Low awareness of COPD among physicians

Introduction: Early identification of patients with chronic obstructive pulmonary disease (COPD) in the health care system followed by successful smoking cessation may prevent rapid lung function deterioration, development of severe COPD and respiratory failure. Objectives: The aim of this study was to determine the frequency of under‐diagnosed chronic obstructive lung diseases among current smokers. Materials and methods: The under‐diagnosis of COPD among smokers was determined in subjects who participated in a screening procedure aimed at recruiting COPD patients for a smoking cessation programme. In order to identify current smokers, a questionnaire was sent out to persons who had been on sick leave for various reasons certified by a physician for more than 2 weeks. Subjects who stated that they currently smoked more than eight cigarettes per day were invited to perform a lung function test. Results: A total of 3887 subjects performed spirometry, i.e. forced expiratory volume in 1 s and forced expirations, and among these, 674 (17.3%) had COPD according to the European Respiratory Society (ERS) consensus guidelines. Of those, 103 (17.3%) had physician‐diagnosed COPD. Productive cough was reported by 16.6% of the COPD subjects. Despite the fact that smokers were on sick leave certified by a physician, more than 80% of those with COPD had no previous diagnosis. As the COPD diagnosis cannot be based on reported symptoms, a spirometry on persons at risk must be performed. Conclusion: The awareness of COPD among primary care physicians has to increase and smokers above the age of 40, with and without respiratory symptoms, have to undergo spirometry if it is regarded important to establish the COPD diagnosis at an early stage. Please cite this paper as: Sundblad B‐M, Larsson K and Nathell L. Low awareness of COPD among physicians. The Clinical Respiratory Journal 2008; 2: 11–16.     

Increasing PAs' awareness and understanding of self-help groups. An educational model

A model for inclusion of information about self-help groups into a PA training program is provided based on the results of a study of 26 PA students enrolled in a patient-counseling class. Interactions with self-help groups yield more positive beliefs and greater intentions to collaborate with self-help groups than training programs that do not address self-help groups. The experiential component is also useful for increasing understanding of appropriate roles for professionals interacting with self-help groups.     

Increasing awareness of sex differences in airway diseases

There is growing epidemiologic data demonstrating sex differences with respect to prevalence and progression of airway diseases, including asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF) and non‐CF‐related bronchiectasis. In asthma, for example, young boys have increased exacerbations and higher morbidity than girls which distinctly reverses after adolescence and into adulthood. In COPD, a disease that was historically considered an illness of men, the number of women dying per year is now greater than in men. Finally, women with CF‐related bronchiectasis have a decreased median life expectancy relative to men and a higher risk of respiratory infections despite equal prevalence of the disease. A number of studies now exist demonstrating mechanisms behind these sex differences, including influences of genetic predisposition, sex hormones and comorbidities. The notable sex disparity has potential diagnostic, therapeutic and prognostic implications and for the practicing respiratory or general physician, a familiarity with these distinctions may augment effective management of patients with airway diseases. This review seeks to concisely summarize the data regarding gender‐based differences in airway diseases, outline the current understanding of contributing factors and discuss therapeutic implications for clinicians.     

Pathogenesis of COPD. Part III. Inflammation in COPD.

Chronic obstructive pulmonary disease (COPD) is mostly caused by cigarette smoking and affects up to 25% of smokers. Air pollution and occupational exposure to dust and fumes can also induce COPD. COPD is characterised by airflow limitation that is not fully reversible and chronic inflammation of the lung. Most patients with COPD also have evidence of tissue remodelling in the smaller airways. How the different pathological features are linked remains unknown. The inflammation of the COPD lung is initially caused by cigarette smoke and the increased infiltration of immune cells into the lung, but it is not clear why the inflammation persists after smoking cessation, while other pathologies partly reverse. Furthermore, anti-inflammatory treatments are not very successful and only control the symptoms but do not cure the disease. Animal models suggest that the imbalance of proteases and antiproteases is central to the major pathologies in the COPD lung. However, this hypothesis was never fully confirmed in humans and may only explain the degenerative stage of the disease, emphysema. The role of tissue-forming cells in the pathogenesis of COPD has not been adequately studied and indicates a deregulated synthesis of growth factors and cytokines in COPD. Finally, recent studies indicate that alpha-1-antitrypsin activity plays a role in all forms of COPD.     

COPD management. Part I. Strategies for managing the burden of established COPD.

