Relationship between Chronic Obstructive Pulmonary Disease and Asthma - Coursework Example

"The Relationship between Chronic obstructive Pulmonary Disease and Asthma" Aim To study the relationship between Chronic Obstructive Pulmonary Disease (COPD) and Asthma. Abstract Asthma and Chronic Obstructive Pulmonary Disease (COPD), which encompass emphysema and chronic bronchitis, are the widespread diseases of lungs with obstructed airflow. It is imperative to discriminate with accuracy between asthma and Chronic Obstructive Pulmonary Disease to minimize the risk of improper treatment of the disease. Much attention has been given to Asthma while COPD remained quite neglected over the years. The inflammatory responses in both these conditions show variations. In asthma, eosinophilic inflammation occur causing airway tenderness, whereas in COPD neutrophilic inflammation causes the obstruction in air passage. The lung parenchyma destruction is the irreversible characteristic of COPD, which is not depicted in asthma; therefore, corticosteroids fail to alter the progression of Chronic Obstructive Pulmonary Disease (Barnes, 2000). A deep insight is given in the study conducted to establish a co-relation between these two closely related diseases. Introduction Asthma and Chronic obstructive pulmonary disease (COPD) are the major reasons for the morbidity and mortality due to loss of lung function and are the prevalent and enduring conditions of lungs in UK. Both these conditions are caused by obstruction in airflow and have inflammatory components (Barnes, 2000). The symptoms of both these conditions include cough, wheeze and breathlessness. (Crockett, T). Some triggering elements or allergies can induce asthma like house dust or dust mites, insects like cockroaches, mold or pet danders and even pollens, cold air or even exercise causing exacerbations whereas in COPD there is no such trigger by allergens and are caused by respiratory tract infections (RTI) (Brian, A). Moreover asthma patients display episodic chest symptoms at night or when exposed to allergic triggers while COPD patients depict morning cough with mucus and their chest symptoms persevere all through the day (Brian, A). Thus, asthma includes bronchial hyper-responsiveness, airway inflammation, and the presence of airflow obstruction, which may be relieved spontaneously or with medication (National Asthma Education and Prevention Program, 1997) while COPD is a chronic and usually progressive disease characterized by airflow limitation but it is not fully reversible (WHO). Asthma is diagnosed during childhood and is associated with atopy and eosinophilic inflammation while Chronic Obstructive Pulmonary Disease (COPD) is usually diagnosed during the middle or later life and is associated with neutrophilic inflammation (Barnes, 2000). It is manifested that asthma and COPD have shown that the two diseases over time may develop physiologic features that are quite similar (Barnes, 2000). Research studies have shown that history of smoking is the foremost cause of COPD and it becomes more devastating with its persistence and can lead to permanent lung damage, it is also reported that patients with asthma also exacerbate with smoking, some of the patients display both these chronic conditions, they have asthma in past with persistence of many years and then bring their lungs to permanent damage with the development of COPD (Brian, A). It is evident that efforts are being made to comprehend the cellular and molecular mechanisms of asthma. COPD although is not widely studied and therefore initially formulated as poorly responsive asthma (Barnes, 2000). Asthma and COPD diversify in stipulations like cellular mechanisms, inflammatory mediators, inflammatory effects and also in terms of response to therapy provided (Barnes, 2000). Almost in 10% of the cases patients are reported to have COPD with Asthma (Figure 1, Appendix). COPD and Asthma are caused by obstruction in airflow along with continual inflammatory process and huge dissimilarity in the nature of inflammation (Table 1, Appendix) (Barnes, 2000). In case of asthma lungs can be reverted back to normal condition or nearly normal condition but for COPD patients, it's hard to spend a day without symptoms (National Asthma Education and Prevention Program, 1995). It is