Chronic Obstructive Pulmonary Disease (COPD) and Lung Cancer are common diseases amongst smokers and they often co-exist making management challenging. There has been a clear association between these disorders but the aetiological factors are unclear. In this review we examine the pathogenic links between these two common disorders and the important management issues in dealing with both diseases.
Examination of bronchoalveolar lavage, induced sputum, and peripheral blood indicate that cysteinyl leukotriene receptor blockers decrease inflammatory cells in asthma but these do not examine airway tissue per se.Our objective was to determine the effect of montelukast, a leukotriene receptor antagonist, on airway tissue inflammatory cells by direct bronchoscopic examination of the bronchial mucosa.Adult subjects with mild asthma (pre-bronchodilator FEV1 ≥ 70% predicted; PC20 of ≤4 mg/mL) were given 10 mg/day oral montelukast (N = 38) or placebo (N = 37) for 6 weeks. Bronchial mucosal eosinophils and mast cells were identified and counted.Change from baseline in numbers of biopsy EG2+ (“activated”) eosinophils was the primary endpoint; numbers of total (chromotrope 2R+) eosinophils and (tryptase+) mast cells were secondary. Unexpectedly, there were many patients with zero EG2+ eosinophils at baseline. There was a within-group decrease in EG2+ cells, from 13.54 cells/mm (at baseline) to 0.79 cells/mm at 6 weeks in the montelukast group (LS mean change; 95% confidence interval = −13.59 [−25.45, −1.74] cells/mm; P < 0.05), a change not observed in the placebo group (−1.17 [−13.26, 10.91] cells/mm; NS). The zero-inflated Poisson statistical model demonstrated that montelukast significantly reduced post-treatment EG2+ cells by 80% compared with placebo (95% CI [70.6–86.8%]; P < 0.0001). The data for total eosinophils showed similar changes. The reduction in mast cell numbers was 12% (95% CI [7.9, 16.0]; P < 0.0001).Direct examination of airway tissue confirms that montelukast decreases the number of eosinophils and mast cells in asthma.
To evaluate the inter-rater and intra-rater reliability of the hand held dynamometer in measuring muscle strength in people with interstitial lung disease (ILD).Test retest reliability of hand-held dynamometry for elbow flexor and knee extensor strength between two independent raters and two testing sessions.Physiotherapy department within a tertiary hospital.Thirty participants with ILD of varying aetiology were included. Twenty participants completed the inter-rater reliability protocol (10 idiopathic pulmonary fibrosis, mean (SD) age 73 (10) years, 11 male) and 21 participants completed the intra-rater reliability protocol (10 idiopathic pulmonary fibrosis, mean age 71 (10) years, 11 male).Mean muscle strength (kg). Agreement between the two raters and testing sessions was analyzed using Bland–Altman plots and reliability was estimated using intraclass correlation coefficients (ICC).For elbow flexor strength there was a mean difference between raters of −0.6 kg (limits of agreement (LOA) −5.6 to 4.4 kg) and within raters of −0.3 kg (LOA −2.8 to 2.3 kg). The ICCs were 0.95 and 0.98, respectively. For knee extensor strength there was a mean difference between raters of −1.5 kg (LOA −6.9 to 3.9 kg) and within raters of −0.7 kg (LOA −3.9 to 2.4 kg). The ICCs were 0.95 and 0.97, respectively.Hand-held dynamometry is reliable in measuring elbow flexor and knee extensor strength in people with ILD.
The generalized alternating method of Schwarz was applied to boundary value problems for a multiply connected domain in the prior work Part I [62]. Approximate analytical formulas for the effective properties of dispersed composites with the exactly derived precision of their validity in concentration and in contrast parameter were derived. The present paper is devoted to comparison study of the formulas from Part I and the previously used engineering approximations. It is demonstrated that self-consistent methods (effective medium approximation, mean field, Mori-Tanaka methods etc) can be considered as the first order approximation of Schwarz's method. Implementation of the reiterated homogenization by means of Schwarz's method is also analyzed. This investigation explains a plenty of illusory different formulas which are actually reduced to the same lower order estimations for dilute composites. Some self-consistent methods violate the principles of homogenization and lead to methodologically misleading approaches.
Systemic inflammation is a well-established feature of Chronic Obstructive Pulmonary Disease, COPD, but less is known about inflammation in the upper airways in the disease. In the current study, we investigated the inflammatory profile in the upper airway and in serum in a cohort of patients with COPD.Patients were examined with inflammatory profiles measured on material from the upper airway and in serum using a 14-plex Bioplex multiplex immunoassay containing the following cytokines: IL-1-beta, IL-3, IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, IL-17, IL-18, Interferon-gamma, Tumour Necrosis Factor-alpha, Tumour Necrosis Factor beta, and GM-CSF.We evaluated COPD disease burden using the CAT questionnaire and symptoms from the upper airways with the nasal domain of the 22 items Sino Nasal Outcome Test (SNOT22nasal).We included 180 patients (female 55%, age 67 (±8) years, FEV1% 52.4 (±16.6). Using a SNOT22nasal threshold of ≥6, we divided patients into high upper airways symptoms (high UAS), n = 74 (41%) and low upper airway symptoms (low UAS), n = 106 (59%). High UAS was significantly associated with higher levels of IL-1 beta and IL-3 in nasal samples (p = 0.016 and 0.02, respectively) and higher serum levels of IL-1 beta (p = 0.003). Upper airway scores correlated positively with nasal levels of IL-3 (rho = 0.195, p = 0.01) and serum levels of IL-1 beta (rho = 0.226, p = 0.005).Patients with COPD and high upper airway symptoms displayed signs of eosinophilic and neutrophilic inflammation with elevated levels of IL-1 beta and IL-3 in the nose and elevated IL-1 beta in serum.
