RESUMEN
Objective To investigate the therapeutical effect and mechanism of tiotropium bromide in patients with stable phase midrange and severe chronic obstructive pulmonary disease (COPD). Methods Seventy-eight patients with stable phase midrange and severe COPD were selected, and they were divided into observation group (40 cases) and control group (38 cases) according to treatment method. All patients were given conventional treatment. The patients in observation group were given tiotropium bromide, and the patients in control group were given terbutaline according to the needs for 12 weeks. The changes of dyspnea, 6 min walking distance, pulmonary function, leukotrienes C4 (LTC4), interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-ɑ) before and after treatment, and drug adverse reaction were observed. Results The dyspnea score after treatment in observation group was significantly lower than that in control group:(2.9±0.5) scores vs. (3.5±0.7) scores, 6 min walking distance in observation group was significantly longer than that in control group: (427.67±70.36) m vs. (365.41±61.42) m, forced expired volume in 1 second (FEV1) and FEV1/forced vital capacity in observation group were significantly higher than those in control group:(1.76±0.89) L vs. (1.29±0.53) L and (67.43±9.52)%vs. (56.32±8.51)%, LTC4, IL-8 and TNF-αlevels in observation group were significantly lower than those in control group: (397.41± 198.57)μg/L vs. (1 181.95±207.54)μg/L, (434.81±176.05) ng/L vs. (823.37±165.43) ng/L and (0.15±0.02) ng/L vs. (0.25 ±0.02) ng/L, there were significant differences ( P<0.01). Pearson correlation analysis result showed that serum LTC4 level was negatively related to FEV 1 (r=-0.578, P=0.024);and the serum IL-8 level was negatively related to FEV1 (r=-0.542, P=0.019). There was no obvious drug adverse reaction in the two groups. Conclusions Tiotropium bromide can significantly improve the clinical manifestations in patients with COPD. Tiotropium bromide may take effects by blocking various inflammatory factors release in the stable phase of COPD.