The following associations emerged among respiratory symptom/disease cumulative incidence and risk factor exposure changes: a two-to-five fold higher risk for COPD, phlegm, cough, dyspnoea, asthma attacks, airway obstruction in persistent smokers; a two-to-three fold higher risk for COPD in remittent smokers; a two-fold higher risk for AR, phlegm and a four-fold higher risk for asthma in subjects with persistent occupational exposure; a two-fold higher risk for cough, phlegm, dyspnoea, AR in subjects with incident occupational exposure; a two-fold higher risk for AR, asthma attacks, COPD in subjects with incident traffic exposure.
<i>Methods:</i> We retrospectively compared the effect of an ambulatory PR program in nonsmoking patients with severe asthma and airway obstruction (FEV1/FVC ratio <70% and FEV1 < 80% measured twice, not under an exacerbation) and sex-, age-, FEV1-, and BMI-matched COPD controls.
Two hundred eighty-two subjects had a positive questionnaire; 190 completed portable spirometry, and approximately 34% (65 of 190 subjects) reported respiratory impairment; of these 65 subjects, 33 completed diagnostic spirometry, and 66.7% (22 of 33) showed evidence of COPD, including 2 subjects with severe airway obstruction (GOLD stage 3, according to the Global Initiative for Chronic Obstructive Lung Disease).
The development of pulmonary hypertension (PH) during the course of COPD is a well-known phenomenon, with the prevalence depending on the severity of airway obstruction.
Asthma and COPD appear as a result of different mechanisms triggered by different pathogeneses and although they present different features and symptoms of airway inflammation and airway obstruction, there are also cases that present the features of both asthma and COPD.
Although identifying the degree of airway obstruction remains important for informing the clinical status of the patient with COPD, FEV<sub>1</sub> is no longer used to direct the therapeutic approach.
This study was conducted in order to investigate the diversity of respiratory physiology, including the respiratory impedance and reversibility of airway obstruction, based on quantitative computed tomography (CT) in patients with COPD.
In some patients with COPD, eosinophils contribute to inflammation that promotes airway obstruction; approximately a third of stable COPD patients have evidence of eosinophilic inflammation.
Thus, simultaneous measurement of pentosidine and VEGF levels may be a promising approach to discriminate the severity of small airways obstruction and alveolar destruction in the lower respiratory tract of COPD.
However, although bronchodilators represent the standard of care in the treatment of airway obstruction associated with asthma or COPD, controversy persists regarding the mechanism(s) by which these agents alleviate cough.
In patients with COPD, diaphragmatic mobility seems to be associated with airway obstruction and lung hyperinflation, as well as with ventilatory capacity and the perception of dyspnea, although not with PADL.
To investigate the effectiveness of voluntary lung function screening in bringing to light patients with previously unknown COPD and to evaluate the relationships among symptoms, smoking status, and airway obstruction.
Airway obstruction was defined as FEV<sub>1</sub>/FVC ratio below lower limit of normal (LLN) before bronchodilation, and COPD was defined as an FEV<sub>1</sub>/FVC ratio below LLN after bronchodilation.
Chronic hypoxia is a critical pathological factor associated with the development of PH resulting from airway obstruction (COPD, sleep apnea), diffusion impairment (interstitial lung disease), developmental lung abnormalities, or high altitude exposure (World Health Organization [WHO]; Group III).
Although current therapies for COPD (primarily based on anti-inflammatory agents) contribute to the reduction of airway obstruction and minimize COPD exacerbations, none can avoid disease progression or reduce mortality.
The β-catenin-Snail1-Twist transcription factor cluster is up-regulated and nuclear translocated in smokers and COPD, and their expression is closely related to both EMT activity and airway obstruction.
The identification of these genes and the pathways in which they are enriched is essential to understand the pathophysiology of airway obstruction and to identify novel therapeutic targets and biomarkers for COPD, including drugs that reverse the COPD gene signature in silico.
Airway obstruction is generated in the large and small airways both in asthma and COPD, and this small airway obstruction is located more proximally in asthma, yet is found more distally in severe and older individuals with asthma, comparable to COPD.
Since smoking patients who are Gly16 homozygotes have an increased risk of airway obstruction we hypothesized that beta2-adrenoreceptor gene polymorphisms may be also a cofounder for COPD development and disease severity.
We conclude that there is increased inflammation and IL-4 gene expression in the mucus-secreting glands and the airway mucosa of smokers with bronchitis: both are lower in those with CB and coexisting COPD suggesting that airway inflammation in CB is reduced when airway obstruction develops.