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肿瘤坏死因子-α基因多态性在重症急性胰腺炎患者中的意义
作者姓名:Zhang D  Li J  Jiang Z  Yu B  Tang X
作者单位:210002,南京大学医学院,南京军区南京总医院普通外科研究所
基金项目:全军“十五”医药卫生重点课题基金资助项目(0 13 0 12 )
摘    要:目的 观察肿瘤坏死因子 (TNF α)基因启动子区域中 - 30 8基因多态性即TNF2及外周血浆TNF α、TNF受体浓度与重症急性胰腺炎 (ASP)及其并发症———严重脓毒症之间的关系。方法 本研究组包括 72例ASP患者和 74个正常人 ,采用聚合酶链反应 (PCR)、NcoI消化及电泳技术检测其多态性。ASP患者血浆TNF α、可溶TNF受体 (sTNF RⅠ和sTNF RⅡ )浓度检测用EASIA法。结果 (1)TNF2出现的频率在ASP组为 2 1例 (2 9 2 % ) ,对照组为 19例 (2 5 7% ) ,两组差异无显著意义 (P>0 0 5 )。ASP组有 2 6例并发严重脓毒症 ,TNF2出现频率 12例 (46 2 % ) ;而无严重脓毒症组为 9例(19 6 % )。TNF2出现的频率在严重脓毒症组显著高于无并发严重脓毒症组 (P <0 0 5 )。 (2 )在严重脓毒症组 ,血浆基础TNF α、sTNF RⅠ和sTNF RⅡ浓度分别为 36± 30 (ng/L)、5 4± 3 5、11 2± 7 9(μg/L) ,无并发严重脓毒症病人分别为 30± 2 5 (ng/L) ,4 6± 3 8、8 8± 6 6 (ng/L) ,两组比较差异均无显著意义 (P >0 0 5 )。 (3)重症胰腺炎患者中 ,TNF2组血浆基础TNF α浓度为 37± 31(ng/L) ,TNF1组为 31± 2 5 (ng/L) ,两组差异无显著意义 (P >0 0 5 )。结论 TNF2与ASP的发生无关 ,但与其导致的严重脓毒症的易感性有关。血浆基础T

关 键 词:重症急性胰腺炎  肿瘤坏死因子α  肿瘤坏死因子受体  基因多态性  脓毒症  并发症  SAP
修稿时间:2002年4月29日

Significance of tumor necrosis factor-alpha gene polymorphism in patients with acute severe pancreatitis
Zhang D,Li J,Jiang Z,Yu B,Tang X.Significance of tumor necrosis factor-alpha gene polymorphism in patients with acute severe pancreatitis[J].National Medical Journal of China,2002,82(22):1529-1531.
Authors:Zhang Dianliang  Li Jieshou  Jiang Zhiwei  Yu Baojun  Tang Xingming
Affiliation:Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210002, China.
Abstract:OBJECTIVE: To investigate the relation of the frequency of TNF2 allele, a TNF-alpha promoter polymorphism, and plasma concentrations of TNF-alpha and soluble tumor necrosis receptor (sTNF-R) to acute severe pancreatitis (ASP) and its severe complication--sepsis. METHODS: The DNA samples of peripheral white blood cells of 72 ASP patients, 16 of them being complicated by severe sepsis and the other 46 cases being without sepsis, and 89 healthy volunteers were extracted. PCR, NcoI digestion, and electrophoresis were used to examine the polymorphism of the TNF-alpha gene promoter region -308. Plasma concentrations of TNF-alpha, sTNF-R I and sTNF-R II were measured by EASIA. RESULTS: The TNF2 allele frequency of ASP patients was 29.2% (21/72), not significantly different from that of healthy volunteers (25.7%, 25/89) (P > 0.05). The prevalence rate of TNF2 was 46.2% in patients with severe sepsis, significantly higher than that of the patients without asepsis (19.6%, P < 0.05). The plasma levels of TNF-alpha, sTNF-R I, and sTNF-R II were 36 +/- 30 ng/L, 5.4 +/- 3.5 micro g/L, and 11.2 +/- 7.9 micro g/L respectively in patients with ASP, not significantly different from those in the healthy controls (30 +/- 25 ng/L, 4.6 +/- 3.8 micro g/L, and 8.8 +/- 6.6 micro g/L respectively, P > 0.05). There was no significant difference in baseline TNF-alpha levels between the TNF2 group and TNF1 group (37 +/- 31 ng/L vs. 31 +/- 25 ng/L, P > 0.05). CONCLUSION: TNF-2 is not related to the pathogenesis of ASP, and is associated with the susceptibility to severe sepsis complicating ASP. The baseline TNF-alpha and sTNF-R levels have little value in predicting the development of severe sepsis.
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