also reported that in COPD even after the cessation of smoking and bronchodilator use, airflow obstruction is only partially reverted (American Thoracic Society, 1997). One of the leading research findings state that airway inflammation is demonstrated by eosinophilic inflammation in asthma. The allergens cause a rise in activated and degranulating eosinophils in bronchial biopsies, BAL and in induced sputum (Bernes, 1996, Jeffery, 1998). It is also reported that Airway Hyperresponsiveness (ARH) is the distinguishing physiologic abnormality in asthma and is also linked to eosinophilic inflammation. AHR, either to methacholine or histamine, a supportive measures of asthma diagnosis, this is documented in subjects with COPD (Xu X, Rijcken, 1997). In case of COPD a rise in the number of neutrophils occur (Jeffery, 1998). A comparative study was conducted between normal, asthma, smoker (without obstructions) and COPD patients (Keatings, 1996). It is reported that there is an increase in eosinophil basic proteins, cationic proteins and eosinophil peroxidase in sputum of COPD patients with no increase in the number of eosinophils, depicting the degranulation of eosinophils. The study also reports that biopsies of ex-smokers show that inflammation persists in the airway once it is established (Turato, 1995). It is reported that most of the changes occur in the peripheral lining of the airways of COPD patients, showing fibrosis and obliterative bronchiolitis. Research data depicts squamous metaplasia in COPD patients who lack in epithelial shedding. Further, in COPD constriction does not occur if induced with bronchial challenges like exercise and Bradykinin. A major difference between COPD and asthma is mucus hypersecretion in COPD along with metaplasia of submucosal glands and goblet cells, which is rarely depicted in asthma. The reason sorted is cigarette smoking and other irritants and allergens inducing inflammatory response in peripheral airways and lung parenchyma (Barnes, 2000). Reversibility of pulmonary obstruction in response to treatment, a hallmark of asthma, may decrease over time in some patients with moderate or severe asthma, to the point of irreversible or only partially reversible airway obstruction (Vonk, 2003, Hudon, 1997, Reed, 1999, Ulrik, 1999). The overlap in many of these signs and symptoms often makes the distinction between these two diseases obscure, making it difficult to label these subjects, especially in elderly population (Barbee, 1997, Fanta, 1989). The progression in severity of asthma symptoms and the overlap of symptoms seen in some patients with asthma and COPD could be concluded as asthma may be a risk factor for the subsequent development of Chronic Obstructive Pulmonary Disease. Considering all the literature surveyed a study is conducted to study the relationship between COPD and Asthma. In this study an analysis of inflammatory cells in inflamed sputum is done for 4 categories: normal subjects, cigarette smokers, patients with COPD and patients with asthma. As per the research data there should be a significant increase in neutrophils in two categories- smokers and COPD patients with a high in COPD, whereas there is a significant increase in eosinophils in asthma (Keatings et al, 1996). The study is carried out and results are displayed in the project log. It has provided a deep insight into the understanding towards Chronic Obstructive Pulmonary Disease and asthma. Method Primary- Normally, the first-line (primary) maintenance therapy for asthma patients is an inhaled corticosteroid, and if required, bronchodilator is added (National Asthma Education and Prevention Program, 1997). In case of COPD, bronchodilators are the first-line maintenance (Pauwels et al, 2001). The study becomes more imperative as it is a must to treat COPD and asthma as two different lines, since most of the general practitioners do not follow this. Reports from The Netherlands about 14 GPs' state that 175 patients were monitored of the age >18 years with asthma and COPD, they analyzed relation between quality of life and GPs' medication prescription, GPs' advice on smoking cessation, patient level of education and counseling (Jacob et al, 2001). Method Secondary- Induction of sputum was done with the inhaled hypertonic saline (Pin et al, 1992). This was used