摘要
目的探讨清胰汤对重症急性胰腺炎(SAP)并发感染患者单核细胞HLA—DR表达的影响。方法33例SAP合并感染患者随机分成3组:SAP并发感染组(Ⅱ组)、GM-CSF治疗组(Ⅲ组)、清胰汤治疗组(Ⅳ组);选取7例SAP未并发感染患者为对照组(Ⅰ组);各组均予常规治疗,Ⅲ、Ⅳ组在常规治疗基础上加用GM-CSF或清胰汤治疗,一周后检测外周血WBC,血淀粉酶,ET,CRP,IL-6以及单核细胞HLA—DR表达率。结果Ⅱ、Ⅲ、Ⅳ组患者在各项血清学指标均高于Ⅰ组,单核细胞HLA-DR表达水平低于Ⅰ组(P〈0.05);而Ⅲ、Ⅳ组患者各项指标较Ⅱ组明显改善(P〈0.05)。结论SAP并发感染患者存在单核细胞免疫功能缺陷,而清胰汤治疗能够改善这种免疫功能障碍以及过度炎症反应。
Objective To investigate the effect of Qingyi decoction on HLA-DR expression of the monocytes in the infectious patients with severe acute pancreatitis ( SAP ) . Method 33 infectious patients with SAP were randomly divided into three groups: SAP complicated by infection group ( Ⅱ ) , SAP complicated by infection treated by GM-CSF ( Ⅲ) , SAP complicated by infection treated by Qingyi decoction ( Ⅳ ) . Besides, 7 SAP patients without infection were recruited to control group ( Ⅰ ). All patients received routine comprehensive treatment after hospitalization, while group Ⅲ and group Ⅳ patients additionally received GM-CSF or Qingyi decoction as an adjutant therapy. All groups were treated for 7 days. The peripheral blood WBC, amylase, ET, IL-6, CRP were detected, and HLA-DR expression of monocytes were detected. Result The HLA-DR expression level of group Ⅱ, group Ⅲ and group IV patients were lower than groupⅠ ( P〈0.05 ) , and the every serum index in them were higher than group Ⅰ ( P〈0.05 ) . Compared with the patients in group Ⅱ, the every serum index and the HLA-DR expression level of patients in groupllI and group IV were ameliorated ( P〈0.05 ) . Conclusion Monocyte anergy is present in patients with severe acute pancreatitis, and SAP patients with infection are more severe. Furthermore, the treatment of Qingyi decoction can ameliorate monocytes-mediated immune function of SAP patients with infection and soften excessive inflammatory response.
出处
《浙江临床医学》
2014年第1期16-18,共3页
Zhejiang Clinical Medical Journal
基金
浙江省卫生厅资助项目(2013RCA039)
关键词
清胰汤
重症急性胰腺炎合并感染
单核细胞免疫功能
人类白细胞抗原DR
炎症反应
Qingyi decoction Severe acute pancreatitis with infection Monocytes-mediated immune function
human leukocyte antigen DR inflammatory response