Year in Review 2014: COPD

Restrepo, Ruben D

doi:10.4187/respcare.04227

Cited by 6 publications

(8 citation statements)

References 17 publications

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“…There is no curative treatment, the available therapy is restricted to corticosteroids, adrenergic b 2 receptor agonists and acetylcholine muscarinic receptor antagonists that can only slow down the progression and alleviate the symptoms (Vestbo et al, 2013). However, these have limited effect in a relatively small patient population (Restrepo, 2015). Therefore, there is an urgent need to find novel therapeutic targets in COPD.…”

Section: Introductionmentioning

confidence: 99%

Integrative characterization of chronic cigarette smoke-induced cardiopulmonary comorbidities in a mouse model

Kemény

Csekő

Szitter

et al. 2017

Environmental Pollution

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Cigarette smoke-triggered inflammatory cascades and consequent tissue damage are the main causes of chronic obstructive pulmonary disease (COPD). There is no effective therapy and the key mediators of COPD are not identified due to the lack of translational animal models with complex characterization. This integrative chronic study investigated cardiopulmonary pathophysiological alterations and mechanisms with functional, morphological and biochemical techniques in a 6-month-long cigarette smoke exposure mouse model. Some respiratory alterations characteristic of emphysema (decreased airway resistance: Rl; end-expiratory work and pause: EEW, EEP; expiration time: Te; increased tidal mid-expiratory flow: EF50) were detected in anaesthetized C57BL/6 mice, unrestrained plethysmography did not show changes. Typical histopathological signs were peribronchial/perivascular (PB/PV) edema at month 1, neutrophil/macrophage infiltration at month 2, interstitial leukocyte accumulation at months 3-4, and emphysema/atelectasis at months 5-6 quantified by mean linear intercept measurement. Emphysema was proven by micro-CT quantification. Leukocyte number in the bronchoalveolar lavage at month 2 and lung matrix metalloproteinases-2 and 9 (MMP-2/MMP-9) activities in months 5-6 significantly increased. Smoking triggered complex cytokine profile change in the lung with one characteristic inflammatory peak of C5a, interleukin-1α and its receptor antagonist (IL-1α, IL-1ra), monokine induced by gamma interferon (MIG), macrophage colony-stimulating factor (M-CSF), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) at months 2-3, and another peak of interferon-γ (IFN-γ), IL-4, 7, 13, 17, 27 related to tissue destruction. Transient systolic and diastolic ventricular dysfunction developed after 1-2 months shown by significantly decreased ejection fraction (EF%) and deceleration time, respectively. These parameters together with the tricuspid annular plane systolic excursion (TAPSE) decreased again after 5-6 months. Soluble intercellular adhesion molecule-1 (sICAM-1) significantly increased in the heart homogenates at month 6, while other inflammatory cytokines were undetectable. This is the first study demonstrating smoking duration-dependent, complex cardiopulmonary alterations characteristic to COPD, in which inflammatory cytokine cascades and MMP-2/9 might be responsible for pulmonary destruction and sICAM-1 for heart dysfunction.

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Section: Introductionmentioning

confidence: 99%

Integrative characterization of chronic cigarette smoke-induced cardiopulmonary comorbidities in a mouse model

Kemény

Csekő

Szitter

et al. 2017

Environmental Pollution

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“…[2] With the spread of air pollution, COPD has become one of the heaviest economic burdens associated with hospitalization, work absence, and disability. [3,4] There is compelling evidence supporting the hypothesis that COPD results from complex interactions between genetic factors and environmental exposure. [5–7] Genetic susceptibility is characterized by familial clustering; COPD risk in subjects with COPD family history is approximately 2 to 3 times higher than subjects from the general population.…”

Section: Introductionmentioning

confidence: 99%

Smoking status and gene susceptibility play important roles in the development of chronic obstructive pulmonary disease and lung function decline

