重症急性胰腺炎肠屏障功能障碍的相关研究

Pathogenesis and prevention of intestinal barrier dysfunction in severe acute pancreatitis

目的探讨重症急性胰腺炎(SAP)肠屏障功能障碍的发病机制及其防治方法。方法将2010年1月至2011年12月间我院收治的SAP患者84例随机分为研究组和对照组,每组42例,对照组患者给予禁食、解痉镇痛、胃肠减压、抗炎抗感染治疗,维持电解质和酸碱平衡,并给予奥曲肽治疗;研究组患者在此基础上给予乌司他丁20万U+5%葡萄糖250ml静滴,2次/d,病情改善后改为1次/d,治疗10d,并在入院确诊后接受微创腹腔引流加肠内营养。在治疗第1、5、7、14天分别测定两组患者TNF-α、IL-6、hs-CRP、血浆内毒素、二胺氧化酶(DAO)、尿乳果糖与甘露醇比值(L/M)、白蛋白、前白蛋白等变化。结果①治疗后两组患者TNF-α、IL-6、hs-CRP、血浆内毒素、DAO、L/M均有所下降,治疗第5、7、14天研究组上述指标明显低于对照组(P<0.05)。②治疗后研究组患者白蛋白、前白蛋白水平明显高于对照组(P<0.05)。③研究组治疗总有效率为90.5%(38/42),对照组总有效率为73.8%(31/42),两组差异有统计学意义(P<0.01)。结论炎症介质及内毒素升高在SAP肠屏障功能障碍的发病中具有重要作用,早期给予抗炎、抗酶治疗并给予微创腹腔引流加肠内营养对于提高SAP的治疗水平、改善预后、提高患者生存率有重要意义。

Objective To investigate the pathogenesis and prevention of intestinal barrier dysfunction in severe acute pancreatitis. Methods Eighty-four patients with severe acute pancreatitis were randomly divided into the study group and the control group, with 42 cases in each group. The patients in both groups were given fasting, spasm and pain, gastrointestinal decompression, anti-inflammatory and anti-infection, and as well as octreotide, to maintain electrolyte and acid-base balance. On the basis of the control group, patients in study group were given ulinastatin 200 000 U combined with 5% glucose 250 ml, twice per day, then once per day, for 10 days, as well as minimally invasive abdominal drainage and enteral nutrition. TNF-α, IL-6, hs-CRP, diamine oxidase （DAO）, lactulose and mannitol ratio （L/M）, albumin, prealbu- min on the 1st, 5st, 7st, 14th day after treatment were determined. Results After the treatment, levels of TNF-α, IL-6, hs-CRP, endotoxin, the DAO, L/M were decreased, and these parameters in the study group were significantly lower than those in the control group on the 5th, 7th, 14th day （P〈0.05）. After the treatment, albumin, prealbumin levels in study group were significantly increased （P〈0.05）. The total effective rate of the study group was 90.5% （38/42）, and the total effective rate of the control group was 73.8% （31/42）, with statistically significant difference between the two groups （P〈0.01）. Conclusion The elevated inflammatory mediators and endotoxin plays an important role in the pathogenesis of intestinal barrier dysfunction in SAP. It is important to give early anti-inflammatory, anti-enzyme therapy minimally invasive abdomi- nal drainage, and enteral nutrition for improving the prognosis and the survival rate of patientswith SAP.