Susan J M Hoonhorst1, Adèle T Lo Tam Loi2, Jorine E Hartman1, Eef D Telenga1, Maarten van den Berge1, Leo Koenderman2, Jan Willem J Lammers2, H Marike Boezen3, Dirkje S Postma1, Nick H T Ten Hacken4. 1. University of Groningen, University Medical Center Groningen, Department of Pulmonary Diseases, Groningen, the Netherlands; University of Groningen, University Medical Center Groningen, GRIAC research institute, Groningen, the Netherlands. 2. University Medical Center Utrecht, Department of Respiratory Medicine, Utrecht, the Netherlands. 3. University of Groningen, University Medical Center Groningen, Department of Pulmonary Diseases, Groningen, the Netherlands; University of Groningen, University Medical Center Groningen, Department of Epidemiology, Groningen, the Netherlands. 4. University of Groningen, University Medical Center Groningen, Department of Pulmonary Diseases, Groningen, the Netherlands; University of Groningen, University Medical Center Groningen, GRIAC research institute, Groningen, the Netherlands. Electronic address: n.h.t.ten.hacken@umcg.nl.
Abstract
BACKGROUND: Cigarette smoking is the main cause of chronic obstructive pulmonary disease (COPD) inducing oxidative stress and local tissue injury, resulting in pulmonary inflammation. Advanced glycation end products (AGEs) are produced by glycation and oxidation processes and their formation is accelerated in inflammatory conditions. In this study we assessed whether AGE accumulation in the skin is elevated in COPD and associates with disease severity. METHODS: 202 mild-to-very-severe COPD patients and 83 old (40-75 years) and 110 young (18-40 years) healthy smokers and never-smokers were included. AGEs were measured by skin autofluorescence (SAF). Demographic variables, smoking habits, co-morbidities and lung function values were obtained. RESULTS: COPD patients (FEV₁=55% predicted) had significantly higher SAF values than old and young healthy controls: 2.5 vs. 1.8 and 1.2 (arbitrary units, p<0.05). No differences in SAF values were found between GOLD stages I-IV (2.4, 2.3, 2.5, 2.5 respectively). Lower function (FEV₁/FVC, MEF₅₀/FVC, RV/TLC) and higher number of packyears were significantly associated with SAF (p<0.05). CONCLUSIONS: SAF is increased in mild-to-very severe COPD patients compared with healthy controls. Interestingly, SAF was not associated with disease severity as values were comparable between different GOLD stages (stage I-IV) of COPD. This may suggest that AGEs play a role in the induction phase of COPD in susceptible smokers. Future studies should further investigate the mechanisms underlying AGEs formation and accumulation in COPD.
BACKGROUND: Cigarette smoking is the main cause of chronic obstructive pulmonary disease (COPD) inducing oxidative stress and local tissue injury, resulting in pulmonary inflammation. Advanced glycation end products (AGEs) are produced by glycation and oxidation processes and their formation is accelerated in inflammatory conditions. In this study we assessed whether AGE accumulation in the skin is elevated in COPD and associates with disease severity. METHODS: 202 mild-to-very-severe COPDpatients and 83 old (40-75 years) and 110 young (18-40 years) healthy smokers and never-smokers were included. AGEs were measured by skin autofluorescence (SAF). Demographic variables, smoking habits, co-morbidities and lung function values were obtained. RESULTS:COPDpatients (FEV₁=55% predicted) had significantly higher SAF values than old and young healthy controls: 2.5 vs. 1.8 and 1.2 (arbitrary units, p<0.05). No differences in SAF values were found between GOLD stages I-IV (2.4, 2.3, 2.5, 2.5 respectively). Lower function (FEV₁/FVC, MEF₅₀/FVC, RV/TLC) and higher number of packyears were significantly associated with SAF (p<0.05). CONCLUSIONS:SAF is increased in mild-to-very severe COPDpatients compared with healthy controls. Interestingly, SAF was not associated with disease severity as values were comparable between different GOLD stages (stage I-IV) of COPD. This may suggest that AGEs play a role in the induction phase of COPD in susceptible smokers. Future studies should further investigate the mechanisms underlying AGEs formation and accumulation in COPD.
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Authors: Robert P van Waateringe; Marjonneke J Mook-Kanamori; Sandra N Slagter; Melanie M van der Klauw; Jana V van Vliet-Ostaptchouk; Reindert Graaff; Helen L Lutgers; Karsten Suhre; Mohammed M El-Din Selim; Dennis O Mook-Kanamori; Bruce H R Wolffenbuttel Journal: PLoS One Date: 2017-06-20 Impact factor: 3.240
Authors: Susan J M Hoonhorst; Adèle T Lo Tam Loi; Simon D Pouwels; Alen Faiz; Eef D Telenga; Maarten van den Berge; Leo Koenderman; Jan-Willem J Lammers; H Marike Boezen; Antoon J M van Oosterhout; Monique E Lodewijk; Wim Timens; Dirkje S Postma; Nick H T Ten Hacken Journal: Respir Res Date: 2016-04-26
Authors: Robert P van Waateringe; Sandra N Slagter; Melanie M van der Klauw; Jana V van Vliet-Ostaptchouk; Reindert Graaff; Andrew D Paterson; Helen L Lutgers; Bruce H R Wolffenbuttel Journal: Eur J Clin Invest Date: 2016-04-15 Impact factor: 4.686