Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease

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Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease. / Lange, Peter; Celli, Bartolome; Agustí, Alvar; Jensen, Gorm Boje; Divo, Miguel; Faner, Rosa; Guerra, Stefano; Marott, Jacob Louis; Martinez, Fernando D; Martinez-Camblor, Pablo; Meek, Paula; Owen, Caroline A; Petersen, Hans; Pinto-Plata, Victor; Schnohr, Peter; Sood, Akshay; Soriano, Joan B; Tesfaigzi, Yohannes; Vestbo, Jørgen.

I: New England Journal of Medicine, Bind 373, Nr. 2, 09.07.2015, s. 111-122.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Lange, P, Celli, B, Agustí, A, Jensen, GB, Divo, M, Faner, R, Guerra, S, Marott, JL, Martinez, FD, Martinez-Camblor, P, Meek, P, Owen, CA, Petersen, H, Pinto-Plata, V, Schnohr, P, Sood, A, Soriano, JB, Tesfaigzi, Y & Vestbo, J 2015, 'Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease', New England Journal of Medicine, bind 373, nr. 2, s. 111-122. https://doi.org/10.1056/NEJMoa1411532

APA

Lange, P., Celli, B., Agustí, A., Jensen, G. B., Divo, M., Faner, R., Guerra, S., Marott, J. L., Martinez, F. D., Martinez-Camblor, P., Meek, P., Owen, C. A., Petersen, H., Pinto-Plata, V., Schnohr, P., Sood, A., Soriano, J. B., Tesfaigzi, Y., & Vestbo, J. (2015). Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease. New England Journal of Medicine, 373(2), 111-122. https://doi.org/10.1056/NEJMoa1411532

Vancouver

Lange P, Celli B, Agustí A, Jensen GB, Divo M, Faner R o.a. Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease. New England Journal of Medicine. 2015 jul. 9;373(2):111-122. https://doi.org/10.1056/NEJMoa1411532

Author

Lange, Peter ; Celli, Bartolome ; Agustí, Alvar ; Jensen, Gorm Boje ; Divo, Miguel ; Faner, Rosa ; Guerra, Stefano ; Marott, Jacob Louis ; Martinez, Fernando D ; Martinez-Camblor, Pablo ; Meek, Paula ; Owen, Caroline A ; Petersen, Hans ; Pinto-Plata, Victor ; Schnohr, Peter ; Sood, Akshay ; Soriano, Joan B ; Tesfaigzi, Yohannes ; Vestbo, Jørgen. / Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease. I: New England Journal of Medicine. 2015 ; Bind 373, Nr. 2. s. 111-122.

Bibtex

@article{8fde35c9d32948b1b68b8d0122550bfa,
title = "Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease",
abstract = "BACKGROUND: Chronic obstructive pulmonary disease (COPD) is thought to result from an accelerated decline in forced expiratory volume in 1 second (FEV1) over time. Yet it is possible that a normal decline in FEV1 could also lead to COPD in persons whose maximally attained FEV1 is less than population norms.METHODS: We stratified participants in three independent cohorts (the Framingham Offspring Cohort, the Copenhagen City Heart Study, and the Lovelace Smokers Cohort) according to lung function (FEV1 ≥80% or <80% of the predicted value) at cohort inception (mean age of patients, approximately 40 years) and the presence or absence of COPD at the last study visit. We then determined the rate of decline in FEV1 over time among the participants according to their FEV1 at cohort inception and COPD status at study end.RESULTS: Among 657 persons who had an FEV1 of less than 80% of the predicted value before 40 years of age, 174 (26%) had COPD after 22 years of observation, whereas among 2207 persons who had a baseline FEV1 of at least 80% of the predicted value before 40 years of age, 158 (7%) had COPD after 22 years of observation (P<0.001). Approximately half the 332 persons with COPD at the end of the observation period had had a normal FEV1 before 40 years of age and had a rapid decline in FEV1 thereafter, with a mean (±SD) decline of 53±21 ml per year. The remaining half had had a low FEV1 in early adulthood and a subsequent mean decline in FEV1 of 27±18 ml per year (P<0.001), despite similar smoking exposure.CONCLUSIONS: Our study suggests that low FEV1 in early adulthood is important in the genesis of COPD and that accelerated decline in FEV1 is not an obligate feature of COPD. (Funded by an unrestricted grant from GlaxoSmithKline and others.).",
keywords = "Adult, Aged, Cohort Studies, Disease Progression, Female, Forced Expiratory Volume, Humans, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive, Smoking, Young Adult",
author = "Peter Lange and Bartolome Celli and Alvar Agust{\'i} and Jensen, {Gorm Boje} and Miguel Divo and Rosa Faner and Stefano Guerra and Marott, {Jacob Louis} and Martinez, {Fernando D} and Pablo Martinez-Camblor and Paula Meek and Owen, {Caroline A} and Hans Petersen and Victor Pinto-Plata and Peter Schnohr and Akshay Sood and Soriano, {Joan B} and Yohannes Tesfaigzi and J{\o}rgen Vestbo",
year = "2015",
month = jul,
day = "9",
doi = "10.1056/NEJMoa1411532",
language = "English",
volume = "373",
pages = "111--122",
journal = "New England Journal of Medicine",
issn = "0028-4793",
publisher = "Massachusetts Medical Society",
number = "2",

