表达水平比治疗前明显下降（P〈0.05）,而应答不佳者治疗3个月时血清IL-6表达水平与治疗前相比无明显差异（P=0.667;P=0.186）。结论：IL-6可能在PBC发病的免疫机制中发挥着重要的作用。目前尚不能认为PBC患者治疗前血清IL-6表达水平能独立评价UDCA疗效,但是治疗三个月后患者血清IL-6水平下降趋势能够提示PBC患者对UDCA的应答情况。

英文摘要：

Objective： To observe the serum IL-6 levels in patients with primary biliary cirrhosis（PBC） and explore the association between the serum IL-6 levels with the therapeutic effects of Ursodeoxycholic acid（UDCA）. Methods： 40 PBC patients and 40 healthy individuals who were visited the Xijing Hospital of Digestive Diseases between 2013 and 2015 were included in our study. Their clinical data and serum samples were selected for research. The serum levels of IL-6 were measured by ELISA and the results were further analyzed. Results： 1） The basal serum level of IL-6 in PBC patients was significantly higher than that of healthy controls（P〈0.001）.2） After treatment with UDCA, the serum IL-6 levels in the third month, the sixth month and the twelfth months all showed remarkable decrease when compared to their basal levels（P〈0.05）. Besides, the decline in the third month was the most obvious. 3） The results showed no significant difference of the basal serum IL-6 levels between UDCA responders and UDCA non-responders according to Paris I criteria or Barcelona criteria（P=0.373; P=0.409）. However, the serum IL-6 level of UDCA responders showed significant decrease after treatment for 3 months（P〈0.05）, while UDCA non-responders demonstrated no difference in the third months after UDCA treatment（P=0.667; P=0.186）. Conclusions： IL-6 may play a significant role in the immunologic mechanism of PBC. The decline of serum IL-6levels may contribute to prompt the therapeutic effects of UDCA, but we could not assess the subsequent response to UDCA by the serum IL-6 levels independently.