Asthma-COPD overlap syndrome (ACOS) or asthma-COPD overlap captures the subset of patients with airways disease who have features of both asthma and chronic obstructive pulmonary disease (COPD). ...Although definitions of ACOS vary, it is generally thought to encompass persistent airflow limitation in a patient older than 40 years of age with either a history of asthma or large bronchodilator reversibility. ACOS affects about a quarter of patients with COPD and almost a third of patients who previously had asthma. Compared with their counterparts with asthma or COPD alone, patients with ACOS have significantly worse respiratory symptoms, poorer quality of life, and increased risk of exacerbations and hospital admissions. Whether this condition emerges after gradual shifts in airway remodelling and inflammation in a patient with COPD, as the result of noxious exposures in a patient with asthma, or even as a de novo disease with its own pathology is yet to be determined. Nevertheless, using treatments developed for asthma or COPD that target eosinophilic, neutrophilic, or paucigranulocytic airway inflammation may be a helpful approach to these patients until further clinical trials can be performed.
COVID-19 and COPD Leung, Janice M; Niikura, Masahiro; Yang, Cheng Wei Tony ...
The European respiratory journal,
08/2020, Letnik:
56, Številka:
2
Journal Article
Asthma-COPD overlap (ACO) is a heterogeneous condition that describes patients who show persistent airflow limitation with clinical features that support both asthma and COPD. Although no single ...consensus definition exists to diagnose this entity, common major criteria include a strong bronchodilator reversibility or bronchial hyperreactivity, a physician diagnosis of asthma, and a ≥ 10-pack-year cigarette smoking history. The prevalence of ACO ranges from 0.9% to 11.1% in the general population, depending on the diagnostic definition used. Notably, patients with ACO experience greater symptom burden, worse quality of life, and more frequent and severe respiratory exacerbations than those with asthma or COPD. The underlying pathophysiologic features of ACO have been debated. Although emerging evidence supports the role of environmental and inhalational exposures in its pathogenesis among patients with a pre-existing airway disease, biomarker profiling and genetic analyses suggest that ACO may be a heterogeneous condition, but with definable characteristics. Early-life factors including childhood-onset asthma and cigarette smoking may interact to increase the risk of airflow obstruction later in life. For treatment options, the population with ACO historically has been excluded from therapeutic trials; therefore strong, evidence-based recommendations are lacking beyond first-line inhaler therapies. Advanced therapies in patients with ACO are selected according to disease phenotypes and are based on extrapolated data from asthma and COPD. Research focused on defining biomarkers and evidence-based treatment options for ACO is needed urgently.
The aims of this systematic review were to determine which blood-based molecules have been evaluated as possible biomarkers to diagnose chronic obstructive pulmonary disease (COPD) exacerbations ...(AECOPD) and to ascertain the quality of these biomarker publications. Patients of interest were those that have been diagnosed with COPD. MEDLINE, EMBASE, and CINAHL databases were searched systematically through February 2015 for publications relating to AECOPD diagnostic biomarkers. We used a modified guideline for the REporting of tumor MARKer Studies (mREMARK) to assess study quality. Additional components of quality included the reporting of findings in a replication cohort and the use of receiver-operating characteristics area-under-the curve statistics in evaluating performance. 59 studies were included, in which the most studied biomarkers were C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). CRP showed consistent elevations in AECOPD compared to control subjects, while IL-6 and TNF-α had variable statistical significance and results. mREMARK scores ranged from 6 to 18 (median score of 13). 12 articles reported ROC analyses and only one study employed a replication cohort to confirm biomarker performance. Studies of AECOPD diagnostic biomarkers remain inconsistent in their reporting, with few studies employing ROC analyses and even fewer demonstrating replication in independent cohorts.
Despite substantial progress in reducing the global impact of many non-communicable diseases, including heart disease and cancer, morbidity and mortality due to chronic respiratory disease continues ...to increase. Many factors have contributed to what must now be considered a public health emergency: failure to limit the sale and consumption of tobacco products, unchecked exposure to environmental pollutants across the life course, and the ageing of the global population (partly as a result of improved outcomes for other conditions). In particular, we advocate for: broader understanding of risk factors (including the devastating effects of global poverty) and the preventive measures necessary to avoid future cases of COPD, disruptive approaches to diagnosis that are not solely based on spirometric airflow limitation but also involve identification of early pathological changes that are more amenable to reversal, classification of the disease into types that share pathophysiological similarities and could lead to novel preventive and therapeutic approaches, and a new approach to the diagnosis and assessment of exacerbations of COPD that focuses on disease mechanisms. An acute worsening of COPD is termed an exacerbation, and such episodes account for a substantial proportion of the attributable cost of the disease and are associated with accelerated lung function loss, prolonged impairments in quality of life, and similar prognosis to many stage III or IV solid organ malignancies.
Chronic obstructive pulmonary disease (COPD) is a global health issue with high social and economic costs. Concomitant chronic cardiac disorders are frequent in patients with COPD, likely owing to ...shared risk factors (e.g., aging, cigarette smoke, inactivity, persistent low-grade pulmonary and systemic inflammation) and add to the overall morbidity and mortality of patients with COPD. The prevalence and incidence of cardiac comorbidities are higher in patients with COPD than in matched control subjects, although estimates of prevalence vary widely. Furthermore, cardiac diseases contribute to disease severity in patients with COPD, being a common cause of hospitalization and a frequent cause of death. The differential diagnosis may be challenging, especially in older and smoking subjects complaining of unspecific symptoms, such as dyspnea and fatigue. The therapeutic management of patients with cardiac and pulmonary comorbidities may be similarly challenging: bronchodilators may have cardiac side effects, and, vice versa, some cardiac medications should be used with caution in patients with lung disease. The aim of this review is to summarize the evidence of the relationship between COPD and the three most frequent and important cardiac comorbidities in patients with COPD: ischemic heart disease, heart failure, and atrial fibrillation. We have chosen a practical approach, first summarizing relevant epidemiological and clinical data, then discussing the diagnostic and screening procedures, and finally evaluating the impact of lung-heart comorbidities on the therapeutic management of patients with COPD and heart diseases.
Globally, nearly 400 million persons have COPD, and COPD is one of the leading causes of hospitalisation and mortality across the world. While it has been long-recognised that COPD is an inflammatory ...lung disease, dissimilar to asthma, type 2 inflammation was thought to play a minor role. However, recent studies suggest that in approximately one third of patients with COPD, type 2 inflammation may be an important driver of disease and a potential therapeutic target. Importantly, the immune cells and molecules involved in COPD-related type 2 immunity may be significantly different from those observed in severe asthma. Here, we identify the important molecules and effector immune cells involved in type 2 airway inflammation in COPD, discuss the recent therapeutic trial results of biologicals that have targeted these pathways and explore the future of therapeutic development of type 2 immune modulators in COPD.
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