for 16 normal subjects who could not produce sputum normally, 12 smokers, 14 COPD patients and 22 asthma patients. The success rate and security of the technique the reproducibility of cell counts, and variation in cell counts between the asthmatic, smokers, COPD and normal groups were examined. The subjects were asked to inhale hypertonic saline solution 3-5% for up to 30 minutes after inhalation of salbutamol (PIN et al, 1992). After the induction, the subjects were asked to expectorate sputum every five minutes. The value of the sample was achieved on the amount of plugs and the level of salivary contamination. For total cell count, plugs from the lower respiratory tract were preferred and direct smear was preferred for differential cell counts of eosinophils and metachromatic cells (mast cells and basophils) (Pin et al, 1992). Notwithstanding, Chronic Obstructive Pulmonary Disease is often misdiagnosed, and persons with COPD are treated as an alternative for asthma (American Thoracic Society, 1995). A survey of 75 primary care physicians was conducted which found that they prescribe analogous medications for COPD and asthma although the suitable treatments differ (Kesten, 1993). Result Plenty of samples (76% of first attempts) obtained from lower respiratory tract were obtained. A fall is reported as low as 5.3% and maximum of 20% in the forced expiratory volume (FEV1) during inhalation of saline. There was a reliability coefficient of 0.8 for Eosinophil and 0.7 for metachromatic cell counts respectively. This data was reproducible. A comparative data was estimated between sputum from normal subjects, sputum from asthmatic patients contained a significantly higher proportion of eosinophils (mean 18.5% (SE 3.8%) v 1.9% (0.6%)) and metachromatic cells (0.50% (0.18%) v 0.039% (0.014%)) (Pin et al, 1992). The results obtained by Jacob et al show that in the span of 15 months, 175 patients went for 537 consultations. In 57% patients' impairment in their quality of life was reported. The given data is associated with subsequent GP interventions and patients' education and counseling. A multivariate logistic regression analysis was performed based on physical complaints and a change in medication prescription was done along with education about control regimen. Various studies are being performed to understand and also discriminate COPD and asthma in one of the studies direct and indirect costs associated with asthma and chronic obstructive pulmonary disease (COPD) in Sweden in 1980 and 1991, was performed to classify trends in the use of outpatient concern, drugs and inpatient concern, and the development of momentary morbidity, permanent disability and mortality for asthma and COPD (Jacobson, 2000). It is reported that Asthma and COPD jointly account for approximately 2% of the economic cost of all diseases. The total costs associated with each disease were alike, the allocation of the different cost mechanisms and changes differ with time. As reported (Jacobson, 2000), during 1980s, the cost of drugs and out-patient care increased for both diseases on the contrary, the cost of inpatient concern for asthma decreased, but for COPD increased (Jacobson, 2000). Discussion Asthma and COPD are lung-associated diseases and share many common features. The study conducted depicts that there is a vast differentiation in the aetiology and their management. It is therefore imperative to understand the key distinguishing attributes to reduce the patients' risk of receiving inappropriate treatment, advice and overall management. Smoking has been described as the main risk factor for the development of COPD. It is manifested that < 20% of cigarette smokers acquire COPD, suggesting that other factors convey significant additional risk (Mannino, 2002). These may encompass rare deficiency of '1-antitrypsin and also exposure to occupational and environmental gases (Liberman, 1969). Results from various studies have depicted that asthma and AHR are important risk factors contributing to an increased rate of decline in FEV1 and therefore to the development of COPD. Fletcher et al compared the rates of decline in FEV1 among subjects with physician-diagnosed asthma and subjects without asthma and found that the rate of decline in FEV1 adjusted for smoking was significantly higher among