Search

COPD is a chronic inflammatory disease characterized by progressive airflow obstruction. Tobacco smoking is the main cause of COPD (COPD-TS), but chronic exposure to biomass smoke (COPD-BS), mainly wood smoke, is the second risk factor; both are considered to cause different phenotypes of COPD. COPD-BS is more eosinophilic than COPD-TS. The objective of the present study was to evaluate the serum level of interleukins involved in eosinophil maturation, recruitment, and survival, and their association with small airway obstruction, measuring cytokines by multiplex test (Bio-Plex) and evaluating the central airway resistance with impulse oscillometry (IOS), comparatively in patients with COPD due to biomass and smoking. The results showed that IL-1ra, IL-2, IL-4, IL-8, IL-9, IL-13, IL-17, and eotaxin were increased in COPD-BS related to COPD-TS. Resistance parameters showed that R5, X5, AX (area reactance), and R5-R20 were significantly higher in COPD-BS than in the COPD-TS group (p < 0.05). R20 was not different between the groups. These data suggest that the cytokines involved in the effect of eosinophils on airway inflammation in COPD-BS were increased compared with COPD-TS, which appears to be related to a predominance of peripheral airway obstruction in patients with COPD-BS more than in COPD-TS

Patients with biomass exposure-related COPD (BE-COPD) is a prevalent disease in developing countries and requires a detailed study of its clinical and inflammatory characteristics, specifying interventions that may differ from tobacco exposure-related COPD (TE-COPD). The objective was to describe clinical characteristics, biomarkers of inflammation, T-helper cells, and microbiological agents during a COPD exacerbation in BE-COPD in comparison with TE-COPD.A prospective observational study in patients with moderate or severe exacerbation was recruited either in the emergency room or the COPD clinic. At enrollment, nasopharyngeal swabs and sputum were collected to identify viral and bacterial pathogens. Blood samples were also collected to measure inflammatory biomarkers and T-helper cells levels. Days of hospitalization and mechanical ventilation requirement was evaluated.Clinical characteristics, vaccination history, hospitalization, history of exacerbations, and microbiological pattern between BE-COPD and TE-COPD were similar. The Th2 profile was higher in BE-COPD than in TE-COPD (2.10 [range 1.30-3.30] vs. 1.40 [range 1.20-1.80], p = 0.001). The Th2/Th1 ratio was higher in BE-COPD than TE-COPD (1.22 [range 0.58-2.57 ] vs. 0.71 [range 0.40-1.15], p = 0.004). The need of mechanical ventilation (MV) was higher in TE-COPD than BE-COPD (13% vs. 31.1%, p = 0.01). Nonvaccination history and high CRP levels were significantly associated with hospitalization [OR 1.48 (CI 95% 1.30-4.61, p = 0.005) and OR 1.17 (CI 95% 1.10-1.24, p = 0.001), respectively].Clinical characteristics, inflammatory markers, and microbiological isolates were similar in both groups but BE-COPD show a tendency to present higher inflammatory Th2 cells and low requirement MV compared with TE-COPD.

Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation and systemic inflammation. The main causes of COPD include interaction between genetic and environmental factors associated with tobacco smoking (COPD-TS) and/or exposure to biomass smoke (COPD-BS). Several microRNAs (miRNAs) control posttranscriptional regulation of COPD-TS associated gene expression. The miR-22-HDAC4-IL-17 axis was recently characterized. It is still unknown, however, whether this axis, participates in COPD-BS. To investigate, 50 patients diagnosed with severe-to-very severe COPD GOLD (Global Initiative for Chronic Obstructive Lung Disease) stages III/IV, were recruited, 25 women had COPD-BS (never smokers, exposed heavily to BS) and 25 had COPD-TS. Serum levels of miRNA-22-3p were measured by RT (Reverse Transcription)-qPCR, while the concentration of HDAC4 (Histone deacetylase 4) was detected by ELISA. Additionally, we looked for association between serum HDAC4 and DLCOsb (Single-breath diffusing capacity of the lung for carbon monoxide), as % of predicted by age, height, and gender, one of the main differences described between COPD-BS and COPD-TS. Women with COPD-BS were older and shorter and had a higher DLCOsb %P (percent predicted) compared to COPD-TS. Serum miR-22-3p was downregulated in COPD-BS relative to COPD-TS. In contrast, the concentration of HDAC4 was higher in COPD-BS compared to COPD-TS. Furthermore, a positive correlation between serum HDAC4 levels and DLCOsb %P was observed. We concluded that the miR-22-HDAC4-DLCO axis behaves differently in patients with COPD-BS and COPD-TS.

BackgroundChronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities. The main causes of COPD are Gene-environment interactions associated with tobacco smoking (COPD-TS) and biomass smoke (COPD-BS). It is well know that microRNAs (miRNAs) participate in the control of post-transcriptional regulation and are involved in COPD-TS; nevertheless, those miRNAS are participating in the COPD-BS are unidentified. Thus, we studied which miRNAs are involved in COPD-BS (GOLD stages I–II).MethodsIn the screening phase, the profile of the miRNAs was analyzed in serum samples (n = 3) by means of a PCR array. Subsequently, the miRNAs were validated with RT-qPCR (n = 25) in the corresponding study groups. Additionally, the serum concentration of Notch1 was measured comparing COPD-BS vs COPD-TS.ResultsmiR-34a was down-regulated in COPD- BS vs COPD-TS. In the other study groups, three miRNAs were differentially expressed: miR-374a was down-regulated in COPD-BS vs C, miR-191-5p was up-regulated in COPD-BS vs H-BS, and miR-21-5p was down-regulated in COPD-TS compared to the C group. Moreover, the serum concentration of Notch1, one of the targets of miR-34a, was increased in COPD-BS compared to women with COPD-TS.ConclusionsThis is the first study in patients with COPD due to biomass that demonstrates miRNA expression differences between patients. The observations support the concept that COPD by biomass has a different phenotype than COPD due to tobacco smoking, which could have important implications for the treatment of these diseases.

Background The main causes of COPD are tobacco smoking (COPD-TS) and biomass smoke exposure (COPD-BS). COPD-TS is known to induce changes in adipokines, incretins, and peptide hormones, frequent biomarkers of inflammation; however, it is unknown if similar changes occur in COPD-BS. Methods Clinical and physiological characteristics, and serum concentration of C-peptide, ghrelin, GIP, GLP-1, glucagon, insulin, leptin, PAI-1, resistin, and visfatin were measured in women with COPD-BS, COPD-TS, and healthy controls. Data were compared with one-way ANOVA and Tukey’s post hoc test; nonparametric were expressed as median (interquartile ranges), with Kruskal-Wallis and Dunn’s post-hoc test. Multivariate analysis, age, BMI, MS, and FEV1% pred with levels of inflammatory mediators in COPD women. Results FEV1% pred, FVC% pred, and FEV1/FVC ratio were decremented in COPD. In COPD-TS increased C-peptide, ghrelin, GIP, GLP-1, and leptin, and reduced glucagon, PAI-1, resistin, and visfatin. In COPD-BS enlarged ghrelin, insulin, leptin, and PAI-1 comparatively with COPD-TS and control, while C-peptide and GLP-1 relatively with controls; conversely, glucagon, and resistin were reduced. Multivariate analysis showed association of ghrelin, insulin, PAI-1, and visfatin with BS exposure. Conclusions women with COPD-BS have a distinct profile of adipokines, incretins, and peptide hormones, and specifically with ghrelin, insulin, PAI-1, and visfatin related to BS exposure.

