How does Smoking Affect the Condition of Patients with Chronic Obstructive Pulmonary Diseases - Literature review Example

Literature Review The argument on how smoking affects the condition of patients with chronic obstructive pulmonary diseases (COPD) has been rife among different scholars with others providing evidence-based reports that when compared to non-smokers, smoking cessation is the cornerstone of COPD management. To provide succinct understanding on the topic, fourteen research materials are reviewed with an aim of establishing their key findings, limitations, and suggestions for future researches on the topic, "How does smoking affect the condition of patients with COPD, compared to those patients who do not smoke?" To begin with, Goren et al. (2015) took a randomized crossover study in China sampling 1421 patients of over 40 years of age within a hospital setting. After regressing smokers and non-smokers with COPD, the authors found that COPD smokers experienced poorer health outcomes compared to non-smokers. Unlike previous studies that included quit attempters, Goren et al. (2015) failed to indicate if there were cases that reported having used prescription cessation treatments. Based on the limitation, it is apparent that there is still paucity of information from the research on the treatment patterns to be used on patients who attempt to quit smoking. This study is related to Ishikawa et al. (2015) that reviewed patients from Japanese hospitals. After their thematic analysis, Ishikawa et al. (2015) found that COPD in Japanese patients is a multicomponent disease where smokers have higher chances for COPD compared to non-smokers. Unlike previous studies, Ishikawa et al. (2015) went deeper by observing levels of inflammatory cells as well as biomarkers in blood and sputum in COPD. This approach indeed challenged previous reports in Western studies that only employed biomarkers in blood. However, from the methodology of the study, Ishikawa et al. (2015) fails to establish whether anti-inflammatory therapy could be essential in the management of COPD in Japan. Different approach in the understanding of the topic was given by Hagstad et al. (2014). Their study concluded that environmental tobacco smoke was independently associated with COPD compared to non-smokers. This finding was based on three cross-sectional studies within the Obstructive Lung Disease in Northern Sweden where sample cases were examined separately unlike previous studies such as Hoogendoorn et al. (2010) that confined the sample population. This study is consistent with latest findings from authors such as Goren et al. (2015) who indicated that smoking is strongest risk factor for COPD. One notable concern from the study is whether the methodology was interested in ascertaining systematic inflammation or airway obstruction. Owing to the challenges that have masked the understanding of smoking and COPD, authors have attempted to undertake randomised controll trials by sampling studies into current or ex-smoking controls, non-smoking and COPD patients. This was the case with the research conducted by Hoogendoorn et al. (2010). After several trails the study revealed that smoking cessation improves COPD. However, it has to be noted that for clearer understanding of the sample, factors such as environmental tobacco smoke or passive smoking has to be given consideration. In as much as Hoogendoorn et al. (2010) noted that previous studies that included environmental tobacco smoke and passive smoking yielded similar research as theirs, it is not possible to associate COPD with environmental tobacco smoke in either single or multiple settings. Similarly, as Hessel et al. (2014) found, smoking and COPD are associated with decreased mucociliary clearance, and healthy smokers have shorter cilia in the large airway than nonsmokers. This research indicates that when smokers and non-smokers with COPD are compared, smoking affect COPD patients. One notable contribution of this study to the general understanding of the topic is that loss of cilia length is a contributor to defective mucociliary clearance in COPD. It even supports earlier researches such as Van Overveld et al. (2006) that COPD and smoking are linked with decreased mucociliary clearance. However, since Hessel et al. (2014) adopted descriptive and thematic analysis it is not clear how smoking may induce changes in the expression of IFT-linked genes in the airway of smokers with COPD. Different approach was provided by Ito et al. (2015) 93 samples of smokers and non-smokers with COPD. After one year of study, their findings indicated that after smoking cessation, subjects with COPD had improved mucociliary. What this research contributes to the new knowledge is that with COPD who quit smoking will likely have improved mucociliary clearance when compared to patients who continued to smoke. This study challenges previous assumptions made by Van Overveld et al. (2006) by providing in their regression that ex-smokers with COPD were likely to have lower exhaled carbon dioxide. The challenge was that the findings with ex-smokers were statistically insignificant. This study is consistent with Kotz and Van Schayck (2011) who took randomised cross-sectional study design on 96 cases to ascertain the link between smoking and COPD. The study concluded that smoking reduced life expectancy, especially in a vulnerable group like patients with COPD. The challenge with the their findings was that with descriptive and thematic analysis as it was the case with 96 cases Kotz and Van Schayck (2011) undertook, it was not easy to ascertain the effects of varenicline on smoking cessation in patients with COPD. This study realizes that smoking cessation has been the central theme among scholars who have researched on the effects of smoking on COPD patients. In a case study that was conducted in Finish University Hospitals Kupiainen et al. (2012) found that smoking cessation is the cornerstone of COPD management, but difficult to achieve in clinical practice. The challenge this study offers is that it relied