Effective management of chronic obstructive pulmonary disease (COPD) is dependent on an accurate diagnosis and assessment of severity. COPD is a clinical diagnosis, based on a history of exposure to known risk factors and the presence of airway obstruction that is not fully reversible. Maximal therapy and support for smoking cessation should be offered to all patients. Symptoms may only develop when a significant loss of lung function has occurred, and the diagnosis is frequently made late in the course of the disease. Earlier diagnosis is dependent on a high index of suspicion, particularly in current and ex-smokers or those exposed to occupational dusts and indoor pollution, and accurate performance and interpretation of spirometry. Established COPD associated with symptoms should initially be treated with bronchodilators as needed, but long-acting bronchodilators should be used when symptoms persist and inhaled corticosteroids added for moderate to severe airflow limitation, particularly when associated with exacerbations. Combination long-acting bronchodilators and inhaled corticosteroids reduce the exacerbation rate and improve the quality of life and symptoms, but they have not been shown to improve survival. Exacerbations are associated with worsening health status and can be managed effectively at home. When symptoms worsen despite optimal treatment for exacerbations, hospital admission is necessary. Non-invasive ventilation has reduced the need for mechanical ventilation, but hospital admission and respiratory failure are associated with a significantly worse prognosis. Pulmonary rehabilitation plays an important role in improving exercise capacity at all severities of COPD, and should be widely available.     

Microsatellite DNA instability in COPD.

STUDY OBJECTIVES: Cigarette smoking is the prime cause of COPD; however, only a few smokers develop the disease. In a previous study, we demonstrated that microsatellite DNA instability (MSI) is a detectable phenomenon in sputum cells of COPD patients. Therefore, we hypothesize that this genetic alteration may indicate susceptibility to COPD. DESIGN: In order to investigate this hypothesis, we compared smokers who developed COPD with smokers who did not develop COPD (referred to as non-COPD smokers). SETTING: Seven highly polymorphic microsatellite markers were targeted on the DNA of sputum cells and of WBCs. PATIENTS AND PARTICIPANTS: We studied 60 non-COPD smokers and 59 severe COPD patients with a similar smoking history (mean +/- SD) of 48+/-25 and 54+/-33 pack-years, respectively (p = 0.77). Non-COPD smokers were tested once; COPD smokers were tested twice, with an interval of 24 months between tests. RESULTS: MSI was detected in 14 COPD patients (24%) but in none of the non-COPD smokers. In 10 COPD patients, MSI was exhibited by one microsatellite marker; in the remaining 4 COPD patients, MSI was exhibited by two different alleles. The most commonly affected marker was THRA1 on chromosome 17 (43%). No significant differences were found between MSI-positive and MSI-negative COPD patients for clinical or laboratory parameters, survival, and development of lung cancer. No change in the microsatellite alleles was found between the tests performed with a 24-month interval. CONCLUSIONS: This study demonstrated that MSI was found exclusively in the sputum cells of smokers with COPD. The results support the hypothesis that MSI could be part of the complex genetic basis of COPD, and it could be a marker of the genetic alteration caused by smoking that allows COPD to develop.     

Bacteria, antibiotics and COPD.

Bacterial infection is one of several important causes of exacerbations of chronic obstructive pulmonary disease (COPD) that may coexist. COPD is a heterogeneous condition and the incidence of bacterial infection is not uniform; mucus hypersecretion may be an important risk factor. The bacteriology of infections varies depending on the severity of the underlying airway disease. There is now a much better understanding of the pathogenesis of bacterial infections of the respiratory mucosa. Lower airway bacterial colonization may be a stimulus for chronic inflammation and may influence the interval between exacerbations. Antibiotic resistance has increased in all the major pathogens. Antibiotics are an important part of the treatment of acute exacerbations of COPD and the decision about whether to give an antibiotic can be made on clinical grounds. It is more difficult to decide, on the available evidence, whether patient characteristics and the risk of antibiotic resistance should influence choice of empiric antibiotic treatment. Most new antibiotics are modifications of existing structures, suggesting that every effort should be made to conserve the sensitivity of current antibiotics by using them appropriately.     

End-of-life care for COPD patients.

Patients with chronic obstructive pulmonary disease (COPD) receive poor end-of-life (EoL) care, in part because their disease course is not predictable. If the family physician would not be surprised at the patient's death within a year, then EoL issues should be raised for discussion. Embarking on such a discussion has the potential to enhance the patient's quality of life and EoL care, thereby avoiding unnecessary treatments or interventions. An Advance Health Care Directive can be useful. Appropriately-used systemic (not nebulised) opioids are safe and effective for managing dyspnoea. The family physician is in an excellent position to provide comprehensive EoL care for COPD patients.     

Future Advances in COPD Therapy.

There is a pressing need for more effective drug treatments for COPD. New bronchodilators include a long-acting anticholinergic tiotropium bromide and a dual beta2-dopamine2-receptor agonist. But no treatments prevent the progression of COPD. Mediator antagonists in development include leukotriene B4 antagonists, chemokine receptor antagonists and more potent antioxidants. The inflammation of COPD is resistant to corticosteroids, so new anti-inflammatory drugs need to be developed. These include phosphodiesterase-4 inhibitors, nuclear factor-kappaB inhibitors and p38 MAP kinase inhibitors. Small molecule protease inhibitors, including neutrophil elastase inhibitors and selective matrix metalloproteinase inhibitors are also in development. Future drug targets may be identified by gene array and proteomics.