The main causes of COPD are smoking (COPD-TS) and exposure to biomass smoke (COPD-BS), considered as different phenotypes. The association of COPD-TS with lung cancer (LC) is well established, but not in COPD-BS. Thus, we studied the serum concentration of cytokines that participate in inflammation, angiogenesis, and tumor progression, used frequently as LC biomarkers, in women with COPD-BS compared with COPD-TS (n = 70). Clinical and physiological characteristics and the serum concentration (multiplex immunoassay) of 16 cytokines were evaluated. The analysis revealed that women with COPD-BS were shorter and older, and had lower concentrations of 12 serum cytokines: 6 proinflammatory and angiogenic IL-6Rα, PECAM-1, leptin, osteopontin, prolactin, and follistatin; and 6 that participate in angiogenesis and in tumor progression FGF-2, HGF, sVEGFR-2, sHER2/neu, sTIE-2, G-CSF, and SCF. Notably, there was a significant increase in sEGFR in women with COPD-BS compared to women with COPD-TS. PDGF-AA/BB and sTIE-2 did not change. These findings suggest that women with COPD-BS have markedly decreased proinflammatory, angiogenic, and tumor progression potential, compared to women with COPD-TS, with sEGFR as the predominant mediator, which might reflect a differential pattern of inflammation in women exposed to BS, favoring the development of chronic bronchitis.

Introduction: Use of varenicline for as long as necessary to achieve abstinence has not been studied. The aim of this study was to test whether smokers with mild-to-moderate chronic obstructive pulmonary disease (COPD) are able to quit if they use varenicline for a sufficient length of time. Methods: A total of 30 heavy smokers with COPD took varenicline for sufficiently long enough for smoking cessation. Smokers were allowed to smoke without a fixed quit date. The main endpoints were the time of voluntary abstinence (VA) and the continuous abstinence rate (CAR) at 12 and 18 months. Results: Of 28 subjects, eight subjects continued to smoke and 20 subjects stopped smoking, demonstrating a CAR up to 18 months (71%). Median time of treatment was 6 (range 3–24) and 2 (range 1–8) months for abstainers and non-abstainers, respectively, and the median time of VA for abstainers was 4 (range 1–21) months. Conclusions: Use of varenicline for more than the traditional 12 recommended weeks may be a good strategy to increase the cessation rate in heavy smokers with mild COPD.

For very severe COPD patients with frequent exacerbations, non-invasive positive pressure ventilation (NIPPV) may an alternative to reduce exacerbations. Objective: To evaluate the impact of the high-intensity non-invasive positive pressure ventilation (HI-NIPPV) in patients with stable normocapnic very severe COPD (Forced Expiratory Volume in the first second (FEV 1 ) lower than 30%p) on the frequency of exacerbations. Methods: A randomized, double blind, clinical trial study. Fifty eligible patients were randomized to receive HI-NIPPV (nspiratory positive pressure of 22 cm H2O or higher) or the sham intervention (S-NIV) during one year. The inclusion criteria were the presence of FEV 1 Results: No differences were found at baseline between groups in number of exacerbation, FEV 1 , dyspnea, exercise capacity, gas exchange, and quality of life. The compliance to the NIPPV was in average 10 hours/day and 26 ± 4cmH2O was the IPAP used in the HI-NIPPV group. The overall reduction in the rate of exacerbations mostly explained by mild and moderate exacerbations was observed in the HI-NIPPV treatment group (reduction by 55%) compared with the S-NIV [0.38 (0.24-0.51) versus 0.22 (0.15-0.29), p =0.012]. The 20% reduction in the rate of severe exacerbations with HI-NIPPV group treatment compared with the S-NIV was not significantly different. Only Dyspnea and PaCO2, showed significant improvement with the HI-NIPPV in comparison with the S-NIV. Conclusions: HI-NIPPV may be a useful additional intervention to prevent mild and moderate exacerbations in patients with severe airflow limitation.

