1,721,082 research outputs found
Evaluation by self-monitoring and noninvasive measures
No full textAsthma severity may be defined in various ways. Despite common perception, well-controlled asthma is not synonymous with mild asthma and poorly controlled asthma is not synonymous with severe asthma. Symptoms cannot always be used as the only criteria of severity since the individual tolerance to a given degree of airflow limitation is variable. There are three asthma phenotypes which are generally defined as difficult to treat asthma: brittle asthma, systemic glucocorticoid-dependent asthma, and glucocorticoid-resistant asthma. This article reviews the role of self-monitoring and noninvasive measures in the diagnosis and treatment of difficult to control asthma and therapy-resistant asthma. An objective measure of the overall asthma severity is essential in the diagnosis and treatment of difficult to control asthma and therapy-resistant asthma, because the goal of asthma control is based on self-monitoring/noninvasive measures, essentially history and lung function tests. The role of ..
Prevention of Chronic Obstructive Pulmonary Disease
No full textCOPD is defined as a preventable condition given that environmental/nongenetic factors play a crucial role in the initiation and development of most of the disease’s clinical expressions, which are possibly related to several interconnected preventable traits. Most of the current evidence on COPD pathogenesis originates from cigarette smoking, and to a lesser extent exposure to outdoor, indoor, and occupational pollutants. Therefore, currently available evidence regarding prevention strategies, and particularly primary prevention, is mainly related to these preventable traits. Smoking cessation has the greatest capacity for influencing the natural history of COPD, and smoking avoidance and cessation remains the only proven primary prevention strategy for chronic respiratory diseases. However, even25 years after the publications of the WHO regarding cigarette smoking, there is still no solid evidence indicating that this convention has globally reduced cigarette consumption. Primary prevention of adverse air pollution effects has been focused on developing ambient air quality guidelines; however, many countries have lacked in the enforcement of standards. BMF air pollutants measured in homes in low-income countries
have been greater than the corresponding values in high-income countries, with evidence of a consistent dose-response relationship. Improving cooking fuels and kitchen ventilation could potentially be effective in decreasing COPD incidence in these conditions. However, although primary prevention remains fundamental for COPD and for all chronic diseases, the evidence of its feasibility and effectiveness remains weak. This weakness is emphasized by a National Institutes of Health (NIH) workshop report that provides a detailed list of future research/actions necessary to properly address this important issue (Box 1). Many strategies have been developed for the many identified preventable trait; however, although these are effective in theory, there are no tangible changes in real-world/large-scale conditions.
In addition, there is current accumulating evidence highlighting that the origins of some chronic diseases, including COPD, could already be present shortly after birth and that primary prevention of chronic obstructive respiratory diseases should probably be started during pregnancy and the first years of life
Risk and Prevention of Cardiovacular Events after Exacerbations of Respiratory Symptoms in Patients with COPD
Full text linkMechanism of occupational asthma
No full textInhalation of agents in the workplace can induce asthma in a relatively small proportion of exposed workers. Like nonoccupational asthma, occupational asthma is probably the result of multiple genetic, environmental, and behavioral influences. It is important that occupational asthma be recognized clinically, because it has serious medical and socioeconomic consequences. Environmental factors that can affect the initiation of occupational asthma include the intrinsic characteristics of causative agents, as well as the influence of the level and route of exposure at the workplace. The identification of host factors, polymorphisms, and candidate genes associated with occupational asthma may improve our understanding of mechanisms involved in asthma. High-molecular-weight compounds from biological sources and low-molecular-weight chemicals cause occupational asthma after a latent period of exposure. Although the clinical, functional and pathologic features of occupational asthma caused by low-molecular-weight agents resemble those of allergic asthma, the failure to detect specific immunoglobulin E antibodies against most low-molecular-weight agents has resulted in a search for alternative or complementary physiopathologic mechanisms leading to airway sensitization. Recent advances have been made in the characterization of the immune response to low-molecular-weight agents. In contrast, the mechanism of the form of occupational asthma that occurs without latency after high-level exposure to irritants remains undetermined
Copd, pulmonary fibrosis and ilas in aging smokers: The paradox of striking different responses to the major risk factors
Full text linkAging and smoking are associated with the progressive development of three main pulmonary diseases: chronic obstructive pulmonary disease (COPD), interstitial lung abnormalities (ILAs), and idiopathic pulmonary fibrosis (IPF). All three manifest mainly after the age of 60 years, but with different natural histories and prevalence: COPD prevalence increases with age to >40%, ILA prevalence is 8%, and IPF, a rare disease, is 0.0005–0.002%. While COPD and ILAs may be associated with gradual progression and mortality, the natural history of IPF remains obscure, with a worse prognosis and life expectancy of 2–5 years from diagnosis. Acute exacerbations are significant events in both COPD and IPF, with a much worse prognosis in IPF. This perspective discusses the paradox of the striking pathological and pathophysiologic responses on the background of the same main risk factors, aging and smoking, suggesting two distinct pathophysiologic processes for COPD and ILAs on one side and IPF on the other side. Pathologically, COPD is characterized by small airways fibrosis and remodeling, with the destruction of the lung parenchyma. By contrast, IPF almost exclusively affects the lung parenchyma and interstitium. ILAs are a heterogenous group of diseases, a minority of which present with the alveolar and interstitial abnormalities of interstitial lung disease
Remodeling in response to infection and injury - Airway inflammation and hypersecretion of mucus in smoking subjects with chronic obstructive pulmonary disease
No full textNeutrophils and Asthma
No full textThe importance of inflammation in asthma has been recognized for a long time and recently proved in man and animal models. All inflammatory cells are probably involved in exacerbations of asthma. Neutrophils in particular are present in the airways during and after the spontaneous asthma attacks in man and during asthmatic reactions and airway hyperresponsiveness induced experimentally in man and animals. Depletion of neutrophils prevents these effects and repletion with neutrophils reconstitutes them. Moreover, the supernatant from stimulated human neutrophils causes transient hyperresponsiveness. However, neutrophils are not increased in stable asthmatics with hyperreactive airways and are not involved in airway hyperresponsiveness induced experimentally in some animals (e.g. guinea-pigs). The studies reviewed suggest that neutrophils may be involved in the transient increases of airway responsiveness associated with exacerbations of asthma, but not in the long-lasting hyperresponsiveness of stable asthmatics
- …
