Globally, chronic obstructive pulmonary disease (COPD) is the fourth major cause of mortality and morbidity and projected to rise to third within a decade as our efforts to prevent, identify, diagnose and treat patients at a global population level have been insufficient. The European Respiratory Society and American Thoracic Society, along with the Global Initiative for Chronic Obstructive Lung Disease (GOLD) strategy document, have highlighted key pathological risk factors and suggested clinical treatment strategies in order to reduce the mortality and morbidity associated with COPD. This review focuses solely on issues related to the under- and over-diagnosis of COPD across the main geographical regions of the world and highlights some of the associated risk factors. Prevalence of COPD obtained mainly from epidemiological studies varies greatly depending on the clinical and spirometric criteria used to diagnose COPD,i.e.forced expiratory volume in 1 s to forced vital capacity ratio <0.7 or 5% below the lower limit of normal, and this subsequently affects the rates of under- and over-diagnosis. Although under-utilisation of spirometry is the major reason, additional factors such as exposure to airborne pollutants, educational level, age of patients and language barriers have been widely identified as other potential risk factors. Co-existent diseases, such as asthma, bronchiectasis, heart failure and previously treated tuberculosis, are reported to be the other determinants of under- and over-diagnosis of COPD.Key pointsGlobally, there is large variation in the prevalence of COPD, with 10–95% under-diagnosis and 5–60% over-diagnosis (table 1) due to differences in the definition of diagnosis used, and the unavailability of spirometry in rural areas of low- and middle-income countries where the prevalence of COPD is likely to be high.In order to be diagnosed with COPD, patients must have a combination of symptoms with irreversible airflow obstruction defined by a post-bronchodilator FEV1/FVC ratio of <0.7 or below the fifth centile of the lower limit of normal (LLN), and with a history of significant exposure to a risk factor. Repeat spirometry is recommended if the ratio is between 0.6 and 0.8.Not performing spirometry is the strongest predictor for an incorrect diagnosis of COPD; however, additional factors, such as age, gender, ethnicity, self-perception of symptoms, co-existent asthma, and educational awareness of risk factor by patients and their physician, are also important.COPD can be associated with inhalation of noxious particles other than smoking tobacco.Educational aimsTo summarise the global prevalence of over- and under-diagnosis of COPD.To highlight the risk factors associated with the under- and over-diagnosis of COPD.To update readers on the key changes in the recent progress made regarding the correct diagnosis of COPD.
Background. Adenoviral (Ad)-vectored vaccines are typically administered via intramuscular injection to humans, incapable of inducing respiratory mucosal immunity. However, aerosol delivery of Ad-vectored vaccines remains poorly characterized and its ability to induce mucosal immunity in humans is unknown. This phase 1b trial was to evaluate the safety and immunogenicity of human serotype-5 Ad-vectored tuberculosis (TB) vaccine (AdHu5Ag85A) delivered to humans via inhaled aerosol or intramuscular injection.Methods. 31 healthy, previously BCG-vaccinated adults were enrolled. AdHu5Ag85A was administered by single-dose aerosol using Aeroneb® Solo Nebulizer or by intramuscular (IM) injection. The study consisted of the low dose (LD) aerosol, high dose (HD) aerosol and IM groups.The adverse events were assessed at various times post-vaccination. Immunogenicity data were collected from the peripheral blood and bronchoalveolar lavage samples at baseline and select timepoints post-vaccination.Results. The nebulized aerosol droplets were <5.39µm in size. Both LD and HD of AdHu5Ag85A administered by aerosol inhalation and IM injection were safe and well-tolerated. Both aerosol doses, particularly LD, but not IM, vaccination markedly induced airway tissue-resident memory CD4 and CD8 T cells of polyfunctionality. While as expected, IM vaccination induced Ag85Aspecific T cell responses in the blood, the LD aerosol vaccination also elicited such T cells in the blood. Furthermore, the LD aerosol vaccination induced persisting transcriptional changes in alveolar macrophages. Conclusion.Inhaled aerosol delivery of Ad-vectored vaccine is a safe and superior way to elicit respiratory mucosal immunity. This study warrants further development of aerosol vaccine strategies against respiratory pathogens including TB and COVID-19.Trial registration. This trial is registered with ClinicalTrial.gov, NCT# 02337270.
BackgroundThe individual and combined contribution of viral prevalence in the community to Emergency Department (ED) visits and hospitalizations with respiratory tract infections (RTIs), chronic obstructive pulmonary disease (COPD) and asthma is unclear. Methods A retrospective analysis on daily viral positive tests and daily ED visits and hospitalizations between ResultsThere were 4,365,578 ED visits with RTIs of which 321,719 (7.4%) were admitted to hospital; 817,141 ED visits for COPD of which 260,665 (31.9%) were admitted and 649,666 ED visits with asthma of which 68,626 (10.6%) were admitted. The percentage of positive tests to influenza A and B, respiratory syncytial virus (RSV), parainfluenza and adenovirus prevalence explained 57.4% of ED visits and 63.8% of hospitalizations for RTI, 41.4% of ED visits and 39.2% of hospitalizations with COPD but only 1.5% of ED visits and 2.7% of hospitalizations for asthma. The further addition of human metapneumovirus, rhinovirus and coronavirus over the final 3 years accounted for 66.7% of ED visits and 74.4% of hospitalizations for PLOS ONE | https://doi.
The airway epithelium is the first line of defense for the lungs, detecting inhaled environmental threats through pattern recognition receptors expressed transmembrane or intracellularly. Activation of pattern recognition receptors triggers the release of alarmin cytokines IL-25, IL-33, and TSLP. These alarmins are important mediators of inflammation, with receptors widely expressed in structural cells as well as innate and adaptive immune cells. Many of the key effector cells in the allergic cascade also produce alarmins, thereby contributing to the airways disease by driving downstream type 2 inflammatory processes. Randomized controlled clinical trials have demonstrated benefit when blockade of TSLP and IL-33 were added to standard of care medications, suggesting these are important new targets for treatment of asthma. With genome-wide association studies demonstrating associations between single-nucleotide polymorphisms of the TSLP and IL-33 gene and risk of asthma, it will be important to understand which subsets of asthma patients will benefit most from anti-alarmin therapy.
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