how are asthma and emphysema inter-realated.
Asthma is a chronic inflammatory disease of the airways and unfortunately in today’s world it is quite common. Asthma is known for causing recurring periods of wheezing, chest tightness, shortness of breath, and coughing. Emphysema is a long-term lung disease that is included in a group of diseases called chronic obstructive pulmonary disease or COPD. Emphysema is most often caused by tobacco smoking and long-term exposure to air pollution. The other form of COPD is chronic bronchitis, which can also be caused by smoking. A patient who has features of more than one condition exhibits an overlap syndrome.The pathogenesis of overlapping asthma and COPD may be mediated by inflammatory/immune mechanisms and/or structural alterations. The clinical recognition of overlapping asthma and COPD requires an assessment of increased variability of airflow and incompletely reversible airflow obstruction. Numerous studies have documented the presence of partial reversibility after short-term and long-term bronchodilator administration in patients with COPD. Current guidelines emphasize a fixed or irreversible component to airway obstruction in some patients with asthma. Thus, the use of phenotypic characteristics (e.g., symptoms, allergy, bronchial hyperresponsiveness) may be useful in differentiating disease characteristics and in understanding similarities in the development and progression of both obstructive airway diseases. A recent study found that 17% to 19% of patients with obstructive airway diseases had more than one condition, or overlap.The overlap of asthma and COPD has been confirmed in older patients by objective testing and is becoming an important clinical consideration.
The distinction between the inflammatory profiles of asthma and COPD may be blurred under certain circumstances. Classically, asthmatic airways show a CD4+ lymphocyte-, eosinophil-, and macrophage-rich inflammatory response, whereas prominent increases in CD8+ T cells, neutrophils, and macrophages are seen in the bronchioles and alveoli in COPD. However, compared with mild and moderate asthmatics, severe asthmatics or asthmatics who smoke show higher numbers of neutrophils in bronchoalveolar lavage fluid and biopsies. Conversely, in COPD patients, especially those with acute disease exacerbations, tissue eosinophilia is commonand is associated with a favorable response to steroid therapy.
In asthmatics, there is a predominance of Th2 cytokines, including interleukin (IL)-4, IL-5, and IL-13, and upregulation of chemokines, including regulated on activation, normal T-cell-expressed and secreted (RANTES), eotaxins, and monocyte chemoattractant protein-1. In contrast, Th1-dominated responses such as enhanced production of interferon-γ by CD8+ cells have been documented in COPD patients. Additionally, the main inflammatory mediators involved in the pathogenesis of tissue inflammation in COPD are the neutrophil chemokine IL-8, leukotriene B4, IL-1, and tumor necrosis factor-α.However, in some COPD subjects, the levels of tumor necrosis factor-α indicated the presence of asthma, and allergic inflammatory mediators such as IL-4, IL-5, and IL-13 were produced, particularly during exacerbations.
Alveolar inflammation and the development of lung emphysema are major characteristics of COPD. The distal lung, including the alveolar parenchyma, is an important site of inflammation in asthma, although asthma is classically considered as a chronic inflammatory disease of the airways. Remodeling of various structural components such as airway epithelium, airway smooth muscle, vessel, mucous gland, and extracellular matrix is prominent in asthmatic airways. The pathological changes within the airways that are associated with asthma and COPD are similar. Based on the complexities of the relationships among the clinico-pathobiological features of the two diseases, the 'Dutch hypothesis' was proposed and updated.This hypothesis suggests that asthma and COPD are different expressions of a single disease entity. In contrast, the 'British hypothesis' states that asthma and COPD are separate clinical entities with similar symptoms. The general consensus under either hypothesis is that similar mechanisms are involved in the pathogenesis of both diseases.
A patient who has features of more than one condition exhibits an overlap syndrome.The pathogenesis of overlapping asthma and COPD may be mediated by inflammatory/immune mechanisms and/or structural alterations. The clinical recognition of overlapping asthma and COPD requires an assessment of increased variability of airflow and incompletely reversible airflow obstruction. Numerous studies have documented the presence of partial reversibility after short-term and long-term bronchodilator administration in patients with COPD. Current guidelines emphasize a fixed or irreversible component to airway obstruction in some patients with asthma. Thus, the use of phenotypic characteristics (e.g., symptoms, allergy, bronchial hyperresponsiveness) may be useful in differentiating disease characteristics and in understanding similarities in the development and progression of both obstructive airway diseases. A recent study found that 17% to 19% of patients with obstructive airway diseases had more than one condition, or overlap.The overlap of asthma and COPD has been confirmed in older patients by objective testing and is becoming an important clinical consideration.
The distinction between the inflammatory profiles of asthma and COPD may be blurred under certain circumstances. Classically, asthmatic airways show a CD4+ lymphocyte-, eosinophil-, and macrophage-rich inflammatory response, whereas prominent increases in CD8+ T cells, neutrophils, and macrophages are seen in the bronchioles and alveoli in COPD. However, compared with mild and moderate asthmatics, severe asthmatics or asthmatics who smoke show higher numbers of neutrophils in bronchoalveolar lavage fluid and biopsies. Conversely, in COPD patients, especially those with acute disease exacerbations, tissue eosinophilia is commonand is associated with a favorable response to steroid therapy.
In asthmatics, there is a predominance of Th2 cytokines, including interleukin (IL)-4, IL-5, and IL-13, and upregulation of chemokines, including regulated on activation, normal T-cell-expressed and secreted (RANTES), eotaxins, and monocyte chemoattractant protein-1. In contrast, Th1-dominated responses such as enhanced production of interferon-γ by CD8+ cells have been documented in COPD patients. Additionally, the main inflammatory mediators involved in the pathogenesis of tissue inflammation in COPD are the neutrophil chemokine IL-8, leukotriene B4, IL-1, and tumor necrosis factor-α.However, in some COPD subjects, the levels of tumor necrosis factor-α indicated the presence of asthma, and allergic inflammatory mediators such as IL-4, IL-5, and IL-13 were produced, particularly during exacerbations.
Alveolar inflammation and the development of lung emphysema are major characteristics of COPD. The distal lung, including the alveolar parenchyma, is an important site of inflammation in asthma, although asthma is classically considered as a chronic inflammatory disease of the airways. Remodeling of various structural components such as airway epithelium, airway smooth muscle, vessel, mucous gland, and extracellular matrix is prominent in asthmatic airways. The pathological changes within the airways that are associated with asthma and COPD are similar. Based on the complexities of the relationships among the clinico-pathobiological features of the two diseases, the 'Dutch hypothesis' was proposed and updated.This hypothesis suggests that asthma and COPD are different expressions of a single disease entity. In contrast, the 'British hypothesis' states that asthma and COPD are separate clinical entities with similar symptoms. The general consensus under either hypothesis is that similar mechanisms are involved in the pathogenesis of both diseases.
