Influence and curative effect observation of Montelukast on high -sensitivity C-reactive protein, interleukin-4 and tumor necrosis factor-α levels of cough variant asthma patients

Objective To discuss the influence and curative effect observation of Montelukast on high-sensitivity Creactive protein(hs-CRP),interleukin-4(IL-4) and tumor necrosis factor-α(TNF-α) levels of cough variant asthma patients.Methods 68 cases of cough variant asthma patients from February 2012 to February 2013 collected by Taizhou Integration of Traditional and Western Medicine Hospital were selected and divided into Montelukast group and control group.The patients in two groups were given the inhibition of Salmeterol/Fluticasone Propionate one suc tion per time,for 2 times daily.The patients in Montelukast group were given 10 mg Montelukast dulcets through the mouth one time daily for 12 weeks.The changes of serum hs-CRP,IL-4 and TNF-α levels of patients in two groups before and after medical treatment were observed,and the clinical curative effect and untoward effect observation were carried on as well.Results After 12 weeks' medical treatment,the serum hs-CRP,IL-4 and TNF-α levels of patients in two groups declined obviously than before(t = 3.16,3.57,2.87,2.27,2.43,1.35,P 0.01 or P 0.05),and the declining rate in Montelukast group was much higher than that in control group(t = 2.35,2.39,2.15,P 0.05).Meanwhile,the total clinical efficiency in Montelukast group(94.12%) was much higher than that in control group(76.47%)(χ2=4.22,P 0.05).2 and 5 cases of untoward effect appeared in control group(5.88%) and Montelukast group(14.71%) respectively with light symptom but not serious drug adverse reaction(DAR).After comparing the DAR oc currence rates in two groups,there was no statistically significant difference(χ2=0.64,P 0.05).Conclusion Montelukast has reliable clinical curative effect on cough variant asthma patients with security,whose mechanism of action has close effect on reducing the hs-CRP,IL-4 and TNF-α levels,and the inhibition of airway inflammation.