Bronchiectasis as a Comorbidity of Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis

Du, Qingxia; Jin, Jianmin; Liu, Xiaofang; Sun, Yongchang

doi:10.1371/journal.pone.0150532

Cited by 116 publications

(76 citation statements)

References 41 publications

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“…Although the presence of bronchiectasis in patients with COPD is usually associated with chronic bronchial infection and more frequent exacerbations, mostly of a bacterial etiology,25,31,32 this infective component is not adequately covered by the usual treatment for COPD based on inhaled therapy with bronchodilators, with or without inhaled corticosteroids (ICS). Some recent studies have demonstrated that even patients on triple therapy may suffer from frequent exacerbations 45.…”

Section: Bronchiectasis In Copd: Therapeutic Consequencesmentioning

confidence: 99%

Bronchiectasis in COPD patients: more than a comorbidity?

Martínez-García

Miravitlles

2017

COPD

117

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Computed tomography scan images have been used to identify different radiological COPD phenotypes based on the presence and severity of emphysema, bronchial wall thickening, and bronchiectasis. Bronchiectasis is defined as an abnormal dilation of the bronchi, usually as a result of chronic airway inflammation and/or infection. The prevalence of bronchiectasis in patients with COPD is high, especially in advanced stages. The identification of bronchiectasis in COPD has been defined as a different clinical COPD phenotype with greater symptomatic severity, more frequent chronic bronchial infection and exacerbations, and poor prognosis. A causal association has not yet been proven, but it is biologically plausible that COPD, and particularly the infective and exacerbator COPD phenotypes, could be the cause of bronchiectasis without any other known etiology, beyond any mere association or comorbidity. The study of the relationship between COPD and bronchiectasis could have important clinical implications, since both diseases have different and complementary therapeutic approaches. Longitudinal studies are needed to investigate the development of bronchiectasis in COPD, and clinical trials with treatments aimed at reducing bacterial loads should be conducted to investigate their impact on the reduction of exacerbations and improvements in the long-term evolution of the disease.

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Section: Bronchiectasis In Copd: Therapeutic Consequencesmentioning

confidence: 99%

Bronchiectasis in COPD patients: more than a comorbidity?

Martínez-García

Miravitlles

2017

COPD

117

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“…Recent research has revealed the importance of extrapulmonary effects on treatment, and the contribution of comorbidities, to the overall severity of COPD (Vogelmeier et al, 2017). Much of the financial cost associated with COPD treatment is related to common systemic comorbidities, which are thought to be part of organ-specific inflammatory processes, for example, respiratory inflammation, cardiovascular disease and, most commonly, periodontitis (Du et al, 2016). Microorganisms are thought to be one of the main etiologic factors that exacerbate COPD.…”

Section: Introductionmentioning

confidence: 99%

Saliva Microbiome Changes in Patients With Periodontitis With and Without Chronic Obstructive Pulmonary Disease

Wang

et al. 2020

Front. Cell. Infect. Microbiol.

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Objective: The oral microbiota plays a key part in the initial colonization by pathogens and the chronic inflammatory reaction of the host. We measured variations in the salivary microbiota and evaluated their potential associations with periodontitis and chronic obstructive pulmonary disease (COPD). Methods:We investigated the salivary microbiota of patients with COPD and periodontitis (n = 21) compared with that in patients with periodontitis alone (n = 36) and with healthy controls (HCs; n = 14), using pyrosequencing of polymerase chain reaction-amplified 16s rRNA genes.Results: Bacterial richness and diversity were significantly higher in patients suffering from COPD, and the bacterial family Lachnospiraceae was observed frequently only among patients with COPD and periodontitis. Veillonella, Rothia, Actinomyces, and Fusobacterium were the core bacterial genera that showed significant differences among patients with coincident COPD and periodontitis, patients with periodontitis alone, and HCs (p < 0.05). Veillonella, Rothia, and Actinomyces were observed much more frequently in patients with COPD and periodontitis, compared with that in HCs. All tested populations were divided into subgroups based on sex, smoking, or periodontitis index. In the subgroup with a bleeding index >2, Rothia was significantly different in periodontitis with and without COPD groups compared with HCs. In the subgroup with a plaque index >2.5, Rothia and Veillonella showed significant differences in periodontitis with and without COPD groups compared with HCs.Conclusion: Variations in salivary microbiota may be associated with COPD and periodontitis.

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“…Respiratory comorbidities associated with COPD include bronchiectasis,6 asthma, pulmonary fibrosis,7 and lung cancer,7 but extra thoracic chronic inflammatory disease also co-occurs 8. Cardiovascular diseases are the most common,9 including hypertension,7 venous thromboembolism, ischemic heart disease, arrhythmias,7,10 and heart failure 7,11.…”

Section: Introductionmentioning

confidence: 99%

Is periodontitis a comorbidity of COPD or can associations be explained by shared risk factors/behaviors?

Hobbins¹,

Chapple

Sapey³

et al. 2017

COPD

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COPD is recognized as having a series of comorbidities potentially related to common inflammatory processes. Periodontitis is one of the most common human inflammatory diseases and has previously been associated with COPD in numerous observational studies. As periodontitis and COPD are both chronic, progressive conditions characterized by neutrophilic inflammation with subsequent proteolytic destruction of connective tissue, it has been proposed that they share common pathophysiological processes. The mechanisms proposed to link COPD and periodontitis include mechanical aspiration of oral contents into the respiratory tree, overspill of locally produced inflammatory mediators into the systemic circulation or oral or lung-derived bacteremia activating an acute-phase response and also reactive oxygen species (ROS) and cytokine release by systemic neutrophils at distant sites. Studies of systemic neutrophils in COPD and chronic periodontitis describe altered cellular functions that would predispose to inflammation and tissue destruction both in the lung and in the mouth, again potentially connecting these conditions. However, COPD and periodontitis also share risk factors such as age, chronic tobacco smoke exposure, and social deprivation that are not always considered in observational and interventional studies. Furthermore, studies reporting associations have often utilized differing definitions of both COPD and periodontitis. This article reviews the current available evidence supporting the hypothesis that COPD and inflammatory periodontal disease (periodontitis) could be pathologically associated, including a review of shared inflammatory mechanisms. It highlights the potential limitations of previous studies, in particular, the lack of uniformly applied case definitions for both COPD and periodontitis and poor recognition of shared risk factors. Understanding associations between these conditions may inform why patients with COPD suffer such a burden of comorbid illness and new therapeutic strategies for both the diseases. However, further research is needed to clarify factors that may be directly causal as opposed to confounding relationships.

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Bronchiectasis as a Comorbidity of Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis

Cited by 116 publications

References 41 publications

Bronchiectasis in COPD patients: more than a comorbidity?

Bronchiectasis in COPD patients: more than a comorbidity?

Saliva Microbiome Changes in Patients With Periodontitis With and Without Chronic Obstructive Pulmonary Disease

Is periodontitis a comorbidity of COPD or can associations be explained by shared risk factors/behaviors?

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