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盐酸氨溴索对慢性阻塞性肺疾病急性加重期IL-6及TNF-α的作用

Effects of ambroxol hydrochloride on serum IL-6 and TNF-α in patients with acute exacerbation of chronic obstructive pulmonary disease
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摘要 目的探讨盐酸氨溴索对慢性阻塞性肺疾病(COPD)急性加重期白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)的作用。方法选择2006年10月至2007年11月住院的慢性阻塞性肺疾病急性加重期患者共72例,根据治疗方案的不同分为A组(治疗组,38例)和B组(常规组,34例),另选择30例健康者为C组(对照组)。B组给予低流量吸氧、控制感染等常规治疗,A组除常规治疗外,加用盐酸氨溴索60 mg,2次/d静脉点滴或雾化吸入治疗,两组疗程均为2周左右,达临床稳定期标准。分别观察各组治疗前、后血清IL-6、TNF-α水平。结果①A组、B组治疗后血清IL-6、TNF-α水平均低于治疗前,差异有统计学意义(P<0.01)。A组治疗后血清IL-6、TNF-α低于B组,两组比较差异有统计学意义(P<0.05);②A组、B组治疗前、后血清IL-6、TNF-α水平均高于C组,差异有统计学意义(P<0.01)。结论盐酸氨溴索能够抑制COPD患者血清IL-6、TNF-α的释放,协同抗感染,对COPD患者的急性期有较好的治疗作用。 Objective To investigate the effect of ambroxol hudrochloride on IL-6 and TNF-α in patients with acute exacerbation of chronic obstructive pulmonary disease.Methods Seventy-two patients with AECOPD in October 2006 to November 2007 were enrolled.According to the different treatment,all patients were divided into treatment group(group A,38 cases) and conventional group(group B 34 cases).Thirty healthy people were the control group(group C).In conventional group low-flow oxygen,infection control and other conventional treatment were given.In treatment group routine therapy were given and ambroxol 30 mg inhalation or intravenous drip two times every day.Course of treatment continued about two weeks.The level of IL-6 and TNF-α in serum before-and-after therapy in all groups were detected.Results ①The level of IL-6 and TNF-α in serum of the two groups after therapy were lower than before therapy,with significant differences(P0.01).②The level of IL-6 and TNF-α in serum before-and-after therapy in the two groups were higher than that in the control groups,with significant differences(P0.01).Conclusion Ambroxol can restraint the releasing of IL-6 and TNF-α in serum and have a better therapeutic effect on COPD patients in the acute phase.
出处 《临床医学》 CAS 2010年第9期15-16,共2页 Clinical Medicine
关键词 慢性阻塞性肺疾病 盐酸氨溴索 白细胞介素-6 肿瘤坏死因子-Α Chronic obstructive pulmonary disease Ambroxol hydrochloride Interleukin-6 Tumor necrosis factor-α
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