Is pulmonary tuberculosis a true risk-factor for chronic obstructive pulmonary disease?

This viewpoint discusses the possible relationship of tuberculosis with chronic obstructive pulmonary disease. Pulmonary tuberculosis as a risk factor and/or complication of COPD is reported in several reports from African and Asian countries. History of TB seems to have an important role in the natural history of COPD. It is difficult to conclude whether this is a true causal relationship or merely an incidental observation due to the concurrent presence of the two commonly prevalent diseases and their risk factors. Many of these disease and treatment-related factors can promote and/or aggravate disease condition.     

Pneumocystis: a novel pathogen in chronic obstructive pulmonary disease?

Chronic obstructive pulmonary disease (COPD) results in significant morbidity and mortality. Smoking has long been recognized as the primary risk factor for development of COPD, but factors determining the severity or pattern of disease in smokers are largely unknown. Recent interest has focused on the potential role of infectious agents and the associated host response in accelerating progression of airway obstruction or in perpetuating its progression following discontinuation of tobacco exposure. Pneumocystis jirovecii is a fungal pathogen that causes pneumonia in immunocompromised individuals. Recent evidence has linked this organism with COPD. Using sensitive molecular techniques, low levels of Pneumocystis have been detected in the respiratory tract of certain individuals and termed colonization. Several findings support the theory that colonization with Pneumocystis is involved in the "vicious circle" hypothesis of COPD in which colonization with organisms perpetuates an inflammatory and lung remodeling response. Pneumocystis colonization is more prevalent in smokers and in those with severe COPD. The presence of Pneumocystis in the lungs, even at low levels, produces inflammatory changes similar to those seen in COPD, with increases in numbers of neutrophils and CD8(+) lymphocytes. HIV-infected subjects who have had PCP develop permanent airway obstruction, and HIV-infected patients have a high prevalence of both emphysema and Pneumocystis colonization. In addition, a non-human primate model of colonization shows development of airway obstruction and radiographic emphysema. Additional studies are needed to confirm the role of Pneumocystis in the pathogenesis of COPD, given that this agent might be a treatable co-factor in disease progression.     

Exacerbations in chronic obstructive pulmonary disease: do they contribute to disease progression?

The impact of chronic obstructive pulmonary disease (COPD) exacerbations on decline in FEV(1) has been a controversial topic for decades. We will review some of the key studies in this area and discuss potential contributors to inconsistent results of these studies. Dissecting the heterogeneous COPD syndrome into meaningful subtypes and assessing the genetic and environmental influences on COPD-related phenotypes such as exacerbation frequency could clarify the impact of exacerbations on the natural history of COPD.     

Assessment tools for chronic obstructive pulmonary disease: do newer metrics allow for disease modification?

The change in FEV1 has been the traditional metric used to define the progression of chronic obstructive pulmonary disease in affected patients. Consequently, various treatments have "targeted" the accelerated decline in FEV1 in an attempt to modify or alter the disease process. We propose a broader definition for "disease modification" as any change in a metric related to the disease that is maintained over time. Available longitudinal and/or predictive data on several newer modalities are described that might be considered as alternative metrics to assess disease modification in chronic obstructive pulmonary disease. These include inspiratory capacity, exercise capacity, the 6-minute walk distance, dyspnea measures, health status, multidimensional indices, and acute exacerbations. Finally, we consider the impact of disease modifying therapies on some of these metrics.     

Is vitamin D supplementation a viable treatment for Crohn’s disease?

Vitamin D, important for maintaining bone health in Crohn’s disease (CD), may have potential as a treatment for the core inflammatory disease process. There is plausible evidence in favor of vitamin D as an anti-inflammatory from animal models, epidemiological and cross sectional studies of CD. Few clinical trials, however, have been published and therefore the translation of this promise into clinical benefit for people with CD remains unclear. The purpose of this piece is to consider the viability of vitamin D as a treatment for CD based on the current available evidence.     

Chronic obstructive pulmonary disease: a modifiable risk factor for cardiovascular disease?

Significant cardiac morbidity and mortality exists in patients with COPD. Shared risk factors include age, smoking history and exposure to air pollution and passive smoke. Although the inappropriate under-prescribing of β-blockers contributes, it is now appreciated that the observed cardiac risk is not only due to smoking and conventional cardiovascular risk factors, but also other independent factors. A number of hypotheses exist for the increased cardiovascular morbidity and mortality seen in COPD including inflammation, pulmonary hypertension, lung hyperinflation and shared genetics models. Mounting evidence from large randomised controlled trials suggests that COPD treatment may be cardio-protective. We review the current evidence supporting the aforementioned hypotheses and how their modulation may prevent cardiovascular morbidity and mortality in COPD. The persisting underdiagnosis of COPD may have significant consequences. Further mechanistic studies identifying the onset and impact of individual interventions will develop our understanding of this emerging and highly relevant clinical field.     

Mucosal immunity in asthma and chronic obstructive pulmonary disease: a role for immunoglobulin A?

Despite our knowledge on the role of IgA in mucosal homeostasis and host defense and clinical evidence suggesting deficient first-line defense mechanisms in chronic airway disorders, little is known regarding its role in asthma and chronic obstructive pulmonary disease (COPD). Studies suggest that the mucosal IgA response is impaired in COPD, and a deficient transport of IgA across the bronchial epithelium in COPD has been identified, possibly involving neutrophil proteinases, which may degrade the Ig receptor mediating this transepithelial routing. In contrast, the IgA response to allergens in patients with asthma may play a pathogenic role through eosinophil activation. Thus, secretory IgA can induce eosinophil degranulation in vitro, a feature in keeping with the correlations observed in vivo between airway IgA levels and eosinophil cationic protein during late asthmatic responses. Selective IgA deficiency is associated with an increased prevalence of atopy, and a protective role of IgA has been seen in murine models of asthma, delineating the complexity of the IgA system in the airway mucosa. Future studies will hopefully yield better knowledge of IgA biology and lung mucosal immunity and help to use more efficiently the mucosal route for immunotherapy or target specific genes in inflamed airways.