史立宏,房春燕,李晓民,李金勇,牟华光.抗过敏冲剂治疗慢性荨麻疹及其对血清RANTES、Eotaxin和TNF-α水平的影响[J].,2009,(10):925-928 |
抗过敏冲剂治疗慢性荨麻疹及其对血清RANTES、Eotaxin和TNF-α水平的影响 |
Therapeutic Effect of Anti-anaphylaxis Granule on Chronic Urticaria and Its Impact on Serum Levels of RANTES,Eotaxin and TNF-α |
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DOI: |
中文关键词: 抗过敏冲剂 慢性荨麻疹 调节激活正常T细胞表达和分泌的细胞因子 嗜酸粒细胞趋化因子 肿瘤坏死因子-α |
英文关键词:Anti-anaphylaxis Granules chronic urticaria regulated upon activation normal T cell expressed and secreted eosinophil chemotactic factor tumor necrosis factor-α |
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中文摘要: |
目的观察抗过敏冲剂对慢性荨麻疹患者的疗效及其对血清调节激活正常T细胞表达和分泌的细胞因子(regulated upon activation normal T cell expressed and secreted,RANTES)、嗜酸粒细胞趋化因子(Eotaxin)、肿瘤坏死因子-α(TNF-α)水平的影响。方法将51例慢性荨麻疹患者随机分为抗过敏冲剂组与西替利嗪组,采用ELISA法检测两组治疗前后血清RANTES、Eotaxin及TNF-α水平,并观察疗效。结果抗过敏冲剂组有效率88.5%,西替利嗪组有效率64.0%,两组比较差异有统计学意义(P<0.05);且抗过敏冲剂组复发率[5.6%(1/18)]低于西替利嗪组[41.7%(5/12)],两组比较差异有统计学意义(P<0.05)。慢性荨麻疹患者血清RANTES、Eotaxin及TNF-α水平较健康组明显升高(P<0.01),抗过敏冲剂能显著降低患者血清中过高的RANTES、Eotaxin与TNF-α水平(P<0.01)。结论抗过敏冲剂对慢性荨麻疹具有良好的疗效,调节RANTES、Eotaxin与TNF-α的血清水平可能是其作用机制。 |
英文摘要: |
Objective To investigate the therapeutic effect of Anti-anaphylaxis Granule(AAG)on chronic urticaria and its impact on cytokine of regulated upon activation of normal T cells expressed and secreted(RANTES),eosinophil chemotactic factor(Eotaxin)and tumor necrosis factor-α(TNF-α).Methods The therapeutic effects of AAG and cetirizine on chronic urticaria patients allocated in two groups were observed respectively,and the serum levels of RANTES,Eotaxin and TNF-α in patients were measured by ELISA before and after treatment,and were compared with those in normal subjects.Results The therapeutic effects of AAG group were better in effective rate(88.5% vs 64.0%)and lower in the recurrent rate(5.6% vs 41.9%)than those of cetirizine(all P<0.05).Serum levels of RANTES,Eotaxin and TNF-α in patients were higher than those in normal subjects(P<0.01),and they could be significantly reduced after AAG treatment(P<0.01).Conclusion AAG has favorite effect for treatment of chronic urticaria,its regulation on serum levels of RANTES,Eotaxin and TNF-α may be the mechanism of action. |
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