New target-specific anticoagulants such as the direct thrombin inhibitor dabigatran and the factor Xa inhibitor rivaroxaban are used in an increasing number of patients. Several studies comparing these new oral anticoagulants with vitamin K antagonists revealed a lower risk of severe bleeding complications and reduced thromboembolic events. However, the lack of antidotes is a challenging issue in the treatment of traumatic or spontaneous intracranial hemorrhage.A retrospective analysis of patients with intracranial bleeding under new oral anticoagulants was performed; these patients were admitted to our department between January 2011 and November 2014. Treatment, reversal management of blood coagulopathy, and outcome of the patients were analyzed.Seventeen patients were included. The median age was 80.4 years. Seven patients were treated with dabigatran and 10 with rivaroxaban. Eight patients had traumatic intracranial bleeding and 9 patients had spontaneous intracranial hemorrhage. Complex perioperative hematologic treatment followed. In 9 cases, the clinical outcome was devastating with severe neurologic deficits (n = 2), comatose status (n = 4), or death (n = 3). Patients with the indication for acute surgical treatment had a high risk for a critical clinical outcome.Only a few case reports have analyzed the clinical course and the outcome after intracranial bleeding under new target-specific oral anticoagulants. Here, one of the first larger series is presented. Because of the lack of reversibility of the anticoagulative effects and the overall risks with geriatric patients, surgical treatment should be delayed as long as possible and comorbidities have to be considered.
Skeletal muscle dysfunction is considered to be one of the key systemic co-morbidities in chronic obstructive pulmonary disease (COPD) influencing exercise capacity and quality of life. The loss of skeletal muscle bulk and skeletal muscle strength are now recognised as important predictors of mortality in this patient group. The mechanisms involved in the development of muscle weakness are likely to be multifactorial, and systemic factors including inflammation and oxidative stress are thought to interact with local factors such as muscle inactivity. A greater understanding of the molecular pathways involved in muscle weakness may provide target areas for future treatments as an adjunct to pulmonary rehabilitation, which remains the mainstay of current therapy. Further research is required to increase and sustain the benefits of pulmonary rehabilitation and to develop novel interventions for this chronic, debilitating condition.
Diabetes mellitus and metabolic syndrome are common in patients with chronic obstructive pulmonary disease (COPD). Metabolic disorders are associated with worse cardiovascular and pulmonary outcomes in COPD patients. This review will consider the prevalence, detection and management of metabolic disorders in COPD.
In response to the letter by Ernst and Suissa1 published in the August edition of Thorax , the issue of incomplete ascertainment of vital status information in five of the seven trials included in the pooled analysis was discussed in the paper.2 This would only make a meaningful impact on the overall results if patients in the inhaled corticosteroid group who withdrew were more likely to die than those patients who withdrew from the placebo arm of the trials. There is no …
Chronic obstructive pulmonary disease (COPD) is characterised by intractable dyspnoea, reduced functional capacity and episodes of acute exacerbation. Physiotherapy plays a key role in multidisciplinary interventions. The evidence in relation to airway clearance, pulmonary rehabilitation, inspiratory muscle training and non-invasive ventilation is now robust whilst further evidence is required for other interventions in order to clarify where application, skills and training should be focused. The challenge is to translate sound clinical evidence-based practice into novel models of service with resultant improvements in care for patients with COPD.
Lung volume reduction surgery (LVRS) improves the fit of severely hyperinflated emphysematous lungs to the surrounding chest cavity and thereby improves respiratory mechanics and expiratory airflow. LVRS is a potent and life extending therapy for some patients with severe emphysema and has a low associated operative mortality. The national emphysema treatment trial (NETT) identified characteristics of patients for whom LVRS improves survival, function and health-related quality of life and characteristics of patients who should not have surgery. Patients with upper-lobe predominant distribution of emphysema on high-resolution computed tomogram are most likely to benefit from LVRS vs. optimal medical therapy and rehabilitation. At long-term follow-up, the survival and functional benefits derived from LVRS are durable. In efforts to make lung volume reduction safer and more broadly accessible physician-scientists have developed bronchoscopic lung volume reduction (BLVR) procedures. Early clinical trials of BLVR performed with endobronchial valves (EVB) and sclerosant biogels demonstrate their safety. The ability of BLVR EBV techniques to produce desired atelectasis and lung volume loss is likely limited in those patients with collateral ventilation, incomplete fissures and those unable to achieve complete lobar exclusion. Results from a phase III BLVR EBV trial are in analysis.