Objective. Although prevalence of tobacco smoking is different in the Latin American regions, the consequences on health are similar. Material and Methods. Therefore, guidelines on treatment are needed and ideally speaking must be useful in the different countries. In order to make quick recommendations useful in the region we made a search in PubMed from the last 5 years with the titles “Smoking cessation guidelines” and “Smoking cessation treatment meta-analysis” to know the content of different guidelines and with the titles of “Nicotine replacement therapy”, “Nicotine chewing gum”, “Nicotine patches”, “Nicotine inhaler”, “Bupropion therapy”, “Varenicline therapy” and “Individual and grupal behavioural counselling for smoking cessation” to determine the efficacy of each intervention. Results and conclusion. Our recommendation based on the availability of pharmacotherapy and human resources is that medical advice and behavioural grupal counseling must be primary interventions either adding, or not, first line drugs for smoking cessation

Raúl H Sansores, Mónica Velázquez-Uncal, Oliver Pérez-Bautista, Jaime Villalba-Caloca, Ramcés Falfán-Valencia, Alejandra Ramírez-VenegasTobacco Smoking and COPD Research Department, National Institute of Respiratory Diseases, Ismael Cosio Villegas, Mexico City, MexicoBackground: Physicians do not routinely recommend smokers to undergo spirometry unless they are symptomatic.Objective: To test the hypothesis that there are a significant number of asymptomatic smokers with chronic obstructive pulmonary disease (COPD), we estimated the prevalence of COPD in a group of asymptomatic smokers.Methods: Two thousand nine hundred and sixty-one smokers with a cumulative consumption history of at least 10 pack-years, either smokers with symptoms or smokers without symptoms (WOS) were invited to perform a spirometry and complete a symptom questionnaire.Results: Six hundred and thirty-seven (21.5%) smokers had no symptoms, whereas 2,324 (78.5%) had at least one symptom. The prevalence of COPD in subjects WOS was 1.5% when considering the whole group of smokers (45/2,961) and 7% when considering only the group WOS (45/637). From 329 smokers with COPD, 13.7% were WOS. Subjects WOS were younger, had better lung function and lower cumulative consumption of cigarettes, estimated as both cigarettes per day and pack-years. According to severity of airflow limitation, 69% vs 87% of subjects were classified as Global Initiative for Chronic Obstructive Lung Disease stagesI–II in the WOS and smokers with symptoms groups, respectively (P

SummaryBackgroundEarly diagnosis of chronic obstructive pulmonary disease (COPD) remains the main intervention to prevent disease progression. However, conflicting results exist on the utility of two different diagnostic strategies that preclude freely recommending one strategy in favor of the other. Spirometry was used to determine the effectiveness of a symptom-based (case-finding) strategy vs. a screening strategy to detect COPD in smokers.MethodsThe case-finding strategy was undertaken during the COPD Day campaign in smokers with respiratory symptoms who were willing to submit to lung function testing. Screening was carried out with smokers attending a smoking cessation program. A short standardized questionnaire on respiratory symptoms along with spirometry were carried out and analyzed for both strategies.ResultsWe evaluated 2781 smokers (mean pack/years 23.38): 1999 from the case-finding strategy and 782 from the smoking cessation program strategy (SCS). Prevalence of COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria was 10.1 and 13.3%, respectively (p

Although prevalence of tobacco smoking is different in the Latin American regions, the consequences on health are similar.Therefore, guidelines on treatment are needed and ideally speaking must be useful in the different countries. In order to make quick recommendations useful in the region we made a search in PubMed from the last 5 years with the titles "Smoking cessation guidelines" and "Smoking cessation treatment meta-analysis" to know the content of different guidelines and with the titles of "Nicotine replacement therapy", "Nicotine chewing gum", "Nicotine patches", "Nicotine inhaler", "Bupropion therapy", "Varenicline therapy" and "Individual and group behavioural counselling for smoking cessation" to determine the efficacy of each intervention.Our recommendation based on the availability of pharmacotherapy and human resources is that medical advice and behavioural group counseling must be primary interventions either adding, or not, first line drugs for smoking cessation.