solely on data from medical records without making a follow up questionnaires. This decision ultimately made it difficult to ascertain the success rates in smoking cessation. It is for this reason that Wang et al. (2011) study has stood the test of time in ascertaining that link between smoking among COPD patients and human airway epithelium. The research found that smoking down-regulates the Wnt pathway in the human airway epithelium thus reduces COPD. For researchers such as Ito et al. (2015) who have been concerned with smoking cessation, Wang et al. (2011) provide an understanding that down-regulation as they put it may be a contributor towards the dysregulation of airway epithelium differentiation observable in smoking-linked airway disorders. Cigarette smoking have been found to be contributing to the imbalance of circulation of CD4+ T cell subsets Zhang et al. (2014); Zhai et al. (2014). While Zhai et al. (2014) noted that smoking is the major risk factor for the development of NSCLC-COPD; both researches develop the point that smoking cigarettes is a major risk factor for the development of COPD, especially among patients with squamous cell carcinoma subtype. Both studies agree that even after cessation, the risk of developing COPD remains higher for smokers compared to healthy non-smokers. As the authors put it, little is still known regarding the gene networks linked with the secretion and synthesis of mucins in the human small airway epithelium. Studies have also been concerned with small airway epithelium and human small airway response to cigarette smoking. Studies that have taken this direction have included Van Overveld et al. (2006) and Siedlinski et al. (2011). Beginning with Siedlinski et al. (2011), their sample of 3,424 cases indicated that cigarette smoking was the major environmental risk factor for chronic obstructive pulmonary disease. On the same note, Van Overveld et al. (2006) found that inhaled corticosteroids affects patients with COPD. One notable finding from these studies is that as far as smoking and COPD is concerned, smoking affects the condition of patients with COPD when the effects are compared to those patients who do not smoke. The authors further identified two candidate regions associated with age at smoking initiation in patients with COPD. The significance of this study to future assessments and researches is that to some extent, the case studies revealed that pulmonary capillary apoptosis could be reversible when it comes to smokers who ceased, but there could be continuity in COPD pathogenesis in patients who continued to smoke. These findings are supported by Siedlinski et al. (2011) who noted that cigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD) and COPD severity. References Goren, A., Gupta, S., Dong, P., Feng, Y., Chen, C., & Liu, D. (2015). Burden of smoking among adults with COPD , chronic bronchitis, and emphysema in urban China. International Journal of Clinical Practice, 69(9), 1015-1028. Hagstad, Bjerg, Ekerljung, Backman, Lindberg, Rönmark, & Lundbäck. (2014). Passive Smoking Exposure Is Associated With Increased Risk of COPD in Never Smokers. Chest, 145(6), 1298-1304. Hessel, J., Heldrich, J., Fuller, J., Staudt, M., Radisch, S., Hollmann, C., . . . Tilley, A. (2014). Intraflagellar Transport Gene Expression Associated with Short Cilia in Smoking and COPD. PLoS One, 9(1), PLoS One, Jan 2014, Vol.9(1). Hoogendoorn, M., Feenstra, T. L., Hoogenveen, R. T., & Rutten-van Mölken, M. P. (2010). Long-term effectiveness and cost-effectiveness of smoking cessation interventions in patients with COPD. Thorax, 65(8), 711-718. Ishikawa, Nobuhisa, Hattori, Noboru, Kohno, Nobuoki, Kobayashi, Akihiro, Hayamizu, Tomoyuki, & Johnson, Malcolm. (2015). Airway inflammation in Japanese COPD patients compared with smoking and nonsmoking controls. International Journal of Chronic Obstructive Pulmonary Disease, 10, 185. Ito, Juliana T., Ramos, Dionei, Lima, Fabiano F., Rodrigues, Fernanda M.M., Gomes, Paulo R., Moreira, Graciane L., . . . Ramos, Ercy M.C. (2015). Nasal mucociliary clearance in subjects with COPD after smoking cessation. Respiratory Care, 60(3), 399. Kotz, & Van Schayck. (2011). What Justifies a Placebo-Controlled Trial of Varenicline for Smoking Cessation in Patients With COPD? Chest, 139(4), 968-969. Kupiainen, H., Kinnula, V., Lindqvist, A., Postma, D., Boezen, H., Laitinen, T., & Kilpeläinen, M. (2012). Successful Smoking Cessation in COPD: Association with Comorbidities and Mortality. 2012, 7. Siedlinski, M., Cho, M., Bakke, P., Gulsvik, A., Lomas, D., Anderson, W., . . . Silverman, E. (2011). Genome-wide association study of smoking behaviours in patients with COPD. Thorax, 66(10), 894. Siedlinski, M., Cho, M., Bakke, P., Gulsvik, A., Lomas, D., Anderson, W., . . . Silverman, E. (2011). Genome-wide association study of smoking behaviours in patients with COPD. Thorax, 66(10), 894. Van Overveld, F., Demkow, U., Górecka, D., De Backer, W., & Zieliński, J. (2006). Differences in responses upon corticosteroid therapy between smoking and non-smoking patients with COPD. Journal of Physiology and Pharmacology : An Official Journal of the Polish Physiological Society, 57 Suppl 4, 273-82. Wang, R., Ahmed, J., Hassan, G., Strulovici-Barel, I., Hackett, Y., Crystal, N., . . . Koenigshoff, Melanie. (2011). Down-Regulation of the Canonical Wnt β-Catenin Pathway in the Airway Epithelium of Healthy Smokers and Smokers with COPD (Smoking Suppresses Wnt Pathway). PLoS ONE, 6(4), E14793. Zhai, R., Yu, X., Wei, Y., Su, L., & Christiani, D. (2014). Smoking and smoking cessation in relation to the development of co‐existing non‐small cell lung cancer with chronic obstructive pulmonary disease. International Journal of Cancer, 134(4), 961-970. Zhang, Ming-Qiang, Wan, Yong, Jin, Yang, Xin, Jian-Bao, Zhang, Jian-Chu, Xiong, Xian-Zhi, . . . Chen, Gang. (2014). Cigarette smoking promotes inflammation in patients with COPD by affecting the polarization and survival of Th/Tregs through up-regulation of muscarinic receptor 3 and 5 expression. PloS One, 9(11), E112350. Read More