the asthmatic subjects compared to the non-asthmatic subjects. The study performed where induced sputum was examined for the presence of cells in normal, smokers, COPD patients and asthmatic subjects show that macrophages play vital role in inducing inflammatory response in COPD and may release neutrophil chemotactic factors along with the proteolytic enzymes. The inhaled irritants like cigarette are known to cause activation of macrophages. It is reported that macrophage number increases by five to ten times in COPD patients. It is further reported that macrophages concentrate in the centriacinar zones; emphysema is marked most in this area (Barnes, 2000). It is also reported that number of macrophages and T-lymphocytes and not neutrophils in alveolar wall show a relationship with the destruction of parenchymal cells (Finkelstein, 1995). It is macrophages which are responsible for the constant proteolytic activity in the lungs in case of emphysema. It is also reported that inflammatory mechanisms in COPD induced by cigarette smoke and various other irritants activate macrophages in the respiratory tract and release neutrophil chemotactic factors, including IL-8 and LTB4. It is reported that these cells then liberate proteases responsible for breakdown of connective tissue in the lung parenchyma, ensuing emphysema, and also excite mucus hypersecretion. Normally, enzymes counteracted by protease inhibitors, comprise '1-antitrypsin ('1-At), secretory leukoprotease inhibitor (SLPI), and tissue inhibitor of MMPs (TIMPs). The reports also state about the evidence of Cytotoxic T cells (CD8+) involvement in the inflammatory surge (Barnes, 2000). The cytokines of asthma and COPD are different. Interleukin (IL)-4 and IL-13 are important in case of asthma which is essential for IgE formation, but IL-5 is critical for eosinophilic inflammation (Chung, 1999). Eosinophil chemotactic cytokines (CC chemokines), like eotaxin and RANTES, play imperative role in asthmatic inflammation and selectively enlist prepared eosinophils from the circulation into the airways. In case of COPD, IL-8 is plays a major role and is a selective attractant of neutrophils (Keatings, 1996). Data collected from various studies state that both asthma and COPD are featured with oxidative stress because of great amplification in activated macrophages and neutrophils and also due to cigarettes in COPD (Repine, 1997). It is reported that in case of COPD, markers of oxidative stress increase (Pratico, 1998). Conclusion: Considering all the research data it is concluded that the answer to treatment varies strikingly between asthma and COPD. In case of asthma, the eosinophilic inflammation can be overcome by corticosteroids. The eosinophils are wiped off from the airways and sputum and there is decrease in AHR. In case of COPD, corticosteroids could not show much effect on inflammation. The need for understanding is must for the fact that corticosteroids reduce eosinophils but prolong neutrophils (Meagher, 1996). It is therefore corticosteroids fail in altering the progression of COPD and show the requirement of formulating more anti-inflammatory drugs in future (Barnes, 1998). It is recommended that CPD and asthma patients need clean air and should also avoid being around smokers and fume-laden air and should stay away from the polluted air in order to avoid any kind of irritation and are advised for the use of face masks. It is also recommended that cleaning action in the form of coughing is also imperative and the patient must be advised to clean the mucus every morning and fluid intake can be performed. This helps the patient in thinning out the mucus (Lung- Treatment of COPD and Asthma). References 1. American Lung Association. American Lung Association Fact Sheet: Chronic Obstructive Pulmonary Disease (COPD). Available at: http://www.lungusa.org/diseases/copd_factsheet.html. 2. American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease 1995. Am J Respir Crit Care Med.;152:S77-S120 3. Anthonisen NR, Manfreda J, Warren CPW, Hershfield ES, Harding GKM, Nelson NA. 1987. 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Prehospitalization inhaled corticosteroid use in patients with COPD or asthma. Chest. 1997;111:296-302. 