The prevalence of ischemic heart disease is approximately twofold higher in chronic obstructive pulmonary disease (COPD) cohorts compared to the general population. Likewise, cardiac patients with COPD have a reduced short- and long-term survival. This co-morbidity of COPD with atherosclerotic vessel disease is associated with common risk factors, such as smoking. However, atherosclerosis, in addition, shares many of the inflammatory mechanisms with those found in COPD. Atherosclerotsic lesions, as well as the COPD lung, are sites of local inflammation. Furthermore, a systemic inflammatory response, measured as increased CRP, has been reported in both patient populations. There are a number of inflammatory mediators produced in both the vessel wall and in the lungs, which potentially induce common pathological processes. For example, leukotriene B4, which induces chemotaxis of neutrophils, monocytes, T-lymphocytes and smooth muscle cells, has been suggested as a therapeutic target in both diseases. Furthermore, activation of smooth muscle cells may lead to a narrowing of the lumen in both airways and vessels. Finally, proteolytic activities of matrix metalloproteinases may be involved both in emphysema formation and in atherosclerotic plaque rupture, leading to myocardial infarction and stroke. Taken together, the associated co-morbidity of COPD with atherosclerosis and their potential common pathophysiological mechanisms support a notion of these, and other inflammatory diseases, as manifestations of chronic inflammation.
Chronic Obstructive Pulmonary disease (COPD) is associated with multiple comorbid conditions including ischemic heart disease, peripheral muscular dysfunction, osteoporosis, osteopenia, glaucoma, anemia, anxiety , depression, caquexia and malnutrition. A number of individuals with COPD experience involuntary weight loss as the condition progresses and weight loss, muscle wasting and tissue depletion are commonly seen.
Chronic obstructive pulmonary disease (COPD) is an increasing health problem and one of the leading causes of morbidity and mortality worldwide, but knowledge about its pathogenesis has increased substantially in recent years. The disease results from interaction between individual risk factors (like enzymatic deficiencies) and environmental exposures to noxious agents, like cigarette smoking, occupational dusts, air pollution and infections in childhood. The main mechanisms that may contribute to airflow limitation in COPD are fixed narrowing of small airways, emphysema and luminal obstruction with mucus secretions. COPD is characterised by a chronic inflammatory process in the pulmonary tissue, with a pattern different from bronchial asthma, associated with extrapulmonary effects and is considered now a complex, systemic disease. Optimal therapeutic targeting of COPD depends on a clear understanding of the precise mechanisms of these complex processes and on early and correct evaluation of disease severity. A combination of pharmacological and non-pharmacological approaches is used to treat COPD. Bronchodilators are the mainstay of COPD treatment and can be combined with inhaled corticosteroids for greater efficacy and fewer side effects. The use of LTOT for hypoxemic patients has resulted in increased survival, and expanded drug therapy options have effectively improved dyspnoea and quality of life. Recent studies have documented the benefits of pulmonary rehabilitation. In addition, non-invasive mechanical ventilation offers new alternatives for patients with acute or chronic failure.
This review provides an overview of the randomised controlled trials covering the topic of chronic non-invasive positive pressure ventilation (NIPPV) in severe stable COPD patients. Studies investigating patients receiving bilevel NIPPV via nasal, oronasal or total face mask interfaces for at least 1 week or more, were described.
Patients who suffer from chronic obstructive pulmonary disease (COPD) often experience acute exacerbations, which frequently require hospitalization and lead to increased mortality. The most common causes of exacerbation are viruses, bacteria, and air pollutants. The risk of influenza and pneumococcal-related hospitalization and death has been shown to be high among COPD sufferers of all ages.
Although resection of giant bullae for the purpose of improving the function of underlying compressed lung is an accepted form of surgery for emphysema, there is only limited information regarding long-term improvement in dynamic hyperinflation and exercise tolerance. Our major goal was to investigate the effects of lung resection for giant bullae on pulmonary function, dynamic hyperinflation, and exercise capacity in patients with chronic obstructive pulmonary disease characterized by emphysema.Pulmonary function and exercise testing were assessed prospectively before and 3, 6, 12, 24, and 48 months after surgery in 12 patients who had chronic obstructive pulmonary disease with emphysema who underwent lung resection of giant bullae.Forced expiratory volume, diffusing capacity for carbon monoxide, arterial partial pressure of oxygen, and exercise capacity were significantly increased after resection of surgical bullae. Dynamic hyperinflation, as assessed by reduction in inspiratory capacity and dyspnea Borg scale, were significantly decreased during exercise. Improvement in baseline and exercise functional capacity slightly decreased over time, remaining, however, far above the value before surgery.Altogether, these findings suggest that surgery for resection of giant bullae is an effective procedure for improving airflow, limiting gas exchange, and limiting exercise dynamic hyperinflation over time.
