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目的:探讨孟鲁斯特在特发性肺纤维化(idiopathic pulmonary-fidrosis,IPF)的作用。方法:采用随机、对照的方法,将60例IPF患者分为2组,2组患者给予相同的基础治疗(吸氧、抗感染、化痰、止咳、平喘治疗),治疗组在基础治疗上加用孟鲁斯特片10mg,每晚口服1次,疗程均为6个月;对照组在基础治疗上加用口服甲泼尼松片0.4mg·kg-1·d-1,4周后减量为0.2mg·kg-1·d-1,连续8周之后再减量为4mg·d-1,3个月。治疗前、治疗后3个月和6个月分别记录临床症状、体征;肺部CT;肺功能;动脉血气分析;白介素-2(IL-2)、白介素-4(IL-4)、白介素-8(IL-8);6min步行距离及不良反应等。结果:治疗3,6个月后治疗组临床症状、体征改善均明显优于对照组,组间差异有显著性(P<0.01),总疗效治疗组明显优于对照组(P<0.01);治疗后3,6个月肺功能和PaO2二组都有明显改善(P<0.05),但治疗6个月与3个月比较肺功能和PaO2没有进一步的改善;治疗后治疗组纠正缺氧明显优于对照组(P<0.05),但2组改善肺功能无明显差异;2组患者在治疗前IL-2、IL-4、IL-8增高,治疗3,6个月后在治疗组IL-2、IL-4、IL-8有明显改善(P<0.01),作用明显优于对照组(P<0.01);治疗后3,6个月6min步行距离2组都有明显提高(P<0.01);治疗组明显优于对照组(P<0.01);对照组中有3例出现血糖轻度升高,5例出现兴奋、失眠,而治疗组未见不良反应发生。结论:孟鲁斯特能阻断花生四烯酸脂氧化酶通路,抑制白三烯产生的肺泡炎、成纤维细胞迁移、增殖和细胞外基质的形成。从而改善临床症状提高生活质量,但不能逆转已形成的纤维化。说明孟鲁斯特通过调节细胞因子网络可能为肺纤维化的更有效治疗带来一定的希望。
Objective: To investigate the effect of monastus on idiopathic pulmonary-fidrosis (IPF). Methods: Sixty patients with IPF were divided into two groups according to a randomized and controlled method. The two groups were given the same basic treatment (oxygen, anti-infection, phlegm, cough and asthma). The treatment group was treated on the basis of basic treatment Plus montelukast tablets 10mg, oral once a night, treatment were 6 months; the control group in the basic treatment plus oral methyl prednisone tablets 0.4mg · kg-1 · d-1, 4 weeks The reduction was 0.2 mg · kg-1 · d-1, then reduced to 4 mg · d-1, 3 months after 8 consecutive weeks. Clinical symptoms and signs were recorded before treatment, 3 months and 6 months after treatment. CT, pulmonary function, arterial blood gas analysis, interleukin-2, interleukin-4, interleukin- 8 (IL-8); 6min walking distance and adverse reactions. Results: After treatment for 3 and 6 months, the clinical symptoms and signs of the treatment group were better than those of the control group. There was significant difference between the two groups (P <0.01). The total curative effect was better in the treatment group than in the control group (P <0.01). After 3 and 6 months of treatment, lung function and PaO2 were significantly improved in both groups (P <0.05), but no significant improvement in lung function and PaO2 was observed at 6 and 3 months after treatment IL-2, IL-4 and IL-8 were significantly higher in the two groups before treatment than those in the control group (P <0.05), but no significant difference was found between the two groups in improving lung function 2, IL-4 and IL-8 were significantly improved (P <0.01), and the effect was significantly better than that of the control group (P <0.01) 0.01). The treatment group was significantly better than the control group (P <0.01). In the control group, 3 patients had slight increase of blood glucose, 5 patients showed excitement and insomnia, while no adverse reaction occurred in the treatment group. CONCLUSION: Montelukast can block arachidonic acid oxidase pathway, inhibit leukotriene-induced alveolitis, fibroblast migration, proliferation and extracellular matrix formation. Thus improving clinical symptoms and improving quality of life, but can not reverse the formation of fibrosis. This suggests that Montelukast may provide some hope for more effective treatment of pulmonary fibrosis by regulating the network of cytokines.