25. Jacobs, J., E.,'van de Lisdonk, E., H.,'Smeele, I., van Weel, C., 2001 Management of patients with asthma and COPD: monitoring quality of life and the relationship to subsequent GP interventions Family Practice, Volume 18,'Number 6, pp. 574-580(7) 26. Jacobson, L., Hertzman, P., Lofdahl, C., G., Skoogh, B., E., Lindgren, B. 2000, The economic impact of asthma and chronic obstructive pulmonary disease (COPD) in Sweden in 1980 and 1991. Respiratory medicine Vol. 94 (3), 247-255. 27. Jeffery P., K. 1998 Structural and inflammatory changes in COPD: a comparison with asthma. Thorax ; 53:129-136. 28. Jeffery, P., K., 2001 Remodeling in Asthma and Chronic Obstructive Lung Disease Am. J. Respir. Crit. Care Med., Volume 164, Number 10, S28-S38 29. Keatings VM, Collins PD, Scott DM, et al. 1996 Differences in interleukin-8 and tumor necrosis factor-a induced sputum from patients with chronic obstructive pulmonary disease or asthma. Am J Respir Crit Care Med; 153:530-534 30. Kesten S, Chapman K., R. 1993 Physician perceptions and management of COPD. Chest.;104:254-258. 31. Lieberman, J. 1969. Heterozygous and homozygous '-antitrypsin deficiency in patients with pulmonary emphysema. N Engl J Med; 281:279-284. 32. Lung- Treatment of COPD and Asthma, http://www.nlhep.org/lung_trtmnt.html 33. Mannino, D.,M. 2002. COPD: epidemiology, prevalence, morbidity and mortality, and disease heterogeneity. Chest; 121: 121S-126S. 34. Meagher LC, Cousin JM, Seckl JR, et al. 1996 Opposing effects of glucocorticoids on the rate of apoptosis in neutrophilic and eosinophilic granuloctyes. J Immunol; 156:4422-4428 35. 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Hackettstown, NJ: Snowdrift Pulmonary Conference. 39. Petty T., L, Nett L., M. 1995 Enjoying Life with Chronic Obstructive Pulmonary Disease. 3rd ed. Cedar Grove, NJ: Laennec Publishing. 40. Petty T., L, Doherty D., E. Prevent Emphysema Now. National Lung Health Education Program. 41. Pin,I., Gibson, P., G., Kolendowicz, R., Girgis-Gabardo, A., Denburg, J., A., Hargreave, F., E., Dolovich, J., 1992 Use of induced sputum cell counts to investigate airway inflammation in asthma.Thorax;47:25-29; doi:10.1136/thx.47.1.25. 42. Pratico D, Basili, S, Vieri M, et al. 1998 Chronic obstructive pulmonary disease is associated with an increase in urinary levels of isoprostane F2a-111, an index of oxidant stress. Am J Respir Crit Care Med; 158:1709-1714. 43. Reed C.,E. 1999. The natural history of asthma in adults: the problem of irreversibility. J Allergy Clin Immunol, 103:539-547. 44. Repine J.,E, Bast A, Lankhorst I. 1997 Oxidative stress in chronic obstructive pulmonary disease. Am J Respir Crit Care Med; 156:341-357 45. Scott-Levin media information. Available at: http://www.quintiles.com. 46. Turato G, Di Stefano A, Maestrelli P, et al. Effect of smoking cessation on airway inflammation in chronic bronchitis. Am J Respir Crit Care Med 1995; 152:1262-1267 47. Ulrik, C.,S., Backer, V.1999. Nonreversible airflow obstruction in life-long nonsmokers with moderate to severe asthma. Eur Respir J ; 14:892-896. 48. What Is COPD' Available at: http://www.thebreathingspace.com/libry.htm#What. 49. World Health Organization. The GOLD global strategy for the management and prevention of COPD. Available at:http://www.goldcopd.com. 50. Van Andel A., E, Reisner C, Menjoge S., S, Witek T., J. 1999. Analysis of inhaled corticosteroid and oral theophylline use among patients with stable COPD from 1987 to 1995. Chest.; 115:703-707. 51. Vonk, J.,M., Jongepier, H., Panhuysen, C.,I. 2003. Risk factors associated with the presence of irreversible airflow limitation and reduced transfer coefficient in patients with asthma after 26 years of follow up. Thorax; 58:322-327. 52. Xu X, Rijcken B, Schouten J., P, et al. 1997. Airways responsiveness and development and remission of chronic respiratory symptoms in adults. Lancet; 350:1431-1434. Appendix Figure 1 Overlap between COPD and asthma. Approximately 10% of patients with COPD also have asthma and therefore share pathologic features ('wheezy bronchitis'). Wheezy Bronchitis (Barnes, 2000) Figure 2 Proposed relationship between Asthma and emphysema (Elias, J, 2004). Table 1 Differences Between COPD and Asthma* Inflammation Asthma COPD Inflammatory Mast cells cells Eosinophils Neutrophils CD4+ cells (Th2) CD8+ cells (Tc) Macrophages+ Macrophages++ Inflammatory LTB4, histamine LTB4 mediators