Trends in moderate and severe exacerbations among COPD patients in the UK from 2005 to 2013

Oshagbemi, Olorunfemi A.; Keene, Spencer; Driessen, Johanna H M; Jordan, Rachel; Wouters, Emiel F.M.; Boer, Anthonius de; Vries, Frank de; Franssen, Frits M.E.

doi:10.1016/j.rmed.2018.09.010

Cited by 15 publications

(11 citation statements)

References 37 publications

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“…Of the remaining 177 studies, a further 7 (4%) used a definition of COPD that had been previously validated against a reference standard in the same database used for their research. Additional studies referred to their case definition being “based on” validated definitions, but used code sets different to those validated [ 21 – 23 ], or did not report the codes they used [ 18 , 24 , 25 ].…”

Section: Resultsmentioning

confidence: 99%

Identifying COPD in routinely collected electronic health records: a systematic scoping review

et al. 2021

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Although routinely collected electronic health records (EHR) are widely used to examine outcomes related to chronic obstructive pulmonary disease (COPD), consensus regarding the identification of cases from electronic healthcare databases is lacking. We systematically examine and summarise approaches from the recent literature.MEDLINE via EBSCOhost was searched for COPD-related studies using EHR published from January 1, 2018 to November 30, 2019. Data were extracted relating to the case definition of COPD and determination of COPD severity and phenotypes.From 185 eligible studies, we found widespread variation in the definitions used to identify people with COPD in terms of code sets used (with 20 different code sets in use based on the ICD-10 classification alone) and requirement of additional criteria (relating to age (n=139), medication (n=31), multiplicity of events (n=21), spirometry (n=19) and smoking status (n=9)). Only 7 studies used a case definition which had been validated against a reference standard in the same dataset. Various proxies of disease severity were used since spirometry results and patient-reported outcomes were not often available.To enable the research community to draw reliable insights from electronic health records and aid comparability between studies, clear reporting and greater consistency of the definitions used to identify COPD and related outcome measures is key.

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Section: Resultsmentioning

confidence: 99%

Identifying COPD in routinely collected electronic health records: a systematic scoping review

et al. 2021

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“…A different spectrum of symptom presentation in exacerbations is also evident. First, women appear to experience more exacerbations than men by the current treatment‐defined criteria 160 . In a Spanish study, although women were younger, smoked less and had better resting oxygenation, they experienced more exacerbations in the last year 161 .…”

Section: Is Gender Important In Copd?mentioning

confidence: 98%

Contemporary perspectives in COPD: Patient burden, the role of gender and trajectories of multimorbidity

et al. 2021

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An individual's experience of COPD is determined by many factors in addition to the pathological features of chronic bronchitis and emphysema and the symptoms that derive directly from them. Multimorbidity is the norm rather than the exception, so most people with COPD are living with a range of other medical problems which can decrease overall quality of life. COPD is caused by the inhalation of noxious particles or gases, in particular tobacco smoke, but also by early life disadvantage impairing lung development and by occupations where inhaled exposures are common (e.g. industrial, farming and cleaning work). Wealthy people are therefore relatively protected from developing COPD and people who do develop the condition may have reduced resources to cope. COPD is also no longer a condition that predominantly affects men. The prevalence of COPD among women has equalled that of men since 2008 in many high‐income countries, due to increased exposure to tobacco, and in low‐income countries due to biomass fuels. COPD is one of the leading causes of death in women in the USA, and death rates attributed to COPD in women in some countries are predicted to overtake those of men in the next decade. Many factors contribute to this phenomenon, but in addition to socioeconomic and occupational factors, there is increasing evidence of a higher susceptibility of females to smoking and pollutants. Quality of life is also more significantly impaired in women. Although most medications (bronchodilators and inhaled corticosteroids) used to treat COPD demonstrate similar trends for exacerbation prevention and lung function improvement in men and women, this is an understudied area and clinical trials frequently have a preponderance of males. A better understanding of gender‐based predictors of efficacy of all therapeutic interventions is crucial for comprehensive patient care. There is an urgent need to recognize the increasing burden of COPD in women and to facilitate global improvements in disease prevention and management in this specific population. Many individuals with COPD follow a trajectory of both lung function decline and also multimorbidity. Unfavourable lung function trajectories throughout life have implications for later development of other chronic diseases. An enhanced understanding of the temporal associations underlying the development of coexisting diseases is a crucial first step in unravelling potential common disease pathways. Lessons can be learned from exploring disease trajectories of other NCD as well as multimorbidity development. Further research will be essential to explain how early life risk factors commonly influence trajectories of COPD and other diseases, how different diseases develop in relation to each other in a temporal way and how this ultimately leads to different multimorbidity patterns in COPD. This review integrates new knowledge and ideas pertaining to three broad themes (i) the overall burden of disease in COPD, (ii) an unappreciated high burden in women and (iii) the contrast...

