scholarly journals Profile of a Brazilian population with severe chronic obstructive pulmonary disease

2003 ◽  
Vol 29 (2) ◽  
pp. 64-68 ◽  
Author(s):  
Mateo Sainz Yaksic ◽  
Mauro Tojo ◽  
Alberto Cukier ◽  
Rafael Stelmach

Chronic obstructive pulmonary disease (COPD) is a public health problem. Tobacco smoking is the major cause, but not the only one. Air pollution, exposure to chemicals, environmental smoke exposure, and passive smoking are among other contributing causes; being viral and bacterial infections also risk factors. Gender and weight are associated to the severity of the disease. Co-morbidity is frequent. OBJECTIVE: To characterize a population of COPD outpatients followed at an outsourced medical service. METHODS: Questionnaires were applied to patients with COPD. The data included gender, age, weight, body mass index (BMI), oxygen delivery users, and FEV1, exposure to tobacco smoke, exposure to wood smoke, history of tuberculosis and co-morbid diseases. RESULTS: Of the 70 patients enrolled in the study, 70% (49) were men with an average age of 64 ± 10 years, average weight of 63 ± 16 kg and average BMI of 22 ± 5 kg/m². Mean FEV1 was 35 ± 14% and 45.7% were oxygen dependent. Nine (12.8%) patients never smoked, while 78.8% had quit tobacco smoking, (38 ± 11 pack/years was the average). Nine (12.8%) smoked corn husk cigarettes. Eighteen (25.7%) were exposed to wood smoke. Eleven (15.7%) patients had tuberculosis, 5.7% complained of asthma symptoms, 2.8% had bronchiectasis, 11.4% diabetes mellitus, 51.4% hypertension, and 20% Cor pulmonale. CONCLUSION: Other possible COPD etiologies must be investigated. Determinants of the pulmonary injury could be environmental smoke exposure associated to former infections. Men with low BMI are typically representative of this severe patient population. Hypertension and Cor Pulmonale are frequent co-morbidity factors.

2021 ◽  
Author(s):  
Carlos A. Torres-Duque ◽  
Felipe Severiche-Bueno ◽  
Mauricio González-García

Around 41% of the world’s population continue using solid fuels, including wood and other types of biomass, for cooking or heating their homes. Long-term indoor exposure to wood smoke, and biomass smoke in general, is a risk factor for developing chronic obstructive pulmonary disease (COPD). In some regions of the world, biomass exposure is a more frequent cause of COPD than exposure to cigarette smoke. Recently it has been described notable differences between COPD associated with wood smoke (WS-COPD) and that caused by tobacco smoking (TS-COPD): significantly less emphysema and more airway inflammation in WS-COPD. Recognizing these differences, some authors have suggested that WS-COPD should be considered a new COPD phenotype. This chapter summarizes the differences between WS-COPD and TS-COPD. The information about the characteristics of COPD caused by other types of biomass fuels, different from wood, is very scarce. Accepting that the smoke derived from wood burning and tobacco smoking have some differences (etiology), the inhalation patterns are different (pathogenesis) and the physiopathological mechanisms they induce may also differ, we analyze if the disease caused by indoor chronic exposure to wood smoke should be considered as another COPD phenotype or a distinct nosological entity.


2011 ◽  
Vol 59 (3) ◽  
pp. 587-592 ◽  
Author(s):  
Alberto Guzmán-Grenfell ◽  
Nayeli Nieto-Velázquez ◽  
Yessica Torres-Ramos ◽  
Araceli Montoya-Estrada ◽  
Alejandra Ramírez-Venegas ◽  
...  

2008 ◽  
pp. 60-65
Author(s):  
E. A. Titova ◽  
A. I. Algazin ◽  
T. A. Kornilova ◽  
I. P. Sokol ◽  
E. M. Reutskaya ◽  
...  

Fifty-two patients with chronic obstructive pulmonary disease (COPD) aged 44 to 71 yrs were examined. Of them, 26 ones suffered from type 2 diabetes mellitus (DM). We established that in patients with concomitant DM, COPD has more severe course with more advanced respiratory failure and chronic cor pulmonale and more frequent exacerbations. COPD patients with concomitant DM more often have co-morbidity, such as obesity, ischemic heart disease, chronic heart failure. Co-morbidity of COLD and DM requires more extensive pharmacotherapy.