IL-4, IL-5, IL-13 TNF-' Eotaxin, RANTES IL-8, GRO-' Oxidative stress+ Oxidative stress+++ Inflammatory All airways Peripheral airways effects AHR+++ AHR' Epithelial shedding Epithelial metaplasia Fibrosis+ Fibrosis++ No parenchymal Parenchymal destruction involvement Mucus secretion+ Mucus secretion +++ Response to Corticosteroids +++ ' *Th2 = T-helper type 2. (Barnes, 2000) Table 2 Asthma vs COPD: History (Crockett, T) History Asthma COPD Childhood problems Common Irrelevant Atopic features Common Irrelevant Smoking Irrelevant Very common Night symptoms Common Very common Cough & sputum Intermittent/ rare Daily/ common Age of onset Any Over 40 Project Log Abstract Airway inflammation is measured to be significant in asthma but is comparatively unreachable to study. Fewer insidious techniques of obtaining sputum from patients not capable of creating it impulsively should offer a useful investigational tool in asthma. Asthma and chronic obstructive lung disease (COPD) are lung inflammatory conditions linked with structural "remodeling" unfortunate to protect normal lung function. The clinically pragmatic distinctions between asthma and COPD are reflected by divergence in the remodeling progression, the prototype of inflammatory cells and cytokines. In case of asthma the epithelium appears to be more delicate than that of COPD. In case of COPD, the epithelial reticular basement membrane (RBM) is extensively thicker, and depicts an enlargement of the mass of bronchial smooth muscle. Emphysema is not reported in asthmatic nonsmoker. COPD depicts epithelial mucous metaplasia, airway wall fibrosis, and inflammation associated with thrashing of nearby alveolar attachments to the external wall of small airways: bronchiolar smooth muscle is amplified. Emphysema is a feature of severe COPD: the vicious process, alveolar wall thickening and focal fibrosis may be distinguished. The hypertrophy of submucosal mucus-secreting glands is similar in extent in asthma and COPD. The number of bronchial vessels and the area of the wall engaged by them increase in severe corticosteroid-dependent asthma: it is likely that these increases also occur in severe COPD. Pulmonary vasculature is remodeled in COPD. In asthma numerous of these structural modifications begin early in the disease process, even in the child. In COPD the changes instigate later in life and the associated inflammatory reaction differs from that in asthma. The following study defines and compares the key remodeling processes. Method of Project Log Day 1 Searched Library to collect the information regarding the relationship between Asthma and COPD Day 2 Assimilated the information and formulated the hypothesis to compare the key remodeling processes for COPD and Asthma Day 3 Prepared the protocol to carry out the study Day 4 Fixed the appointment with the hospital authorities, patients of COPD and Asthma and normal volunteers and take their consent for sputum examination for eosinophils and neutrophils. Day 5 Performed the first round of study with all the four categories of subjects' viz. COPD patients, Asthma patients, Smokers and Normal subjects. Day 6 Performed the second round of study with all the four categories of subjects. Day 7 Results were calculated, studied and concluded. Result Plenty of samples (76% of first attempts) obtained from lower respiratory tract were obtained. A fall is reported as low as 5.3% and maximum of 20% in the forced expiratory volume (FEV1) during inhalation of saline. There was a reliability coefficient of 0.8 for Eosinophil and 0.7 for metachromatic cell counts respectively. This data was reproducible. A comparative data was estimated between sputum from normal subjects, sputum from asthmatic patients contained a significantly higher proportion of eosinophils (mean 18.5% (SE 3.8%) v 1.9% (0.6%)) and metachromatic cells (0.50% (0.18%) v 0.039% (0.014%)) (Pin et al, 1992). The results obtained by Jacob et al show that in the span of 15 months, 175 patients went for 537 consultations. In 57% patients' impairment in their quality of life was reported. The given data is associated with subsequent GP interventions and patients' education and counseling. A multivariate logistic regression analysis was performed based on physical complaints and a change in medication prescription was done along