title: Plasminogen activator inhibitor-1 is elevated in patients with COPD independent of metabolic and cardiovascular function.
abstract: BACKGROUND
  Plasminogen activator inhibitor-1 (PAI-1), a major inhibitor of fibrinolysis, is associated with thrombosis, obesity, insulin resistance, dyslipidemia, and premature aging, which all are coexisting conditions of chronic obstructive pulmonary disease (COPD). The role of PAI-1 in COPD with respect to metabolic and cardiovascular functions is unclear.
  
  
  METHODS
  In this study, which was nested within a prospective cohort study, the serum levels of PAI-1 were cross-sectionally measured in 74 stable COPD patients (Global Initiative for Chronic Obstructive Lung Disease [GOLD] Stages I-IV) and 18 controls without lung disease. In addition, triglycerides, high-density lipoprotein cholesterol, fasting plasma glucose, waist circumference, blood pressure, smoking status, high-sensitive C-reactive protein (hs-CRP), adiponectin, ankle-brachial index, N-terminal pro-B-type natriuretic peptide, and history of comorbidities were also determined.
  
  
  RESULTS
  The serum levels of PAI-1 were significantly higher in COPD patients than in controls, independent of a broad spectrum of possible confounders including metabolic and cardiovascular dysfunction. A multivariate regression analysis revealed triglyceride and hs-CRP levels to be the best predictors of PAI-1 within COPD. GOLD Stages II and III remained independently associated with higher PAI-1 levels in a final regression analysis.
  
  
  CONCLUSIONS
  The data from the present study showed that the serum levels of PAI-1 are higher in patients with COPD and that moderate-to-severe airflow limitation, hypertriglyceridemia, and systemic inflammation are independent predictors of an elevated PAI-1 level. PAI-1 may be a potential biomarker candidate for COPD-specific and extra-pulmonary manifestations.
authors.affiliation: Pneumology, LungenClinic Grosshansdorf, Grosshansdorf, Germany; Pulmonary Research Institute at LungenClinic Grosshansdorf, Grosshansdorf, Germany; Airway Research Center North (ARCN), German Center for Lung Research (DZL), Grosshansdorf, Germany.
authors.forename: Benjamin
authors.initials: B
authors.lastname: Waschki
authors.affiliation: Pulmonary Research Institute at LungenClinic Grosshansdorf, Grosshansdorf, Germany; Airway Research Center North (ARCN), German Center for Lung Research (DZL), Grosshansdorf, Germany.
authors.forename: Henrik
authors.initials: H
authors.lastname: Watz
authors.affiliation: Fraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany; Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), German Center for Lung Research (DZL), Hannover, Germany.
authors.forename: Olaf
authors.initials: O
authors.lastname: Holz
authors.affiliation: Pulmonary Research Institute at LungenClinic Grosshansdorf, Grosshansdorf, Germany; Airway Research Center North (ARCN), German Center for Lung Research (DZL), Grosshansdorf, Germany.
authors.forename: Helgo
authors.initials: H
authors.lastname: Magnussen
authors.affiliation: Department of Medicine, Trelleborg Hospital, Trelleborg, Sweden.
authors.forename: Beata
authors.initials: B
authors.lastname: Olejnicka
authors.affiliation: Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), German Center for Lung Research (DZL), Hannover, Germany; Department of Respiratory Medicine, Hannover Medical School, Hannover, Germany.
authors.forename: Tobias
authors.initials: T
authors.lastname: Welte
authors.affiliation: Pneumology, LungenClinic Grosshansdorf, Grosshansdorf, Germany; Airway Research Center North (ARCN), German Center for Lung Research (DZL), Grosshansdorf, Germany.
authors.forename: Klaus F
authors.initials: KF
authors.lastname: Rabe
authors.affiliation: Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), German Center for Lung Research (DZL), Hannover, Germany; Department of Respiratory Medicine, Hannover Medical School, Hannover, Germany.
authors.forename: Sabina
authors.initials: S
authors.lastname: Janciauskiene
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis*; D002319:Cardiovascular System / Q000503:physiopathology*; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology; D007249:Inflammation / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood*; D016014:Linear Models; D008168:Lung / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D011446:Prospective Studies; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology; D012720:Severity of Illness Index; D014280:Triglycerides / Q000097:blood*; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D014280:Triglycerides; D002097:C-Reactive Protein
keywords: N-terminal pro-B-type natriuretic peptide; ankle-brachial index; cardiovascular disease; chronic obstructive pulmonary disease; hypertriglyceridemia; inflammation; plasminogen activator inhibitor-1