Muscle loss phenotype in COPD is associated with adverse outcomes in the UK Biobank
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype (MLP), which is characterized by the loss of muscle mass, muscle strength, or loss of both muscle and fat mass. There are limited data comparing the indiv...
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Published in: | BMC pulmonary medicine Vol. 24; no. 1; p. 186 |
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Abstract | Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype (MLP), which is characterized by the loss of muscle mass, muscle strength, or loss of both muscle and fat mass. There are limited data comparing the individual traits of MLP with clinical outcomes in a large unbiased cohort of COPD patients. Our aim was to determine the proportion of patients who met criteria for MLP in an unbiased sample of COPD patients at the population-level. We also determined if specific MLP features were associated with all-cause and COPD-related mortality.
A retrospective population-based cohort analysis of the UK Biobank was performed. COPD was defined by a FEV1/FVC ratio < 0.7, physician established diagnosis of COPD, or those with a COPD-related hospitalization before baseline assessment. MLP included one or more of the following: 1) Low fat-free mass index (FFMI) on bioelectric impedance analysis (BIA) or 2) Appendicular skeletal muscle index (ASMI) on BIA, 3) Low muscle strength defined by handgrip strength (HGS), or 4) Low muscle and fat mass based on body mass index (BMI). Cox regression was used to determine the association between MLP and all-cause or COPD-related mortality. All models were adjusted for sex, age at assessment, ethnicity, BMI, alcohol use, smoking status, prior cancer diagnosis and FEV1/FVC ratio.
There were 55,782 subjects (56% male) with COPD followed for a median of 70.1 months with a mean(± SD) age at assessment of 59 ± 7.5 years, and FEV1% of 79.2 ± 18.5. Most subjects had mild (50.4%) or moderate (42.8%) COPD. Many patients had evidence of a MLP, which was present in 53.4% of COPD patients (34% by ASMI, 26% by HGS). Of the 5,608 deaths in patients diagnosed with COPD, 907 were COPD-related. After multivariate adjustment, COPD subjects with MLP had a 30% higher hazard-ratio for all-cause death and 70% higher hazard-ratio for COPD-related death.
Evidence of MLP is common in a large population-based cohort of COPD and is associated with higher risk for all-cause and COPD-related mortality. |
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AbstractList | BackgroundChronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype (MLP), which is characterized by the loss of muscle mass, muscle strength, or loss of both muscle and fat mass. There are limited data comparing the individual traits of MLP with clinical outcomes in a large unbiased cohort of COPD patients. Our aim was to determine the proportion of patients who met criteria for MLP in an unbiased sample of COPD patients at the population-level. We also determined if specific MLP features were associated with all-cause and COPD-related mortality.MethodsA retrospective population-based cohort analysis of the UK Biobank was performed. COPD was defined by a FEV1/FVC ratio < 0.7, physician established diagnosis of COPD, or those with a COPD-related hospitalization before baseline assessment. MLP included one or more of the following: 1) Low fat-free mass index (FFMI) on bioelectric impedance analysis (BIA) or 2) Appendicular skeletal muscle index (ASMI) on BIA, 3) Low muscle strength defined by handgrip