Zhao

Chen³

et al. 2017

Medicine

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Background:We conducted this study to identify the influences and synergistic effects of smoking status and polymorphisms in hedgehog interacting protein (HHIP) on chronic obstructive pulmonary disease (COPD) and lung function decline.Methods:A cohort containing 306 COPD patients and 743 healthy subjects was recruited from 25,000 subjects. All selected subjects had chronic cough for over 2 years or a smoking history above 20 pack-years. After 8 years, all subjects were divided into 2 cohorts according to whether they had quit smoking or not. A follow-up of all patients was completed after another period of 10 years. Three variants in HHIP were genotyped to investigate the impacts of gene susceptibility on the development of COPD and lung function decline.Results:During the follow-up tests, forced expiratory volume in 1 s (FEV1) ratios decreased more significantly in COPD patients than in healthy subjects. For variant rs7654947, FEV1 decreased more significantly in CC and CT subjects than in TT subjects. FEV1 in COPD patients with a CC genotype from smoking cohorts reduced markedly when compared to ex-smoking cohorts (case, 30.75% vs. 35.5%; total, 28% vs. 32%).Conclusions:Our results showed that smoking and HHIP variant rs7654947 were associated with COPD development and lung function decline. Moreover, we found that cigarette smoking and gene susceptibility have cooperative effects on COPD risk and lung function decline.

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“…Many patients have suffered from COPD for years and have endured comorbidities and complications that impacted therapy, prognosis, and quality of life, and then died of the disease or its complications prematurely. [3,4] …”

Section: Introductionmentioning

confidence: 99%

“…[3,4] The prevalence of COPD is apparently increasing and should be a crucial issue for future health care providers due to continued exposure of the global population to risk factors for COPD, as well as worldwide demographic trends toward aging populations. [3,4] Moreover, the WHO predicts that morbidity and mortality trends in COPD will increase significantly and will grow to become the third leading cause of death by 2030. [3,4] …”

Section: Introductionmentioning

confidence: 99%

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Association of chronic obstructive pulmonary disease and hemorrhoids

et al. 2017

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According to traditional Chinese medicine (TCM) theory, a specific physiological and pathological relationship exists between the lungs and the large intestine. The aim of this study is to delineate the association of chronic obstructive pulmonary disease (COPD) and hemorrhoids in order to verify the “interior–exterior” relationship between the lungs and the large intestine. A retrospective cohort study is conceived from the National Health Insurance Research Database, Taiwan. The 2 samples (COPD cohort and non-COPD cohort) were selected from the 2000 to 2003 beneficiaries of the NHI, representing patients age 20 and older in Taiwan, with the follow-up ending on December 31, 2011. The COPD cohort (n = 51,506) includes every patient newly diagnosed as having Chronic Obstructive Pulmonary Disease (COPD, ICD-9-CM: 490–492, 494, 496), who have made at least 2 confirmed visits to the hospital/clinic. The non-COPD cohort (n = 103,012) includes patients without COPD and is selected via a 1:2 (COPD: non-COPD) matching by age group (per 5 years), gender, and index date (diagnosis date of COPD for the COPD cohort). Compared with non-COPD cohorts, patients with COPD have a higher likelihood of having hemorrhoids and the age-, gender- and comorbidies-adjusted hazard ratio (HR) for hemorrhoids is 1.56 (95% confidence intervals [CI]:1.50–1.62). The adjusted HR of hemorrhoids for females is 0.79 (95% CI: 0.77–0.83), which is significantly less than that for males. The elderly groups, 40 to 59 years and aged 60 or above, have higher adjusted HRs than younger age groups (20–39 years), 1.19 (95% CI: 1.14–1.26), and 1.18 (95% CI: 1.12–1.24), respectively. Patients with COPD may have a higher likelihood to have hemorrhoids in this retrospective cohort study. This study verifies the fundamental theorem of TCM that there is a definite pathogenic association between the lungs and large intestine.

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Year in Review 2014: COPD

Cited by 6 publications

References 17 publications

Integrative characterization of chronic cigarette smoke-induced cardiopulmonary comorbidities in a mouse model

Integrative characterization of chronic cigarette smoke-induced cardiopulmonary comorbidities in a mouse model

Smoking status and gene susceptibility play important roles in the development of chronic obstructive pulmonary disease and lung function decline

Association of chronic obstructive pulmonary disease and hemorrhoids

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