with education about control regimen. Various studies are being performed to understand and also discriminate COPD and asthma in one of the studies direct and indirect costs associated with asthma and chronic obstructive pulmonary disease (COPD) in Sweden in 1980 and 1991, was performed to classify trends in the use of outpatient concern, drugs and inpatient concern, and the development of momentary morbidity, permanent disability and mortality for asthma and COPD (Jacobson, 2000). It is reported that Asthma and COPD jointly account for approximately 2% of the economic cost of all diseases. The total costs associated with each disease were alike, the allocation of the different cost mechanisms and changes differ with time. As reported (Jacobson, 2000), during 1980s, the cost of drugs and out-patient care increased for both diseases on the contrary, the cost of inpatient concern for asthma decreased, but for COPD increased. (Jacobson, 2000). Cell count(% total) for all the four categories Normal (n=16), Smokers (n= 12), COPD (n=14), Asthma (n=12) Conclusion It can be concluded that induced sputum is capable of detecting differences in cell counts between normal and asthmatic subjects and virtues further development of drugs and therapies as a potential means of assessing airway inflammation in asthma. It is clear from these studies that there are populations of patients with COPD and asthma that can be readily distinguished from one another based on their physiology, natural history, and/or disease pathogenesis. It is also clear from these studies that there are many patients who appear to have features of both these disorders (Figure 1). The study conclude that different lines of therapy must be followed by the physicians for both COPD and Asthma once the cell count report is confirmed. It will be a definite help to the physician treating COPD and Asthma patients and will help to combat COPD which is proving to be the fourth leading causes of mortality in US (Confronting COPD in America: Executive Summary). Recommendation: In asthma episodic coughing, wheezing, and shortness of breath has been recognized since ancient times. In concurrence with the medical importance of asthma, the study was performed diligently to define and characterize asthma and COPD. As a result of these efforts, our concept of asthma pathogenesis has evolved from the prior supposition that asthma is caused by an essential irregularity in airway smooth muscle to our present conceptualization that asthma is a chronic inflammatory disorder of the airway. COPD is a complex term that is used to explain a variety of diseases including chronic bronchitis and emphysema. Like asthma, COPD is characterized by a variable airflow obstruction, can be seen with AHR, and evident as episodic shortness of breath, dyspnea, and wheezing. The airways obstruction in COPD is characteristically irreversible or partly reversible, and the mucous metaplasia of chronic bronchitis and the alveolar destruction of emphysema cause a chronic, progressive loss of lung function. The protease-antiprotease hypothesis has dominated our thoughts about COPD over the past 40 years. It proposes that there is a balance between proteases such as matrix metalloproteases (MMPs), cathepsins and serine proteases, and antiproteases, such as tissue inhibitors of metalloproteases, leukocyte proteinase inhibitor. As compared to healthy lung, an antiprotease shield is believed to predominate, preventing proteolytic parenchymal injury. Emphysema is proposed to occur when there is amplification in proteases or a decrease in antiproteases, a process that can be initiated by oxidant lung injury and/or lung inflammation. The affiliation between asthma and COPD has been contemplated on and investigated. The British hypothesis has held scientific and clinical influence in recent years. It proposes that asthma and COPD are distinct entities that are generated by distinct mechanisms. A variety of lines of evidence have been cited to support this idea (British Thoracic Society, 1997). A constant effort and awareness is desired to overcome the mortality caused by COPD and asthma. Drugs targeting COPD must be designed explicitly to combat the disease. It is recommended that patient must practice breathing exercises by means of relaxation, leaning forward while