strength (HGS), or 4) Low muscle and fat mass based on body mass index (BMI). Cox regression was used to determine the association between MLP and all-cause or COPD-related mortality. All models were adjusted for sex, age at assessment, ethnicity, BMI, alcohol use, smoking status, prior cancer diagnosis and FEV1/FVC ratio.ResultsThere were 55,782 subjects (56% male) with COPD followed for a median of 70.1 months with a mean(± SD) age at assessment of 59 ± 7.5 years, and FEV1% of 79.2 ± 18.5. Most subjects had mild (50.4%) or moderate (42.8%) COPD. Many patients had evidence of a MLP, which was present in 53.4% of COPD patients (34% by ASMI, 26% by HGS). Of the 5,608 deaths in patients diagnosed with COPD, 907 were COPD-related. After multivariate adjustment, COPD subjects with MLP had a 30% higher hazard-ratio for all-cause death and 70% higher hazard-ratio for COPD-related death.ConclusionsEvidence of MLP is common in a large population-based cohort of COPD and is associated with higher risk for all-cause and COPD-related mortality. Abstract Background Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype (MLP), which is characterized by the loss of muscle mass, muscle strength, or loss of both muscle and fat mass. There are limited data comparing the individual traits of MLP with clinical outcomes in a large unbiased cohort of COPD patients. Our aim was to determine the proportion of patients who met criteria for MLP in an unbiased sample of COPD patients at the population-level. We also determined if specific MLP features were associated with all-cause and COPD-related mortality. Methods A retrospective population-based cohort analysis of the UK Biobank was performed. COPD was defined by a FEV1/FVC ratio < 0.7, physician established diagnosis of COPD, or those with a COPD-related hospitalization before baseline assessment. MLP included one or more of the following: 1) Low fat-free mass index (FFMI) on bioelectric impedance analysis (BIA) or 2) Appendicular skeletal muscle index (ASMI) on BIA, 3) Low muscle strength defined by handgrip strength (HGS), or 4) Low muscle and fat mass based on body mass index (BMI). Cox regression was used to determine the association between MLP and all-cause or COPD-related mortality. All models were adjusted for sex, age at assessment, ethnicity, BMI, alcohol use, smoking status, prior cancer diagnosis and FEV1/FVC ratio. Results There were 55,782 subjects (56% male) with COPD followed for a median of 70.1 months with a mean(± SD) age at assessment of 59 ± 7.5 years, and FEV1% of 79.2 ± 18.5. Most subjects had mild (50.4%) or moderate (42.8%) COPD. Many patients had evidence of a MLP, which was present in 53.4% of COPD patients (34% by ASMI, 26% by HGS). Of the 5,608 deaths in patients diagnosed with COPD, 907 were COPD-related. After multivariate adjustment, COPD subjects with MLP had a 30% higher hazard-ratio for all-cause death and 70% higher hazard-ratio for COPD-related death. Conclusions Evidence of MLP is common in a large population-based cohort of COPD and is associated with higher risk for all-cause and COPD-related mortality. Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype (MLP), which is characterized by the loss of muscle mass, muscle strength, or loss of both muscle and fat mass. There are limited data comparing the individual traits of MLP with clinical outcomes in a large unbiased cohort of COPD patients. Our aim was to determine the proportion of patients who met criteria for MLP in an unbiased sample of COPD patients at the population-level. We also determined if specific MLP features were associated with all-cause and COPD-related mortality. A retrospective population-based cohort analysis of the UK Biobank was performed. COPD was defined by a FEV1/FVC ratio < 0.7, physician established diagnosis of COPD, or those with a COPD-related hospitalization before baseline assessment. MLP included one or more of the following: 1) Low fat-free mass index (FFMI) on bioelectric impedance analysis (BIA) or 2) Appendicular skeletal muscle index (ASMI) on BIA, 3) Low muscle strength defined by handgrip strength (HGS), or 4) Low muscle and fat mass based on body mass index (BMI). Cox regression was used to determine the association between MLP and all-cause or COPD-related mortality. All models were adjusted for sex, age at assessment, ethnicity, BMI, alcohol use, smoking status, prior cancer diagnosis and FEV1/FVC ratio. There were 55,782 subjects (56% male) with COPD followed for a median of 70.1 months with a mean(± SD) age at assessment of 59 ± 7.5 years, and FEV1% of 79.2 ± 18.5. Most subjects had mild (50.4%) or moderate (42.8%) COPD. Many patients had evidence of a MLP, which was present in 53.4% of COPD patients (34% by ASMI, 26% by HGS). Of the 5,608 deaths in patients diagnosed with COPD, 907 were COPD-related. After multivariate adjustment, COPD subjects with MLP had a 30% higher hazard-ratio for all-cause death and 70% higher hazard-ratio for COPD-related death. Evidence of MLP is common in a large population-based cohort of COPD and is associated with higher risk for all-cause and COPD-related mortality. Background Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype (MLP), which is characterized by the loss of muscle mass, muscle strength, or loss of both muscle and fat mass. There are limited data comparing the individual traits of MLP with clinical outcomes in a large unbiased cohort of COPD patients. Our aim was to determine the proportion of patients who met criteria for MLP in an unbiased sample of COPD patients at the population-level. We also determined if specific MLP features were associated with all-cause and COPD-related mortality. Methods A retrospective population-based cohort analysis of the UK Biobank was performed. COPD was defined by a FEV1/FVC ratio < 0.7, physician established diagnosis of COPD, or those with a COPD-related hospitalization before baseline assessment. MLP included one or more of the following: 1) Low fat-free mass index (FFMI) on bioelectric impedance analysis (BIA) or 2) Appendicular skeletal muscle index (ASMI) on BIA, 3) Low muscle strength defined by handgrip strength (HGS), or 4) Low muscle and fat mass based on body mass index (BMI). Cox regression was used to determine the association between MLP and all-cause or COPD-related mortality. All models were adjusted for sex, age at assessment, ethnicity, BMI, alcohol use, smoking status, prior cancer diagnosis and FEV1/FVC ratio. Results There were 55,782 subjects (56% male) with COPD followed for a median of 70.1 months with a mean([+ or -] SD) age at assessment of 59 [+ or -] 7.5 years, and FEV1% of 79.2 [+ or -] 18.5. Most subjects had mild (50.4%) or moderate (42.8%) COPD. Many patients had evidence of a MLP, which was present in 53.4% of COPD patients (34% by ASMI, 26% by HGS). Of the 5,608 deaths in patients diagnosed with COPD, 907 were COPD-related. After multivariate adjustment, COPD subjects with MLP had a 30% higher hazard-ratio for all-cause death and 70% higher hazard-ratio for COPD-related death. Conclusions Evidence of MLP is common in a large population-based cohort of COPD and is associated with