title: Soluble receptor of advanced glycation end-products and endothelial dysfunction in COPD.
abstract: BACKGROUND
  Chronic obstructive pulmonary disease (COPD) is accompanied by an increased cardiovascular risk which is aggravated by the incidence of acute exacerbations (AE). Endothelial function, as well as the soluble receptor for advanced glycation end-products (sRAGE), both markers of cardiovascular risk, has been shown to be decreased in stable COPD.
  
  
  OBJECTIVE
  We aimed to investigate a possible link between sRAGE and endothelial function in AE of COPD. We hypothesize that circulating levels of sRAGE and endothelial function are impaired during AE and improve after clinical recovery, respectively.
  
  
  METHODS
  We enrolled patients admitted to hospital due to an AE of COPD without overt cardiovascular comorbidities. Study related procedures comprised spirometry, measurement of plasma sRAGE levels and the quantification of endothelial function by means of the flow-mediated dilation technique (FMD). All measurements were scheduled during hospitalization and after confirmed clinical stability.
  
  
  RESULTS
  We recruited 29 patients (27% female) with moderate to severe COPD. Median sRAGE concentration was 525 pg/mL (371-770, 1st-3rd quartile) and mean FMD 6.7 ± 3.6% at AE. There was a significant increase of sRAGE levels to 876 pg/mL (633-1371, 1st-3rd quartile, p < 0.001) and a simultaneous improvement in FMD (10.0 ± 3.4%, p < 0.001) after clinical recovery. There was a significant positive association between sRAGE and FMD (regression coefficient = 2.43; p = 0.01) in our study sample.
  
  
  CONCLUSIONS
  Our results indicate a substantial decrease in sRAGE levels and endothelial function during AE, with evidence of improvements after clinical recovery. sRAGE may contribute to cardiovascular risk in COPD.
authors.affiliation: Department of Respiratory and Critical Care Medicine, Ludwig Boltzmann Institute for COPD, Otto Wagner Hospital, Sanatoriumstrasse 2, 1140 Vienna, Austria.
authors.forename: Matthias H
authors.initials: MH
authors.lastname: Urban
authors.affiliation: Department of Respiratory and Critical Care Medicine, Ludwig Boltzmann Institute for COPD, Otto Wagner Hospital, Sanatoriumstrasse 2, 1140 Vienna, Austria.
authors.forename: Arschang
authors.initials: A
authors.lastname: Valipour
authors.affiliation: Hartmann Hospital, Nikolsdorfergasse 26-36, 1050 Vienna, Austria.
authors.forename: Dora
authors.initials: D
authors.lastname: Kiss
authors.affiliation: St. Anna Children's Hospital, Kinderspitalgasse 6, 1090 Vienna, Austria.
authors.forename: Philipp
authors.initials: P
authors.lastname: Eickhoff
authors.affiliation: Department of Respiratory and Critical Care Medicine, Ludwig Boltzmann Institute for COPD, Otto Wagner Hospital, Sanatoriumstrasse 2, 1140 Vienna, Austria. Electronic address: georg-christian.funk@wienkav.at.
authors.forename: Georg-Christian
authors.initials: GC
authors.lastname: Funk
authors.affiliation: Department of Respiratory and Critical Care Medicine, Ludwig Boltzmann Institute for COPD, Otto Wagner Hospital, Sanatoriumstrasse 2, 1140 Vienna, Austria.
authors.forename: Otto C
authors.initials: OC
authors.lastname: Burghuber
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000209:etiology*; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications* / Q000503:physiopathology; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000378:metabolism*; D014797:Vital Capacity / Q000502:physiology
chemical_list: D015415:Biomarkers; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic
keywords: COPD; Exacerbation; FMD; Nitric oxide; sRAGE