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Resumen: Objetivo: Determinar la tasa de decepción o concordancia entre la respuesta de los pacientes con enfermedad pulmonar obstructiva crónica (EPOC) sobre su hábito tabáquico y la medición del mismo por cooximetría en una consulta monográfica EPOC. Diseño: Estudio observacional prospectivo para determinar la concordancia entre los valores de cooximetría y la respuesta a entrevista clínica sobre hábito tabáquico. Emplazamiento: Consulta monográfica de EPOC, Neumología, Sevilla. Participantes: Pacientes con diagnóstico confirmado de EPOC en cualquier grado. Intervenciones: Entrevista clínica y medición de monóxido de carbono mediante cooximetría. Mediciones principales: Valores de cooximetría, respuestas sobre hábito tabáquico, variables sociodemográficas. Resultados: Se incluyó un total de 169 pacientes (n: 169) de los cuales, 107 presentaron valores menores o iguales 6 ppm frente a 62 con valores mayores a 6 ppm, determinando una prevalencia de tabaquismo activo del 36,7%.La tasa de decepción fue del 19,5% del total de la muestra (24,3% de entre todos los que afirmaban no fumar), con una kappa de Cohen de 0,48 y p < 0,000. El 40% de los pacientes confesó no haber dicho la verdad.No se encontró ninguna relación de este dato con la edad, el consumo acumulado de tabaco ni el FEV1. Se halló una relación significativa con el sexo (tasa de decepción: 31,8% en las mujeres vs. 15,2% en los hombres, p 0,017). Conclusiones: A pesar de nuestros intentos para que los pacientes dejen de fumar, la tasa de decepción en nuestra consulta fue considerable, mayor entre las mujeres, exfumadores recientes o en proceso de abandono, por lo que sería fundamental incorporar medidas objetivas como el cooxímetro en el abordaje de este tipo de pacientes. Summary: Objective: To determine the deception rate or concordance between the interview on smoking and cooximetry in COPD patients from a monographic consultation. Design: Prospective observational study to evaluate the concordance between the values of cooximetry and the response to a clinical interview on smoking. Setting: COPD monographic consultation, Pneumology, Seville. Participants: Patients with a confirmed diagnosis of COPD in any degree. Interventions: Clinical interview and measurement of carbon monoxide by cooximetry. Main measurements: Cooximetry values, responses on smoking, sociodemographic variables. Results: n: 169. 107 patients presented values less than or equal to 6 ppm compared to 62 with values greater than 6 ppm, determining a prevalence of active smoking of 36.7%.The deception rate was 19.5% of the total sample (24.3% of all those who claimed not to smoke), with a Cohen kappa of 0.48 and p < 0.000. 40% of patients confessed not having told the truth.No relationship of this data was found with age, accumulated tobacco consumption or FEV1. A significant relationship with sex was found (deception rate: 31.8% in women vs. 15.2% in men, p 0.017). Conclusions: In spite of our attempts to make patients stop smoking, a considerable deception rate was found in our consultation; higher among women, recent ex-smokers or in the process of abandonment, so it would be essential to incorporate objective measures such as the cooximeter in the approach of this type of patient.

Objective: Smoking is a modifiable cardiovascular risk factor closely related to arterial stiffness (AS). However, data are lacking regarding the chronic effects of smoking on AS, especially in ex-smoker (ES) who faces remnant cardiovascular risk when compared to never-smokers (NS). Methods: Among 1722 health screening participants, we retrospectively evaluated 652 healthy men with different smoking history [240 current smoker (CS) vs. 228 ES vs. 184 NS]. To assess AS, augmentation index (AIx), pulse pressure amplification (PPamp), and carotid-femoral pulse wave velocity (cfPWV) were measured and compared. Results: Baseline characteristics were similar except age and triglyceride level. AIx was lowest in NS, followed by ES, and was highest in CS. PPamp was highest in NS, lowest in CS, and ES was of intermediate level. The differences were more robust after adjustment for baseline covariates (AIx, p = 0.005; PPamp: p = 0.001). On the other hand, no significant intergroup difference was observed for cfPWV in our middle-aged population. With the regression analyses revealing an independent association between smoking duration and AS in ES, subgroup analysis demonstrated that long-term ES (smoking duration ≥20 years) had significantly higher AS than short-term ES (