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“…The pathogenesis of COPD is closely associated with factors, including smoking, exposure to air pollution and inhalation of dust (25,26). Pathological changes observed in COPD include chronic bronchitis, emphysema, airway reconstruction and pulmonary artery reconstruction (27).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of the hyperplasia suppressor gene inactivates airway fibroblasts obtained from a rat model of chronic obstructive pulmonary disease by inhibiting the Wnt signaling pathway

Yang

Zhou

et al. 2019

Mol Med Report

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The present study aimed to investigate the effects of hyperplasia suppressor gene (HSG) overexpression on the activation of airway fibroblasts in a rat model of chronic obstructive pulmonary disease (COPD) and assess the underlying molecular mechanisms. The rat model of COPD was established by injection of papain and confirmed by hematoxylin and eosin staining. Airway fibroblasts were identified using immunofluorescence, and HSG expression was facilitated by an HSG vector. Cell viability, apoptosis and the levels of matrix metallopeptidase-9 (MMP-9), platelet-derived growth factor (PDGF), and transforming growth factor-β1 (TGF-β1) were measured via Cell Counting Kit-8, flow cytometry and ELISA analyses, respectively, and potential mechanisms were detected by reverse transcription-quantitative polymerase chain reaction and western blotting. Airway fibroblasts from COPD rats were isolated and identified based on vimentin expression. Compared with the control group, HSG overexpression reduced cell viability, promoted apoptosis, and reduced the protein levels of TGF-β1, MMP-9 and PDGF. Additionally, HSG overexpression reduced β-catenin and Ras homology family member A (RhoA) expression at both the mRNA and protein levels. Conversely, Wnt signaling pathway agonists lithium chloride (LiCl) and 4-ethyl-5,6-dihydro-5-methyl- (1,3)dioxolo(4,5-j)phenanthridine (HLY78), significantly reduced the effects of HSG overexpression (P<0.05 vs. HSG). Cell viability in the HSG + LiCl and HSG + HLY78 groups was increased, whereas apoptosis was reduced compared with HSG treatment alone. The protein levels of TGF-β1, MMP-9 and PDGF were also decreased in the HSG + LiCl and HSG + HLY78 groups compared with the HSG group (P<0.05). Furthermore, the expression of β-catenin and RhoA was higher in the HSG + LiCl and HSG + HLY78 groups compared with the HSG group (P<0.05). Collectively, the results indicated that HSG overexpression inactivated airway fibroblasts from COPD by inhibiting the Wnt signaling pathway.

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Trends in moderate and severe exacerbations among COPD patients in the UK from 2005 to 2013

Cited by 15 publications

References 37 publications

Identifying COPD in routinely collected electronic health records: a systematic scoping review

Identifying COPD in routinely collected electronic health records: a systematic scoping review

Contemporary perspectives in COPD: Patient burden, the role of gender and trajectories of multimorbidity

Overexpression of the hyperplasia suppressor gene inactivates airway fibroblasts obtained from a rat model of chronic obstructive pulmonary disease by inhibiting the Wnt signaling pathway

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