Author(s):  
Kaushlendra Pratap Narayan ◽  
S. K. Verma ◽  
Surya Kant ◽  
R. A. S. Kushwaha ◽  
Santosh Kumar ◽  
...  

Background: Chronic obstructive pulmonary disease (COPD) is a common preventable and treatable disease that is characterised by persistent respiratory symptoms and airflow limitation. COPD is characterised by an intense inflammatory process in the airways, parenchyma, and pulmonary vasculature. It is possible in some cases that the inflammatory process may overflow into the systemic circulation, promoting a generalised inflammatory reaction. Patient with COPD often have concomitant chronic illness (co-morbidities). The aim of this study is to know the pattern of co-morbidities in COPD patients.Methods: This study was a cross sectional observational study conducted on 172 COPD patients (IPD and OPD) diagnosed on the basis of GOLD guideline 2017. Co morbidities were diagnosed as per standard defined criteria laid down in the respective guidelines.Results: 55.3% of the patients with COPD had co morbidities. 18/88(20.5%) patients presented with multiple co-morbidities. 49/88, 55.7% COPD patients were affected with cardiac (either only cardiac or had multiple organs affected besides cardiac), the commonest co-morbidity. Amongst cardiac, hypertension and congestive heart failure (CHF) was the commonest (n=19/49, 38.8% each) followed by CAD/CSA/IWMI/IHD/AF. Others were metabolic (n=14/88, 15.9%), GERD (n=13/88, 14.8%), Depression (n=11/88, 12.5%). Less prevalent co-morbidities were Osteoporosis (n=8/88, 9.1%), Lung cancer (n=6/88, 6.8%), Bronchiectasis (n=5/88, 5.6%) and OSA (n=3/88, 3.4%).Conclusions: Urban indwelling, advancing age and duration of illness, presentation with low mood, loss of pleasure/ interest, appetite disturbances and heart burn with relief on taking proton pump inhibitor can be predictors of co-morbidities in COPD patients. Chance of finding co-morbidities may be multifactorial. Thus, it is important to look out for co morbidities in each and every COPD patients.


2019 ◽  
Vol 14 (1) ◽  
pp. 39-52 ◽  
Author(s):  
Alessia Santoro ◽  
Carlo Tomino ◽  
Giulia Prinzi ◽  
Palma Lamonaca ◽  
Vittorio Cardaci ◽  
...  

Background: The morbidity and mortality associated with tobacco smoking is well established. Nicotine is the addictive component of tobacco. Nicotine, through the non-neuronal α7nicotinic receptor, induces cell proliferation, neo-angiogenesis, epithelial to mesenchymal transition, and inhibits drug-induced apoptosis. Objective: To understand the genetic, molecular and cellular biology of addiction, chronic obstructive pulmonary disease and lung cancer. Methods: The search for papers to be included in the review was performed during the months of July- September 2018 in the following databases: PubMed (http://www.ncbi.nlm.nih.gov), Scopus (http://www.scopus.com), EMBASE (http://www.elsevier.com/online-tools/embase), and ISI Web of Knowledge (http://apps.webofknowledge.com/). The following searching terms: “nicotine”, “nicotinic receptor”, and “addiction” or “COPD” or “lung cancer” were used. </P><P> Patents were retrieved in clinicaltrials.gov (https://clinicaltrials.gov/). All papers written in English were evaluated. The reference list of retrieved articles was also reviewed to identify other eligible studies that were not indexed by the above-mentioned databases. </P><P> New experimental data on the ability of nicotine to promote transformation of human bronchial epithelial cells, exposed for one hour to Benzo[a]pyrene-7,8-diol-9-10-epoxide, are reported. Results: Nicotinic receptors variants and nicotinic receptors upregulation are involved in addiction, chronic obstructive pulmonary disease and/or lung cancer. Nicotine through α7nicotinic receptor upregulation induces complete bronchial epithelial cells transformation. Conclusion: Genetic studies highlight the involvement of nicotinic receptors variants in addiction, chronic obstructive pulmonary disease and/or lung cancer. A future important step will be to translate these genetic findings to clinical practice. Interventions able to help smoking cessation in nicotine dependence subjects, under patent, are reported.


2010 ◽  
Vol 184 (8) ◽  
pp. 4460-4469 ◽  
Author(s):  
Gregory T. Motz ◽  
Bryan L. Eppert ◽  
Brian W. Wortham ◽  
Robyn M. Amos-Kroohs ◽  
Jennifer L. Flury ◽  
...  

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