higher risk for all-cause and COPD-related mortality. Keywords: Cachexia, Chronic obstructive pulmonary disease, Epidemiology, Sarcopenia, Skeletal muscle loss Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype (MLP), which is characterized by the loss of muscle mass, muscle strength, or loss of both muscle and fat mass. There are limited data comparing the individual traits of MLP with clinical outcomes in a large unbiased cohort of COPD patients. Our aim was to determine the proportion of patients who met criteria for MLP in an unbiased sample of COPD patients at the population-level. We also determined if specific MLP features were associated with all-cause and COPD-related mortality. A retrospective population-based cohort analysis of the UK Biobank was performed. COPD was defined by a FEV1/FVC ratio < 0.7, physician established diagnosis of COPD, or those with a COPD-related hospitalization before baseline assessment. MLP included one or more of the following: 1) Low fat-free mass index (FFMI) on bioelectric impedance analysis (BIA) or 2) Appendicular skeletal muscle index (ASMI) on BIA, 3) Low muscle strength defined by handgrip strength (HGS), or 4) Low muscle and fat mass based on body mass index (BMI). Cox regression was used to determine the association between MLP and all-cause or COPD-related mortality. All models were adjusted for sex, age at assessment, ethnicity, BMI, alcohol use, smoking status, prior cancer diagnosis and FEV1/FVC ratio. There were 55,782 subjects (56% male) with COPD followed for a median of 70.1 months with a mean([+ or -] SD) age at assessment of 59 [+ or -] 7.5 years, and FEV1% of 79.2 [+ or -] 18.5. Most subjects had mild (50.4%) or moderate (42.8%) COPD. Many patients had evidence of a MLP, which was present in 53.4% of COPD patients (34% by ASMI, 26% by HGS). Of the 5,608 deaths in patients diagnosed with COPD, 907 were COPD-related. After multivariate adjustment, COPD subjects with MLP had a 30% higher hazard-ratio for all-cause death and 70% higher hazard-ratio for COPD-related death. Evidence of MLP is common in a large population-based cohort of COPD and is associated with higher risk for all-cause and COPD-related mortality. |
ArticleNumber | 186 |
Audience | Academic |
Author | Dasarathy, Srinivasan Hatipoğlu, Umur Engelen, Marielle Pkj Attaway, Amy H Zein, Joe Lopez, Rocio Bellar, Annette Welch, Nicole |
Author_xml | – sequence: 1 givenname: Amy H surname: Attaway fullname: Attaway, Amy H organization: Departments of Pulmonary Medicine, Cleveland Clinic, Cleveland, OH, USA – sequence: 2 givenname: Rocio surname: Lopez fullname: Lopez, Rocio organization: Center for Populations Health Research, Cleveland Clinic, Cleveland, OH, USA – sequence: 3 givenname: Nicole surname: Welch fullname: Welch, Nicole organization: Gastroenterology and Hepatology, Cleveland Clinic, Cleveland, OH, USA – sequence: 4 givenname: Annette surname: Bellar fullname: Bellar, Annette organization: Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, USA – sequence: 5 givenname: Umur surname: Hatipoğlu fullname: Hatipoğlu, Umur organization: Departments of Pulmonary Medicine, Cleveland Clinic, Cleveland, OH, USA – sequence: 6 givenname: Joe surname: Zein fullname: Zein, Joe organization: Department of Medicine, Mayo Clinic, Scottsdale, AZ, USA – sequence: 7 givenname: Marielle Pkj surname: Engelen fullname: Engelen, Marielle Pkj organization: Department of Kinesiology, Texas A&M University, College Station, TX, USA – sequence: 8 givenname: Srinivasan surname: Dasarathy fullname: Dasarathy, Srinivasan email: dasaras@ccf.org, dasaras@ccf.org, dasaras@ccf.org organization: Department of Inflammation and Immunity, Lerner Research Institute, 9500 Euclid Avenue, Cleveland, OH, 44195, USA. dasaras@ccf.org |
