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作 者:金俊哲[1] 吴硕东[1] 苏洋[1] 张振海[1] 张立魁[1] 孔静[1]
机构地区:[1]中国医科大学附属二院普外二科,辽宁省沈阳市110004
出 处:《世界华人消化杂志》2006年第7期727-730,共4页World Chinese Journal of Digestology
摘 要:目的:探讨肠胆反流与胆色素结石形成间的相关性及其可能的作用机制.方法:胆囊息肉组(n=10),胆囊结石组(n= 27)和胆管结石组(n=11)患者48例,术中穿刺获得胆汁标本,行胆汁细菌培养及内毒素测定.另外,胆囊切除、胆道探查、T管引流术后患者41例根据核素检查有无肠胆反流分为反流组(n=16)及无反流组(n=25),随机选择其中26例,比较两组患者胆汁淀粉酶、脂肪酶及β-葡萄糖醛酸酶活性.结果:胆囊息肉组、胆囊结石组、胆管结石组细菌培养阳性率分别为0%,0%,81.8%;胆汁内毒素水平分别为(0.003±0.004)×10-6、 (0.01±0.02)×10-6、(10.12±4.49)×10-6 EU/L: 胆管结石组细菌培养阳性率和胆汁内毒素水平明显高于前两组(P<0.01).16/41例患者检测到十二指肠胆道反流(39.02%),反流组淀粉酶、脂肪酶和外源性β-葡萄糖醛酸酶显著高于无反流组(79 891±91 152 nkat/L vs 582 ±928 nkat/L,P<0.01:86 110±58 255 nkat/ L vs 6 124±7 500 nkat/L,P<0.01;27 789± 13 849 nkat/L vs 15 369±7 533 nkat/L,P<0.01).结论:十二指肠胆道反流可能通过细茵、内毒素、淀粉酶、脂肪酶和外源性β-葡萄糖醛酸酶活性改变,在胆色素结石的形成中发挥作用.AIM: To investigate the possible action and mechanism of duodenal-biliary reflux in the pathogenesis of bile duct pigment gallstone. METHODS: Forty-eight patients were divided into three groups: polyp of gallbladder (PG, n = 10), cholecystolithiasis (CH, n = 27) and calculus of bile duct (CBD, n = 11). Bile samples were collected during operation for bacterial culture and endotoxin examination. Forty-one patients received T tube drainage after cholecystectomy and choledochotomy were divided into reflux (n = 16) and non-reflux group (n = 25) according to radionuclide examination. The activity of biliary amylase, lipase and 13-glucuronidase were detected in 26 of the 41 patients. RESULTS: The positive rate of bacterial culture was 0% in PG group, 0% in CH group and 81.8% in CBD group, and the level of endotoxin in bile was (0.003 ± 0.004) × 10^-6, (0.01 ± 0.02) × 10^-6, and (10.12 ± 4.49) × 10^-6 EU/L the above corresponding group, respectively. Compared with those in the former two groups, the positive rate and endotoxin level were higher in the latter CBD group (P 〈 0.01). Sixteen patients showed duodenal-biliary reflux (39.02%) among 41 patients. The activities of biliary amylase, lipase and exogenous β-glucuronidase in reflux group was significantly higher than those in non-reflux group (amylase: 79 891 ± 91 152 nkat/L vs 582± 928 nkat/L, P 〈 0.01; lipase: 86 110 ± 58 255 nkat/L vs 6 124 ± 7 500 nkat/L, P 〈 0.01; β-glucuronidase: 27 789 β 13 849 nkat/L vs 15 369 β 7 533 nkat/L, P 〈 0.01). CONCLUSION: Duodenal-biliary reflux can promote the formation of pigment gallstone through bacteria, endotoxin, amylase, lipase and exogenous β-glucuronidase.
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