A new approach to assess COPD by identifying lung function break-points.

This international, peer-reviewed Open Access journal by Dove Medical Press focuses on pathophysiological processes underlying Chronic Obstructive Pulmonary Disease (COPD) interventions, patient focused education, and self-management protocols. Sign up for email alerts here.

39,063 Monthly downloads/views I 2.893 Impact Factor I 5.2 CiteScore I 1.16 Source Normalized Impact per Paper (SNIP) I 0.804 Scimago Journal & Country Rank (SJR)

Record: found
Abstract: found
Article: found

Is Open Access

A new approach to assess COPD by identifying lung function break-points.

Author(s): Göran Eriksson, Linnea Jarenbäck, Stefan Peterson, Jaro Ankerst, Leif Bjermer, Ellen Tufvesson

Publication date: 2015

Journal: International Journal of Chronic Obstructive Pulmonary Disease

Publisher: Dove Medical Press Ltd.

Keywords: body plethysmography, break-point, impulse oscillometry, severity, single-breath carbon-monoxide diffusion test, spirometry

Read this article at

ScienceOpenPublisher PMC

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

COPD is a progressive disease, which can take different routes, leading to great heterogeneity. The aim of the post-hoc analysis reported here was to perform continuous analyses of advanced lung function measurements, using linear and nonlinear regressions.

Most cited references 19

Record: found
Abstract: not found
Article: not found

segmented: an R package to fit regression models with broken-line relationships

V. Muggeo, Muggeo VMR, R. Muggeo V. M. … (2008)

0 comments Cited 243 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction.

K F Chung, I M Adcock (2008)

Chronic obstructive pulmonary disease is a leading global cause of morbidity and mortality that is characterised by inexorable deterioration of small airways obstruction with emphysema associated with cellular inflammation and structural remodelling. Other features include apoptosis as well as proliferation of cells, and both tissue repair and lack of tissue repair. Metalloprotease release, together with that of apoptotic factors, may underlie the emphysema, and, conversely, fibrosis of the small airways may be accounted for by the effects of growth factor activation. In advanced disease, influential factors include the development of autoimmunity, with activation of dendritic cells and T-helper cells of both type 1 and 2, and the senescence response. An inability of macrophages to ingest apoptosed cells and bacteria may exacerbate inflammatory responses. Systemic inflammation with concomitant cardiovascular disease and metabolic syndrome may reflect the effect of cigarette smoke on nonpulmonary cells. Corticosteroid resistance may be secondary to oxidative stress mechanisms, such as inactivation of histone deacetylases. The mechanisms of chronic obstructive pulmonary disease may be heterogeneous, according to severity, and clinical phenotypes need to be correlated with cellular and pathological processes. Treatments may be targeted to patients with specific mechanisms.

0 comments Cited 177 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Reference spirometric values using techniques and equipment that meet ATS recommendations.

R. Gardner, R Crapo, A.-B. Morris (1981)

Forced expiratory volumes and flows were measured in 251 healthy nonsmoking men and women using techniques and equipment that meet American Thoracic Society (ATS) recommendations. Linear regression equations using height and age alone predict spirometric parameters as well as more complex equations using additional variables. Single values for 95% confidence intervals are acceptable and should replace the commonly used method of subtracting 20% to determine the lower limit of normal for a predicted value. Our study produced predicted values for forced vital capacity and forced expiratory volume in one second that were almost identical to those predicted by Morris and associates (1) when the data from their study were modified to be compatible with the back extrapolation technique recommended by the ATS. The study of Morris and colleagues was performed at sea level in rural subjects, whereas ours was performed at an altitude of 1,400 m in urban subjects. Either the present study or the study of Morris and co-workers, modified to back extrapolation, could be recommended for predicting normal values.