COPD Wetenschap

Chronic obstructive pulmonary disease and β-blocker treatment in Asian patients with heart failure.
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Chronic obstructive pulmonary disease and β-blocker treatment in Asian patients with heart failure.

ESC Heart Fail. 2017 Oct 21;:

Authors: Kubota Y, Tay WT, Asai K, Murai K, Nakajima I, Hagiwara N, Ikeda T, Kurita T, Teng TK, Anand I, Lam CSP, Shimizu W, ASIA-HF Study investigators

Abstract
AIMS: Chronic obstructive pulmonary disease (COPD) and heart failure (HF) are increasingly frequent in Asia and commonly coexist in patients. However, the prevalence of COPD among Asian patients with HF and its impact on HF treatment are unclear.
METHODS AND RESULTS: We compared clinical characteristics and treatment approaches between patients with or without a history of COPD, before and after 1:2 propensity matching (for age, sex, geographical region, income level, and ethnic group) in 5232 prospectively recruited patients with HF and reduced ejection fraction (HFrEF, <40%) from 11 Asian regions (Northeast Asia: South Korea, Japan, Taiwan, Hong Kong, and China; South Asia: India; Southeast Asia: Thailand, Malaysia, Philippines, Indonesia, and Singapore). Among the 5232 patients with HFrEF, a history of COPD was present in 8.3% (n = 434), with significant variation in geography (11.0% in Northeast Asia vs. 4.7% in South Asia), regional income level (9.7% in high income vs. 5.8% in low income), and ethnicity (17.0% in Filipinos vs. 5.2% in Indians) (all P < 0.05). Use of mineralocorticoid receptor antagonists and diuretics was similar between groups, while usage of all β-blockers was lower in the COPD group than in the non-COPD group in the overall (66.3% vs. 79.9%) and propensity-matched cohorts (66.3% vs. 81.7%) (all P < 0.05). A striking exception was the Japanese cohort in which β-blocker use was high in COPD and non-COPD patients (95.2% vs. 91.2%).
CONCLUSIONS: The prevalence of COPD in HFrEF varied across Asia and was related to underuse of β-blockers, except in Japan.

PMID: 29055972 [PubMed - as supplied by publisher]



Participant selection for lung cancer screening by risk modelling (the Pan-Canadian Early Detection of Lung Cancer [PanCan] study): a single-arm, prospective study.
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Participant selection for lung cancer screening by risk modelling (the Pan-Canadian Early Detection of Lung Cancer [PanCan] study): a single-arm, prospective study.

Lancet Oncol. 2017 Oct 16;:

Authors: Tammemagi MC, Schmidt H, Martel S, McWilliams A, Goffin JR, Johnston MR, Nicholas G, Tremblay A, Bhatia R, Liu G, Soghrati K, Yasufuku K, Hwang DM, Laberge F, Gingras M, Pasian S, Couture C, Mayo JR, Nasute Fauerbach PV, Atkar-Khattra S, Peacock SJ, Cressman S, Ionescu D, English JC, Finley RJ, Yee J, Puksa S, Stewart L, Tsai S, Haider E, Boylan C, Cutz JC, Manos D, Xu Z, Goss GD, Seely JM, Amjadi K, Sekhon HS, Burrowes P, MacEachern P, Urbanski S, Sin DD, Tan WC, Leighl NB, Shepherd FA, Evans WK, Tsao MS, Lam S, PanCan Study Team

