Efficacy of Gushen Dingchuan Pills and Western Medicine in Treating Stable Chronic Obstructive Pulmonary Disease Patients with Syndrome of Lung and Kidney Qi Deficiency / 中国实验方剂学杂志

ABSTRACT

Objective: To observe the efficacy of Gushen Dingchuan pills combined with routine western medicine in treating stable chronic obstructive pulmonary disease (COPD) patients with syndrome of lung and kidney Qi yin deficiency, and investigate its effect on serum levels of S100 calcium binding protein A8/A9 complex (S100A8/A9), nuclear factor (NF) -κB, tumor necrosis factor (TNF) -α, interleukin (IL) -8 and IL-1β. Method:One hundred and ten stable chronic COPD patients were selected and randomly divided into control group (55 cases) and treatment group (55 cases) by the random number table. Cases of control group received routine therapy by reference to the Guidelines for Diagnosis and Treatment for Chronic Obstructive Pulmonary Disease (2013 Revision). In addition to the therapy of control group, cases of treatment group were orally given Gushen Dingchuan pills(1.5-2.0 g/time, tid). Both groups were treated for 12 weeks. Lung function, scores of symptoms of lung and kidney Qi Yin deficiency, life quality St. George's respiratory questionnaire (SGRQ) score, and the efficacy were compared between both groups. Serum levels of S100A8/A9, NF-κB, TNF-α, IL-8 and IL-1β were detected for two groups. Result:After treatment, FEV1% and FEV1/FVC of treatment group were obviously higher, while score of symptoms of lung and kidney Qi deficiency were lower than control group (Pχ2=4.777, PPκB of treatment group were obviously lower than those of control group (Pα, IL-8, IL-1β of treatment group were remarkably lower than control group after treatment (PConclusion:Gushen Dingchuan pills combined with western medicine can treat stable chronic COPD patients with syndrome of lung and kidney Qi Yin deficiency by improving lung function, alleviating symptoms of lung and kidney Qi deficiency, increasing life quality and efficacy and decreasing levels of S100A8/A9 and NF-κB inflammatory factors.