exercising and belly breathing are much help to the patients with pulmonary problems and especially with the cases of COPD and asthma. Supplemental oxygen also help the patients with severe COPD (Lung- Treatment of COPD and Asthma). Summary: Asthma is characterized by eosinophilic and mononuclear cell infiltration, mucous metaplasia, airway remodeling, reversible airflow obstruction, and airway hyper-responsiveness. COPD is typified by nonreversible or incompletely reversible airway obstruction, often accompanied by mucous metaplasia and alveolar destruction. There is considerable overlap in pathogenesis and clinical features between both these conditions. However, asthma and COPD may be distinguished by their respective cytokine profiles. COPD and asthma may represent disease states along a continuum, with varying degrees of each disease often present in the same patient. It is clear from the conducted study, that there are populations of patients with COPD and asthma that can be readily distinguished from one another based on their physiology, natural history, and/or disease pathogenesis. It is also clear that there are many patients who appear to have features of both disorders. As a result of these findings, it is reasonable to hypothesize that in these patients there is a continuum between COPD/emphysema and asthma. At the asthmatic extreme are patients with normal alveoli, normal pulmonary compliance, and minimal tissue proteolysis and injury. As one moves toward COPD and emphysema, there is a progressive increase in alveolar destruction, compliance, and parenchymal injury and remodeling. Using this concept, it is easy to see how varying degrees of asthma and COPD may overlap in the same individual. Bibliography: 1. American Lung Association. American Lung Association Fact Sheet: Chronic Obstructive Pulmonary Disease (COPD). Available at: http://www.lungusa.org/diseases/copd_factsheet.html. 2. Anthonisen NR, Manfreda J, Warren CPW, Hershfield ES, Harding GKM, Nelson NA. 1987. Antibiotic therapy in exacerbations of chronic obstructive pulmonary disease. Ann Intern Med.;106:196-204. 3. Barnes P., J. 1996. Pathophysiology of asthma. Br J Clin Pharmacol; 42:3-10 4. Barnes P., J., 1998 New therapies for chronic obstructive pulmonary disease. Thorax; 53:137-147. 5. Barnes P., J. 1998. Chronic obstructive pulmonary disease: new opportunities for drug development. Trends Pharmacol Sci; 19:415-423 6. Barnes P., J.1999 Managing Chronic Obstructive Pulmonary Disease. London, England: Science Press Ltd. 7. Barnes P., J. 2000. Chronic obstructive pulmonary disease. N Engl J Med.;343:269-280. 8. Chronic Lung Diseases. Available at: http://www.health-center.com/english/body/respiratory/copd.htm. 9. Chung K., F, Barnes P., J. 1999., Cytokines in asthma. Thorax; 54:825-857. 10. Chronic Lung Diseases. Available at: http://www.health-center.com/english/body/respiratory/copd.htm. 11. European Respiratory Society. 1995. ERS consensus statement. Optimal assessment and management of chronic obstructive pulmonary disease (COPD). Eur Respir J.;8:1398-1420. 12. Elias, J. 2004. The Relationship between Asthma and COPD Lessons from Transgenic Mice, Chest; 126: 111S-116S. 13. Jacobs, J., E.,'van de Lisdonk, E., H.,'Smeele, I., van Weel, C., 2001 Management of patients with asthma and COPD: monitoring quality of life and the relationship to subsequent GP interventions Family Practice, Volume 18,'Number 6, pp. 574-580(7) 14. Lung- Treatment of COPD and Asthma, http://www.nlhep.org/lung_trtmnt.html 15. Meagher LC, Cousin JM, Seckl JR, et al. 1996 Opposing effects of glucocorticoids on the rate of apoptosis in neutrophilic and eosinophilic granuloctyes. J Immunol; 156:4422-4428 16. Miravitlles M, Mayordomo C, Art's M, Sanchez-Agudo L, Nicolau F, Seg' J-L. 1999 Treatment of chronic obstructive pulmonary disease and its exacerbations in general practice. Respir Med.;93:173-179. 17. National Asthma Education and Prevention Program. Clinical Practice Guidelines. Expert Panel Report 2. Guidelines for the Diagnosis and Management of Asthma. Bethesda, Md: National Heart, Lung, and Blood Institute, National Institutes of Health, US Dept of Health and Human Services; 1997. NIH publication 97-4051. 18. What Is COPD' Available at: http://www.thebreathingspace.com/libry.htm#What. Top of Form Read More