Subject(s)
Bacteremia/diagnosis , COVID-19/complications , Candidemia/diagnosis , Cross Infection/diagnosis , Intensive Care Units/statistics & numerical data , Bacteremia/microbiology , COVID-19/physiopathology , Candidemia/microbiology , Critical Illness , Cross Infection/microbiology , Female , Humans , Male , Middle AgedABSTRACT
INTRODUCTION: Although smoking cessation is strongly indicated by international guidelines as an effective therapeutic tool for patients with COPD and Asthma, a large proportion of them do not quit smoking and they are regarded as a "difficult" target group. AIM: To study the effectiveness of an intensive smoking cessation program in smokers with COPD and asthma under real-life conditions. METHODS: 166 smokers with COPD, 120 smokers with asthma and 1854 control smokers attended the smoking cessation program in the out-patient patient Smoking Cessation Clinic of the Pulmonary Department in Athens University. Continuous Abstinence Rate (CAR) was evaluated in 3, 6, 9 and 12 months after the target quit date. RESULTS: Short-term CAR (in 3 months) was 49.4% for COPD smokers, 51.7% for asthmatic smokers and 48.0% for the control group of smokers. 12 months after the initial visit the CAR was 13.9%, 18.3% and 15.9%, respectively. No statistically significant differences between groups at any study period were found. Smokers with good compliance with the program had higher long-term CAR after 12 months: 37.7% in COPD smokers, 40.0% in asthmatic smokers and 39.3% in control smokers. High CAR was observed at all stages of COPD severity. CONCLUSION: The results support the view that smokers with respiratory obstructive airway diseases of any severity should be offered an intensive smoking cessation program with regular and long-term follow-up. This will help them to achieve high abstinence rates and prevent relapses.
Subject(s)
Asthma/etiology , Pulmonary Disease, Chronic Obstructive/etiology , Smoking Cessation/methods , Smoking/adverse effects , Adult , Aged , Asthma/physiopathology , Asthma/therapy , Attitude to Health , Female , Forced Expiratory Volume/physiology , Humans , Male , Middle Aged , Motivation , Patient Compliance , Program Evaluation , Pulmonary Disease, Chronic Obstructive/physiopathology , Pulmonary Disease, Chronic Obstructive/therapy , Retrospective Studies , Severity of Illness Index , Smoking Prevention , Vital Capacity/physiologyABSTRACT
Leukotriene E(4) (LTE(4)) is implicated in asthma pathophysiology and possibly in chronic obstructive pulmonary disease (COPD) as one of the causes of persistent bronchoconstriction and mucus hypersecretion. Cigarette smoking stimulates cysteinyl leukotrienes (CysLTs) production. We investigated whether LTE(4) is equally increased in asthma and COPD and whether smoking significantly affects LTE(4) levels. Secondary outcomes involved correlations with inflammatory and functional parameters. We studied 40 patients with COPD [20 smokers], 40 asthmatics [20 smokers] and 30 healthy subjects [15 smokers]. Spirometry (FEV(1)% pred., FEV(1)/FVC) was performed, urine was collected for measurement of LTE(4) and creatinine, induced sputum was collected for differential cell counts and serum for ECP. LTE(4)/creatinine levels (pg/mg) [mean (sd)] were increased in asthmatic patients compared to COPD and controls, [125.6(54.5) vs. 54.5(19) vs. 55.9(18.9)pg/mg, respectively, P<0.0001 for asthma]. Smoking significantly affects LTE(4) levels only in asthmatic patients [164 (48) vs. 87 (26.3), P<0.0001 for smokers]. The only significant correlation was between eosinophils in induced sputum and LTE(4)/creatinine levels in asthmatics. In conclusion, patients with asthma presented higher LTE(4) values compared to normals and patients with COPD. Smoking significantly affects LTE(4) values only in asthmatics indicating a different underlying CysLTs inflammatory process in this condition.
