摘要目的通过研究胆固醇结石患者胆囊胆汁中凝血纤溶状态与交联纤维蛋白生成和降解的关系来探讨胆囊结石的形成机制。方法收集胆固醇结石(简称胆石)患者胆囊胆汁20份和非胆囊结石患者胆囊胆汁15份，测定胆汁中的纤维蛋白特异性降解产物D-二聚体抗原和部分凝血纤溶因子抗原和活性水平。结果胆囊结石组患者胆汁中D-二聚体抗原高于非胆囊结石组（P＜0.01），抗凝血酶Ⅲ抗原高于非胆囊结石组（P＜0.05），抗凝血酶Ⅲ活性低于非胆石组（P＜0.05），胆石组抗凝血酶Ⅲ抗原与活性之比与非胆石组相比明显增高（P＜0.01），胆石组纤溶酶活性较非胆石组增高（P＜0.05），纤溶酶活性与凝血活性指标之比明显低于非胆石组（P＜0.05），两组间纤溶酶原激活物抑制物活性差异无显著性。结论胆固醇结石患者胆囊胆汁中的凝血和纤溶活性均高于非胆石组，但纤溶活性增高的程度与凝血活性相比则明显减低，从而使交联纤维蛋白的生成增多，而降解相对减少，导致成石组胆囊胆汁中交联纤维蛋白积累，促进胆囊结石的形成。

abstractsObjective　To study the effects of coagulatic and fibrinolytic activities on production and degradation of fibrin in normal and calculous human bile.　Methods　Coagulatic and fibrinolytic components and D-Dimer antigen were studied in the biles of patients with gallstones (20 patients) compared with those without gallstones (15).　Results　D-Dimer was significantly higher in gallstones group than in controls (median 1.260 mg/L, vs. 0.234 mg/L, P＜0.01). the concentration of antithronbin Ⅲ antigen (AT-Ⅲ: Ag) was higher in the biles of patients with gallbladder stones than those without gallstones (median 425.45 mg/L, vs. 163.64, P＜0.05). On the contrary, the activity of antithrombin Ⅲ (AT-Ⅲ: Ac) was lower than in controls (median 115.73%, vs. 162.65%, P＜0.05). There was a significant difference in the ratio of AT-Ⅲ：Ag to AT-Ⅲ：Ac in both groups (median 8.47, vs. 0.97, P＜0.01). The activity of plasmin (Plm:Ac) was greater in gallbladder bile of calculous patients than in that of those without gallstones (median 62.83%, vs. 49.95%, P＜0.05), but the ratio of fibrinolytic activity to coagulatic activity was much lower in patients with gallbladder stones than in those without gallstones (median 7.4, vs. 38.6, P＜0.02). There was no significant difference in the activity of plasminogen activator inhibitor (PAI: Ac) in both groups (median 0.368%, vs. 0.678%).　Conclusions　Both coagulatic and fibrinolytic activities were much greater in patients with gallbladder stones than in those without gallstones, but the increment of fibrinolytic activity was lower than that of coagulatic activity. Then the production of crosslinked fibrin would be reinforced in the gallbladder bile of patients with gallstones. Simultaneously, the degradation of crosslinked fibrin also increased in gallstone patients, resulting from the soaring of the fibrinolytic activity. But the increment of degradation was relatively lower then that of the production of crosslinked fibrin. As a result, the crosslinked fibrin would accumulate in patients with gallstones and accelerate the formation of gallstones as a fibrillar network by capturing the sediments of cholesterol and other substance.