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出 处:《河南大学学报(医学科学版)》2004年第3期12-14,共3页
基 金:河南省科技厅科技攻关项目 (编号 :0 0 1170 6 2 9);开封市科技进步二等奖 (编号 :2 0 0 32 1)
摘 要:目的 :探讨肝纤维化、肝硬化不同分期时细胞因子水平变化及其对肝纤维化、肝硬化的形成、发展的影响。方法 :经肝穿刺活检证实慢性乙肝肝纤维化患者 30例、肝硬化患者 75例。肝纤维化患者分S12例、S2 4例、S3 10例、S414例 ,G13例、G2 5例、G3 10例、G412例。肝硬化患者按Child -Pugh分级A级 2 8人、B级 39人、C级 8人。对照组为 2 0例健康人。所有患者肝穿刺活检的同时 ,取血清测一氧化氮 (NO)、肿瘤坏死因子 (TNFa)、内毒素(LPS)。结果 :TNFa随肝炎程度及肝纤维化程度加重而升高 ,具等级相关。r分别为 0 .6 2 3(P <0 .0 5 )、0 .6 4 9(P <0 .0 1) ,NO等级相关性r=0 .32 8(P >0 .0 5 ) ,LPS在肝纤维化阶段尚无明显增高 ,只是在肝功能Child -Pugh分级B、C级时才显著升高。结论 :LPS早期未参与肝病的慢性损伤 ,在肝硬化时与肝功能损害互为因果 ;TNFa在慢性肝炎发展至肝硬化过程中 ,始终起着重要作用 ;Objective: To discuss liver fibrosis , alteration of cellular factors in the different stages of Liver cirrhosis and their influence on the formation and development of liver fibrosis and cirrhosis. Methods: 30 cases of chronic hepatitis B which were confirmed as fibrosis by biopsy of liver puncture, among which 75 cases were diagnosed as liver cirrhosis. The patients with liver fibrosis were classified as S 1 2 cases and S 2 4 cases and S 3 10 cases and S 4 14 cases, G 1 3 cases and G 2 5 cases and G 3 10 cases and G 4 12 cases. Patents with liver cirrhosis were classified as A stage: 28 patients, B stage: 39 patients, and C stage: 8 patients, based on Child-Pugh. 20 regular health persons were in the control group. At the same time of liver biopsy , serum was to be measured for monoxide nitrogen (NO) , the tumor putrescence factor (TNFa) , endotoxin (LPS). Results: TNFa increased as hepatitis and liver fibrosis accelerated, which was related to stages. R was 0.623 (P<0.05 ), 0.649 (P<0.01 ) respectively, NO grade correlation was r = 0.328 (P>05), LPS in liver fibrosis stage do not have yet increased obviously, only when Child-Pugh of liver function grades the B C stages LPS was higher. Conclusion: LPS does not participate in the chronic lesion of liver in the early stage of the disease. When liver is hardened with the infringement of liver function, they have the mutual cause and effect; TNFa plays an important role all along in the development of chronic hepatitis into liver cirrhosis; NO has nothing to do with liver hardening in formation and development of liver cirrhosis in the early stage.
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