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Cites_doi | 10.1002/jcsm.13198 10.1093/gerona/61.10.1059 10.1016/S2213-2600(21)00369-6 10.1111/acer.13425 10.1093/ageing/afy169 10.1016/j.chest.2016.11.033 10.1007/s13539-014-0161-y 10.1513/AnnalsATS.201610-821OC 10.1183/23120541.00522-2020 10.1136/thoraxjnl-2014-206440 10.1056/NEJMoa021322 10.1186/s41232-016-0022-5 10.1183/16000617.0049-2019 10.1513/AnnalsATS.201506-388OC 10.1152/japplphysiol.00790.2012 10.1186/s12890-018-0718-1 10.1002/sim.6804 10.1038/s41586-018-0579-z 10.1161/CIRCOUTCOMES.118.004580 10.1164/rccm.201701-0218PP 10.1113/JP283700 10.1093/aje/kwx246 10.1111/resp.13877 10.1164/rccm.202301-0106PP 10.1371/journal.pone.0180928 10.1183/13993003.02140-2018 10.1183/09031936.00080312 10.1164/rccm.201402-0373ST 10.1183/09031936.00023214 10.1183/09031936.04.00055204 10.1016/j.arr.2018.07.005 10.1016/j.rmed.2021.106725 10.1249/01.MSS.0000078924.61453.FB 10.1186/s12877-018-0768-5 10.1007/s13539-014-0164-8 10.1046/j.1532-5415.2002.50216.x 10.1097/MCP.0b013e328336438d 10.1093/ageing/afz046 10.1002/jcsm.12600 10.1590/S1806-37132015000000040 |
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Keywords | Sarcopenia Cachexia Chronic obstructive pulmonary disease Skeletal muscle loss Epidemiology |
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References | AW Vaes (2999_CR9) 2014; 44 CH Martinez (2999_CR28) 2017; 14 DJ Wilkinson (2999_CR38) 2018; 47 BR Celli (2999_CR14) 2004; 350 2999_CR32 TM Costa (2999_CR7) 2015; 41 JE Morley (2999_CR41) 2014; 5 JS Preisser (2999_CR22) 2016; 35 K Ibrahim (2999_CR27) 2018; 18 2999_CR18 F Maltais (2999_CR39) 2014; 189 W Sepúlveda-Loyola (2999_CR4) 2020; 11 DH Higbee (2999_CR36) 2022; 10 JL Marott (2999_CR10) 2022; 192 E Falaschetti (2999_CR20) 2004; 23 CM Lo Cascio (2999_CR33) 2017; 151 A Suleymanova (2999_CR3) 2019; 54 I Janssen (2999_CR43) 2002; 50 2999_CR1 H Abdel-Qadir (2999_CR21) 2018; 11 CK Ryrsø (2999_CR11) 2018; 18 2999_CR5 PH Quanjer (2999_CR25) 2012; 40 BH Goodpaster (2999_CR15) 2006; 61 AJ Cruz-Jentoft (2999_CR24) 2019; 48 C Bycroft (2999_CR16) 2018; 562 AH Attaway (2999_CR2) 2021; 26 LW Lee (2999_CR6) 2017; 12 AH Attaway (2999_CR35) 2023; 14 2999_CR26 S Ogawa (2999_CR44) 2016; 36 RC Wüst (2999_CR42) 2007; 2 2999_CR45 CH Martinez (2999_CR34) 2015; 12 AH Remels (2999_CR40) 2013; 114 SE Jones (2999_CR8) 2015; 70 RA Rabinovich (2999_CR13) 2010; 16 A Fry (2999_CR30) 2017; 186 J Vestbo (2999_CR12) 2006; 173 S von Haehling (2999_CR23) 2014; 5 AJ Cruz-Jentoft (2999_CR29) 2019; 48 CF Vogelmeier (2999_CR31) 2017; 195 CL Craig (2999_CR19) 2003; 35 J Dasarathy (2999_CR37) 2017; 41 A Agustí (2999_CR17) 2023; 207 |
References_xml | – volume: 14 start-page: 1083 issue: 2 year: 2023 ident: 2999_CR35 publication-title: J Cachexia Sarcopenia Muscle doi: 10.1002/jcsm.13198 contributor: fullname: AH Attaway – ident: 2999_CR18 – volume: 61 start-page: 1059 issue: 10 year: 2006 ident: 2999_CR15 publication-title: J Gerontol A doi: 10.1093/gerona/61.10.1059 contributor: fullname: BH Goodpaster – volume: 10 start-page: 149 issue: 2 year: 2022 ident: 2999_CR36 publication-title: Lancet Respir Med doi: 10.1016/S2213-2600(21)00369-6 contributor: fullname: DH Higbee – volume: 41 start-page: 1419 issue: 8 year: 2017 ident: 2999_CR37 publication-title: Alcohol Clin Exp Res doi: 10.1111/acer.13425 contributor: fullname: J Dasarathy – volume: 48 start-page: 16 issue: 1 year: 