}

RIS

TY - JOUR

T1 - Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease

AU - Lange, Peter

AU - Celli, Bartolome

AU - Agustí, Alvar

AU - Jensen, Gorm Boje

AU - Divo, Miguel

AU - Faner, Rosa

AU - Guerra, Stefano

AU - Marott, Jacob Louis

AU - Martinez, Fernando D

AU - Martinez-Camblor, Pablo

AU - Meek, Paula

AU - Owen, Caroline A

AU - Petersen, Hans

AU - Pinto-Plata, Victor

AU - Schnohr, Peter

AU - Sood, Akshay

AU - Soriano, Joan B

AU - Tesfaigzi, Yohannes

AU - Vestbo, Jørgen

PY - 2015/7/9

Y1 - 2015/7/9

N2 - BACKGROUND: Chronic obstructive pulmonary disease (COPD) is thought to result from an accelerated decline in forced expiratory volume in 1 second (FEV1) over time. Yet it is possible that a normal decline in FEV1 could also lead to COPD in persons whose maximally attained FEV1 is less than population norms.METHODS: We stratified participants in three independent cohorts (the Framingham Offspring Cohort, the Copenhagen City Heart Study, and the Lovelace Smokers Cohort) according to lung function (FEV1 ≥80% or <80% of the predicted value) at cohort inception (mean age of patients, approximately 40 years) and the presence or absence of COPD at the last study visit. We then determined the rate of decline in FEV1 over time among the participants according to their FEV1 at cohort inception and COPD status at study end.RESULTS: Among 657 persons who had an FEV1 of less than 80% of the predicted value before 40 years of age, 174 (26%) had COPD after 22 years of observation, whereas among 2207 persons who had a baseline FEV1 of at least 80% of the predicted value before 40 years of age, 158 (7%) had COPD after 22 years of observation (P<0.001). Approximately half the 332 persons with COPD at the end of the observation period had had a normal FEV1 before 40 years of age and had a rapid decline in FEV1 thereafter, with a mean (±SD) decline of 53±21 ml per year. The remaining half had had a low FEV1 in early adulthood and a subsequent mean decline in FEV1 of 27±18 ml per year (P<0.001), despite similar smoking exposure.CONCLUSIONS: Our study suggests that low FEV1 in early adulthood is important in the genesis of COPD and that accelerated decline in FEV1 is not an obligate feature of COPD. (Funded by an unrestricted grant from GlaxoSmithKline and others.).

AB - BACKGROUND: Chronic obstructive pulmonary disease (COPD) is thought to result from an accelerated decline in forced expiratory volume in 1 second (FEV1) over time. Yet it is possible that a normal decline in FEV1 could also lead to COPD in persons whose maximally attained FEV1 is less than population norms.METHODS: We stratified participants in three independent cohorts (the Framingham Offspring Cohort, the Copenhagen City Heart Study, and the Lovelace Smokers Cohort) according to lung function (FEV1 ≥80% or <80% of the predicted value) at cohort inception (mean age of patients, approximately 40 years) and the presence or absence of COPD at the last study visit. We then determined the rate of decline in FEV1 over time among the participants according to their FEV1 at cohort inception and COPD status at study end.RESULTS: Among 657 persons who had an FEV1 of less than 80% of the predicted value before 40 years of age, 174 (26%) had COPD after 22 years of observation, whereas among 2207 persons who had a baseline FEV1 of at least 80% of the predicted value before 40 years of age, 158 (7%) had COPD after 22 years of observation (P<0.001). Approximately half the 332 persons with COPD at the end of the observation period had had a normal FEV1 before 40 years of age and had a rapid decline in FEV1 thereafter, with a mean (±SD) decline of 53±21 ml per year. The remaining half had had a low FEV1 in early adulthood and a subsequent mean decline in FEV1 of 27±18 ml per year (P<0.001), despite similar smoking exposure.CONCLUSIONS: Our study suggests that low FEV1 in early adulthood is important in the genesis of COPD and that accelerated decline in FEV1 is not an obligate feature of COPD. (Funded by an unrestricted grant from GlaxoSmithKline and others.).

KW - Adult

KW - Aged

KW - Cohort Studies

KW - Disease Progression

KW - Female

KW - Forced Expiratory Volume

KW - Humans

KW - Male

KW - Middle Aged

KW - Pulmonary Disease, Chronic Obstructive

KW - Smoking

KW - Young Adult

U2 - 10.1056/NEJMoa1411532

DO - 10.1056/NEJMoa1411532

M3 - Journal article

C2 - 26154786

VL - 373

SP - 111

EP - 122

JO - New England Journal of Medicine

JF - New England Journal of Medicine

SN - 0028-4793

IS - 2

ER -

ID: 153788008