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慢性肝病患者肠道通透性和炎症因子变化的研究

     

摘要

目的 探讨慢性肝病患者肠黏膜屏障及炎症细胞因子的变化.方法 收集各种慢性肝病患者和正常人的血清,统一采用酶联免疫吸附法和改良分光光度法检测血清D-乳酸(D-Lac)、二胺氧化酶(DAO)、内毒素(ET)、降钙素原(PCT)和肿瘤坏死因子(TNF)水平.结果 各组患者人口学特征无明显差别(P>0.05),从肝炎病毒携带者到慢性重型肝炎,患者血清中D-Lac(从1.52±0.29 μg/ml至4.07±0.43μg/ml).DAO(从1.22±0.34 u/ml至4.07±0.42 μ/ml),ET(从1.39±0.27 pg/ml至25.51±4.42 pg/ml),PCT(从1.22±0.34μg/ml至23.17±5.28 μg/ml) 水平逐渐升高(P<0.05);同样肝硬化失代偿期血清D-Lac,DAO.ET,PCT和TNF-α的水平(4.28±O.70μg/ml,3.64±0.53 u/ml,18.14±3.98 pg/ml,18.75±3.84 μgd和27.12 4±4.64 ng/ml)也较代偿期高(1.93±0.40 μg/ml,1.82±0.58 u/ml,13.03±2.44 pg/ml,2.44±O.52μg/ml和14.73±2.60ng/ml)(P<0.05);酒精性肝病患者血清D-Lac,DAO,ET,PCT和TNF-α的水平(3.35±O.55μg/ml 3.03±0.42 u/ml,14.30±4.06 pg/ml,17.99±3.75μg/ml和32.46±6.84 ng/ml)也高于正常对照(1.68±0.41μg/ml,1.08±0.32u/ml,1.40±O.28pg/ml,1.29±0.25 μg/ml和11.14±1.74 ng/ml)(P<0.05),但较慢性重型肝炎和肝硬化失代偿期低(P<0.05).结论 随着肝损伤程度的加重,慢性肝病患者肠黏膜屏障的通透性,炎症反应和细胞因子同时升高,与肝损伤之间形成恶性循环.%Objective To investigate the alterations of intestinal permeability and serum inflammatory cytokines in patients with chronic liver disease. Method Various chronic liver disease patients were enrolled in this study. The serum samples were taken and cryopreseryed at - 30 ℃. Serum levels of D-lactate(D-Lac),diamine oxidase(DAO), endotoxin(ET), procalcitonin(PCT) and tumor necrosis factor α(TNF-α) were determined by enzyme linked immunosorbent assay(ELISA) and improved spetrophotometry. Results There were no differences in demography characteristics among these groups (P > 0.05). From hepatitis virus caniers to patients with chronic severe hepatitis, the levels of D-Lac(from 1.52 ± 0.29 μg/ml to 40± 0.43 μg/ml). DAO (from 1.22 ± 0.34 μ/ml to 4.07 ± 0.42 μ/ml), ET (from 1.39 ± 0.27 pg/ml to 25.51 ± 4.42 pg/ml), PCT (from 1.22 ± 0.34 μg/ml to 23.17 ± 5.28 μg/ml) were gradually elevated. On the other hand. levels of D-Lac, DAO,ET, PCT and TNFα in patients with decompensated liver cirrhosis(4.28 ± 0.70 μg/ml, 3.64 ± 0.53 μ/ml, 18. 14 ± 3.98 pg/ml, 18.75 ± 3.84 μ g/ml and 27.12 ± 4.64 ng/ml, respectively)were higher than patients with compensated liver cirrhosis (1.93 ± 0.10 μg/ml, 1.82 ± 0.58 μml, 13.03 ± 2.44 pg/ml. 2.44 ± 0.52 μg/ml and 14.73 ±2.60 ng/ml. respectively)(P < 0.05). The levels of D-Lac, DAO, ET, PCT and TNF-α in patients with alcoholic liver disease (3.35 ± 0.55 μg/ml. 3.03 ± 0.42 μ/ml, 14.30 ± 4.06 pg/ml, 17.99 ± 3.75 μg/ml and 32.46 ±6.84 ng/ml, respectively) were also higher than in control group(1.68 ± 0.41 μg/ml, 1.08± 0.32 μ/ml, 1.40 ±0.28 pg/ml. 1.29 ± 0.25 μg/ml and 11.14 ± 1.74 ng/ml respeaively)(P < 0.05), but lower than in chronic severe hepatitis group and decompensated liver cirrhosis group(P < 0.05). Conclusion In the chronic liver diseases, with the aggravation of the liver damage, the patient' intestinal permeabilky and inflamntory cytokines were elevated whicb contributed a vicious circle with the liver damage.

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