Abstract
BACKGROUND: Results from retrospective studies indicate that selecting individuals for low-dose CT lung cancer screening on the basis of a highly predictive risk model is superior to using criteria similar to those used in the National Lung Screening Trial (NLST; age, pack-year, and smoking quit-time). We designed the Pan-Canadian Early Detection of Lung Cancer (PanCan) study to assess the efficacy of a risk prediction model to select candidates for lung cancer screening, with the aim of determining whether this approach could better detect patients with early, potentially curable, lung cancer.
METHODS: We did this single-arm, prospective study in eight centres across Canada. We recruited participants aged 50-75 years, who had smoked at some point in their life (ever-smokers), and who did not have a self-reported history of lung cancer. Participants had at least a 2% 6-year risk of lung cancer as estimated by the PanCan model, a precursor to the validated PLCOm2012 model. Risk variables in the model were age, smoking duration, pack-years, family history of lung cancer, education level, body-mass index, chest x-ray in the past 3 years, and history of chronic obstructive pulmonary disease. Individuals were screened with low-dose CT at baseline (T0), and at 1 (T1) and 4 (T4) years post-baseline. The primary outcome of the study was incidence of lung cancer. This study is registered with ClinicalTrials.gov, number NCT00751660.
FINDINGS: 7059 queries came into the study coordinating centre and were screened for PanCan risk. 15 were duplicates, so 7044 participants were considered for enrolment. Between Sept 24, 2008, and Dec 17, 2010, we recruited and enrolled 2537 eligible ever-smokers. After a median follow-up of 5·5 years (IQR 3·2-6·1), 172 lung cancers were diagnosed in 164 individuals (cumulative incidence 0·065 [95% CI 0·055-0·075], incidence rate 138·1 per 10 000 person-years [117·8-160·9]). There were ten interval lung cancers (6% of lung cancers and 6% of individuals with cancer): one diagnosed between T0 and T1, and nine between T1 and T4. Cumulative incidence was significantly higher than that observed in NLST (4·0%; p<0·0001). Compared with 593 (57%) of 1040 lung cancers observed in NLST, 133 (77%) of 172 lung cancers in the PanCan Study were early stage (I or II; p<0·0001).
INTERPRETATION: The PanCan model was effective in identifying individuals who were subsequently diagnosed with early, potentially curable, lung cancer. The incidence of cancers detected and the proportion of early stage cancers in the screened population was higher than observed in previous studies. This approach should be considered for adoption in lung cancer screening programmes.
FUNDING: Terry Fox Research Institute and Canadian Partnership Against Cancer.

PMID: 29055736 [PubMed - as supplied by publisher]



[COPD: the great unknown? A note on how to improve diagnostic accuracy].
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[COPD: the great unknown? A note on how to improve diagnostic accuracy].

Rev Calid Asist. 2017 Oct 18;:

Authors: Figueira Gonçalves JM, Pérez Rodríguez A

PMID: 29055684 [PubMed - as supplied by publisher]



Non-evidence based medicine: example of the use of systemic corticosteroids in exacerbation of COPD.
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Non-evidence based medicine: example of the use of systemic corticosteroids in exacerbation of COPD.

Rev Clin Esp. 2017 Oct 18;:

Authors: Miravitlles M

PMID: 29055656 [PubMed - as supplied by publisher]



Vitamin K deficit and elastolysis theory in pulmonary elasto-degenerative diseases.
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Vitamin K deficit and elastolysis theory in pulmonary elasto-degenerative diseases.

Med Hypotheses. 2017 Oct;108:38-41

Authors: Janssen R, Vermeer C

Abstract
Elastin is a unique protein providing deformability and resilience to dynamic tissues, such as arteries and lungs. It is an absolute basic requirement for circulation and respiration. Elastin can be degraded by elastases and has a high calcium affinity. Elastin calcification and elastin degradation are two pathological processes that impair elastin's functioning. Furthermore, elastin degradation can be associated to elastin calcification. Matrix Gla Protein (MGP) is probably the most potent natural inhibitor of elastin calcification and requires vitamin K for its activation. Measuring circulating levels of inactive MGP (dp-ucMGP) is a frequently used method to assess vitamin K status. Dp-ucMGP reflects the burden of vitamin K-dependent proteins that have not been activated by vitamin K and could therefore best be regarded as a biomarker of a vitamin K deficit. Dp-ucMGP levels decrease after vitamin K supplementation. Since the amino acids desmosine and isodesmosine (DES) are unique to crosslinked elastin fibers, systemic elastin degradation can be assessed with the plasma DES assay. Recently, we discovered a strong correlation between plasma dp-ucMGP and plasma DES levels in both patients with chronic obstructive pulmonary disease (COPD) and controls. The 'Vitamin K deficit and elastolysis theory' posits that elastin degradation causes a rise in the vitamin K deficit and implies that vitamin K supplementation could be preventing elastin degradation. If this hypothesis holds true and is universally found in every state and condition, it will have an unprecedented impact on the management of every single pulmonary disease characterized by accelerated elastin degradation, such as alpha-1 antitrypsin deficiency, bronchiectasis, COPD and cystic fibrosis. Theoretically, a plasma dp-ucMGP concentration of zero would be associated with a near-complete standstill of elastin degradation and disease progression in patients with any of these debilitating conditions.

PMID: 29055397 [PubMed - in process]



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