2019 ident: 2999_CR29 publication-title: Age Ageing doi: 10.1093/ageing/afy169 contributor: fullname: AJ Cruz-Jentoft – volume: 151 start-page: 1039 issue: 5 year: 2017 ident: 2999_CR33 publication-title: Chest doi: 10.1016/j.chest.2016.11.033 contributor: fullname: CM Lo Cascio – volume: 5 start-page: 253 issue: 4 year: 2014 ident: 2999_CR41 publication-title: J Cachexia Sarcopenia Muscle doi: 10.1007/s13539-014-0161-y contributor: fullname: JE Morley – volume: 14 start-page: 1638 issue: 11 year: 2017 ident: 2999_CR28 publication-title: Ann Am Thorac Soc doi: 10.1513/AnnalsATS.201610-821OC contributor: fullname: CH Martinez – volume: 54 start-page: PA695 issue: suppl 63 year: 2019 ident: 2999_CR3 publication-title: Eur Respir J. contributor: fullname: A Suleymanova – ident: 2999_CR32 doi: 10.1183/23120541.00522-2020 – volume: 70 start-page: 213 issue: 3 year: 2015 ident: 2999_CR8 publication-title: Thorax doi: 10.1136/thoraxjnl-2014-206440 contributor: fullname: SE Jones – volume: 350 start-page: 1005 issue: 10 year: 2004 ident: 2999_CR14 publication-title: N Engl J Med. doi: 10.1056/NEJMoa021322 contributor: fullname: BR Celli – volume: 36 start-page: 17 issue: 1 year: 2016 ident: 2999_CR44 publication-title: Inflamm Regen doi: 10.1186/s41232-016-0022-5 contributor: fullname: S Ogawa – ident: 2999_CR5 doi: 10.1183/16000617.0049-2019 – volume: 12 start-page: 1788 issue: 12 year: 2015 ident: 2999_CR34 publication-title: Ann Am Thorac Soc doi: 10.1513/AnnalsATS.201506-388OC contributor: fullname: CH Martinez – volume: 2 start-page: 289 issue: 3 year: 2007 ident: 2999_CR42 publication-title: Int J Chron Obstruct Pulmon Dis contributor: fullname: RC Wüst – volume: 114 start-page: 1253 issue: 9 year: 2013 ident: 2999_CR40 publication-title: J Appl Physiol (1985) doi: 10.1152/japplphysiol.00790.2012 contributor: fullname: AH Remels – volume: 18 start-page: 154 issue: 1 year: 2018 ident: 2999_CR11 publication-title: BMC Pulm Med doi: 10.1186/s12890-018-0718-1 contributor: fullname: CK Ryrsø – volume: 35 start-page: 1722 issue: 10 year: 2016 ident: 2999_CR22 publication-title: Stat Med doi: 10.1002/sim.6804 contributor: fullname: JS Preisser – volume: 562 start-page: 203 issue: 7726 year: 2018 ident: 2999_CR16 publication-title: Nature doi: 10.1038/s41586-018-0579-z contributor: fullname: C Bycroft – volume: 11 start-page: e004580 issue: 7 year: 2018 ident: 2999_CR21 publication-title: Circ Cardiovasc Qual Outcomes doi: 10.1161/CIRCOUTCOMES.118.004580 contributor: fullname: H Abdel-Qadir – volume: 195 start-page: 557 issue: 5 year: 2017 ident: 2999_CR31 publication-title: Am J Respir Crit Care Med. doi: 10.1164/rccm.201701-0218PP contributor: fullname: CF Vogelmeier – ident: 2999_CR45 doi: 10.1113/JP283700 – volume: 186 start-page: 1026 issue: 9 year: 2017 ident: 2999_CR30 publication-title: Am J Epidemiol doi: 10.1093/aje/kwx246 contributor: fullname: A Fry – volume: 26 start-page: 62 issue: 1 year: 2021 ident: 2999_CR2 publication-title: Respirology doi: 10.1111/resp.13877 contributor: fullname: AH Attaway – volume: 207 start-page: 819 issue: 7 year: 2023 ident: 2999_CR17 publication-title: Am J Respir Crit Care Med doi: 10.1164/rccm.202301-0106PP contributor: fullname: A Agustí – ident: 2999_CR1 – volume: 12 start-page: e0180928 issue: 7 year: 2017 ident: 2999_CR6 publication-title: PLoS ONE doi: 10.1371/journal.pone.0180928 contributor: fullname: LW Lee – volume: 173 start-page: 79 issue: 1 year: 2006 ident: 2999_CR12 publication-title: Am J Respir Crit Care Med contributor: fullname: J Vestbo – ident: 2999_CR26 doi: 10.1183/13993003.02140-2018 – volume: 40 start-page: 1324 issue: 6 year: 2012 ident: 2999_CR25 publication-title: Eur Respir J doi: 10.1183/09031936.00080312 contributor: fullname: PH Quanjer – volume: 189 start-page: e15 issue: 9 year: 2014 ident: 2999_CR39 publication-title: Am J Respir Crit Care Med doi: 10.1164/rccm.201402-0373ST contributor: fullname: F Maltais – volume: 44 start-page: 1199 issue: 5 year: 2014 ident: 2999_CR9 publication-title: Eur Respir J doi: 10.1183/09031936.00023214 contributor: fullname: AW Vaes – volume: 23 start-page: 456 issue: 3 year: 2004 ident: 2999_CR20 publication-title: Eur Respir J doi: 10.1183/09031936.04.00055204 contributor: fullname: E Falaschetti – volume: 47 start-page: 123 year: 2018 ident: 2999_CR38 publication-title: Ageing Res Rev doi: 10.1016/j.arr.2018.07.005 contributor: fullname: DJ Wilkinson – volume: 192 start-page: 106725 year: 2022 ident: 2999_CR10 publication-title: Respir Med doi: 10.1016/j.rmed.2021.106725 contributor: fullname: JL Marott – volume: 35 start-page: 1381 issue: 8 year: 2003 ident: 2999_CR19 publication-title: Med Sci Sports Exerc doi: 10.1249/01.MSS.0000078924.61453.FB contributor: fullname: CL Craig – volume: 18 start-page: 79 issue: 1 year: 2018 ident: 2999_CR27 publication-title: BMC Geriatr doi: 10.1186/s12877-018-0768-5 contributor: fullname: K Ibrahim – volume: 5 start-page: 261 issue: 4 year: 2014 ident: 2999_CR23 publication-title: J Cachexia Sarcopenia Muscle doi: 10.1007/s13539-014-0164-8 contributor: fullname: S von Haehling – volume: 50 start-page: 889 issue: 5 year: 2002 ident: 2999_CR43 publication-title: J Am Geriatr Soc doi: 10.1046/j.1532-5415.2002.50216.x contributor: fullname: I Janssen – volume: 16 start-page: 123 issue: 2 year: 2010 ident: 2999_CR13 publication-title: Curr Opin Pulm Med doi: 10.1097/MCP.0b013e328336438d contributor: fullname: RA Rabinovich – volume: 48 start-page: 601 issue: 4 year: 2019 ident: 2999_CR24 publication-title: Age Ageing doi: 10.1093/ageing/afz046 contributor: fullname: AJ Cruz-Jentoft – volume: 11 start-page: 1164 issue: 5 year: 2020 ident: 2999_CR4 publication-title: J Cachexia Sarcopenia Muscle doi: 10.1002/jcsm.12600 contributor: fullname: W Sepúlveda-Loyola – volume: 41 start-page: 415 issue: 5 year: 2015 ident: 2999_CR7 publication-title: J Bras Pneumol doi: 10.1590/S1806-37132015000000040 contributor: fullname: TM Costa |
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Snippet | Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype (MLP), which... Background Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype... BackgroundChronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype... BACKGROUNDChronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss phenotype... Abstract Background Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder with systemic consequences that can cause a muscle loss... |
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SubjectTerms | Analysis Biobanks Body fat Body mass index Cachexia Care and treatment Chronic obstructive pulmonary disease Development and progression Diagnosis Epidemiology Ethnicity Exercise Fat-free body mass Genotype & phenotype Hospitalization Inflammatory diseases Lung diseases Lung diseases, Obstructive Medical examination Mortality Muscle strength Muscles Musculoskeletal system Phenotype Phenotypes Sarcopenia Skeletal muscle Skeletal muscle loss Spirometry |
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Title | Muscle loss phenotype in COPD is associated with adverse outcomes in the UK Biobank |
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