Abstract Background Tobacco smoking is a recognized risk factor for many chronic diseases and previous study evidences have indicated that smokers receive smoking cessation service after the diagnosis of chronic diseases increases successful rate in quitting. But the prevalence of tobacco related chronic diseases (TCD) among smokers, as well as the role of TCD diagnosis in smoking cessation is still unclear in China. Methods From June 2016 to December 2017, we sampled 36, 698 residents aged over 18 years by a three stage sampling in Songjiang district, Shanghai. We conducted a cross-sectional study to understand the prevalence of TCD among smokers, and the role of TCD diagnosis in smoking cessation among ex-smokers as well as the smoking cessation attempt among current smokers. Results Over all, the prevalence of current smoking is 19.78% (48.36% for male and 0.22% for female). 15.93% of smokers have stopped smoking successfully (1, 376/8, 636). The prevalence of ten selected TCDs among smokers range from 0.63% (Chronic Obstructive Pulmonary Disease, COPD) to 36.31% (hypertension). All of 1, 376 ex-smokers had at least one kind of TCD, and 52.33% of them stop smoking after the diagnosis of TCD, the time interval between TCD diagnosis and smoking cessation ranges from 0 to 65 years, with a median of 9 years. Smokers with TCD had higher prevalence of quit smoking, and current smokers with TCD had higher smoking cessation attempt proportion. Conclusions The prevalence of current smoking is still very high among male residents in rural area of Shanghai, and the occurrence of TCD even non-lethal one could provide an opportunity for doctors to assist the smoking cessation among smokers.

Objective: Although smoking increase the risk of cardiovascular diseases, its quitting leads to weight gain due to increased appetite. The aim of this study was to determine the effect of face to face dietary counseling on metabolic syndrome (MetS) indices in cigarette quitter. Materials and Methods: This 9-week parallel randomized clinical trial was conducted by participation of 50 patients with metabolic syndrome who have recently quit smoking. Participants were assigned randomly into two groups. Intervention group (IG) received weekly nutritional education and consultation, while control group (CG) did not receive any intervention. Before and after the trial, both groups were evaluated nutritionally using 24-hour dietary recall questionnaire, and metabolic syndrome parameters were measured. Paired T-test and ANCOVA were used for statistical analysis. Results: After intervention, weight, body mass index (BMI), triglycerides and systolic blood pressure were significantly different between CG and IG, while indices of low-density lipoprotein (LDL-C), high-density lipoprotein (HDL-C) and diastolic blood pressure were not significantly different between two groups. Amount of energy, lipid, protein, and carbohydrate intake were significantly lower in IG compare to CG. After adjustment of age, duration of smoking and the initial concentration of biochemical and anthropometric factors, significant differences were found between IG and CG in the changes of LDL-C (P-value 0.001), BMI (P-value 0.001), weight (P-value 0.001), waist circumference (P-value 0.002), and triglyceride (P-value 0.001).While the difference in changes of HDL-C, FBS, systolic and diastolic blood pressure, were not significant between two groups. Conclusion: Given the findings of this study, nutritional counseling could improve some indices of MetS in cigarette quitters.

Pulmonary emphysema usually arises in cigarette smokers, and often progresses after smoking cessation and even in ex-smokers. Lung-epithelial cell adhesion molecule 1 (CADM1), an immunoglobulin superfamily member, is extracellularly shed to produce a proapoptotic C-terminal fragment (CTF) within the cell and contribute to the development of emphysema. Here, we made an ex-smoker model using C57BL/6 mice; mice (6-week-old; 5 mice per group) were exposed to passive smoke of eight cigarettes twice a day 5 days a week until 18 weeks of age, and were then left untreated until 30 weeks of age. We calculated the mean linear intercept (Lm) and the alveolar septal thickness in the lung histologic sections to estimate the alveolar space dilatation. At 18 weeks of age, Lm was marginally enlarged (P = 0.023) with a marked increase in the septal thickness (P < 0.001) in comparison with age-matched control mice (5 mice per group), while at 30 weeks, the increase in Lm was much more prominent (P = 0.006) and the septal thickness was normalized, suggesting that emphysema progressed with septal remodeling during smoking cessation. Western blot analyses of the lungs were performed for CADM1, a possible CADM1 sheddase ADAM10, an epithelial marker pan-cytokeratin, and a myofibroblastic marker α-smooth muscle actin to estimate the expression levels of CTF and ADAM10 per epithelial cell and the levels of pan-cytokeratin and αSMA per tissue. CADM1 shedding was increased in the treated mice than in control mice at both ages, in association with an increase in the CTF level at 30 weeks (P = 0.021). In total of the treated and control mice of 30 weeks of age, Lm was positively correlated with the CTF and ADAM10 levels, and pan-cytokeratin was negatively correlated with CTF, suggesting an involvement of CADM1 shedding in emphysema progression. Positive correlations were also found between CTF and ADAM10, and between ADAM10 and αSMA, suggesting that increased septal myofibroblasts might be involved in increased CADM1 shedding. Taken together, persisting increase in ectodomain shedding of CADM1 appeared to contribute to the progression of emphysema in ex-smokers, and might be accounted for by alveolar septal remodeling.