title: Plasminogen activator inhibitor-1, fibrinogen, and lung function in adolescents with asthma and obesity.
abstract: BACKGROUND
  Obesity promotes a low-grade systemic inflammatory state that may act on the lung to exacerbate asthma. There is little information on the relationship between systemic inflammation and lung function in children and adolescents.
  
  
  OBJECTIVE
  To explore the relationship among fibrinogen, plasminogen activator inhibitor-1 (PAI-1), lung function in adolescents with the presence of asthma, and/or obesity.
  
  
  METHODS
  Totally 178 adolescents (boys and girls) were involved; four groups were divided according to their diagnosis: non-obese and non-asthmatic controls (n = 38), non-obese asthmatics (n = 31), obese non-asthmatics (n = 62), obese asthmatics (n = 47). The levels of PAI-1 and fibrinogen were determined in blood samples. The lung function was evaluated with spirometry by measuring forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), and forced expiratory flows between 25 and75% (FEF(25-75%)).
  
  
  RESULTS
  Compared to healthy controls, obese adolescents with or without asthma show higher levels of fibrinogen (289.2 ± 61.5, 328.4 ± 54.9, and 324.9 ± 68.9 mg/dL, respectively), PAI-1 (36.0 ± 17.3, 53.2 ± 22.3, and 52.6 ± 24.7 ng/mL, respectively), and the reduced FEV1/FVC ratio (87.7 ± 7.7, 81.6 ± 8.6, and 81.7 ± 6.9, respectively). In the whole studied subjects, FEV1/FVC ratio shows significant inverse correlation with PAI-1 (r = -0.185), fibrinogen (r = -0.157), body mass index (BMI; r = -0.303), insulin(r = -0.198), and HOMA (r = -0.173). In the 78 asthmatic subjects, FVC correlates positively with BMI.
  
  
  CONCLUSIONS
  Our data demonstrate that the degree of systemic inflammation and the degree of obesity in the whole studied adolescents groups correlate negatively with lung function, suggesting an obstructive pulmonary pattern. Further studies are needed to identify the pathophysiological mechanism for such association.
authors.affiliation: Department of Pharmacology and Toxicology, Hospital Infántil de México Federico Gómez (HIMFG), Mexico City, Mexico.
authors.forename: Fengyang
authors.initials: F
authors.lastname: Huang
authors.forename: Blanca Estela
authors.initials: BE
authors.lastname: del-Río-Navarro
authors.forename: Saúl Torres
authors.initials: ST
authors.lastname: Alcántara
authors.forename: José Alfredo Pérez
authors.initials: JA
authors.lastname: Ontiveros
authors.forename: Dino Roberto Pietropaolo
authors.initials: DR
authors.lastname: Cienfuegos
authors.forename: Santos Albel
authors.initials: SA
authors.lastname: Bello González
authors.forename: Santiago
authors.initials: S
authors.lastname: Villafaña
authors.forename: Guadalupe
authors.initials: G
authors.lastname: Bravo
authors.forename: Enrique
authors.initials: E
authors.lastname: Hong
mesh_terms: D000293:Adolescent; D001249:Asthma / Q000150:complications / Q000503:physiopathology*; D015992:Body Mass Index; D002648:Child; D005260:Female; D005340:Fibrinogen / Q000032:analysis*; D005540:Forced Expiratory Flow Rates; D005541:Forced Expiratory Volume; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D008168:Lung / Q000503:physiopathology*; D008297:Male; D009765:Obesity / Q000150:complications / Q000503:physiopathology*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D014797:Vital Capacity
chemical_list: D017395:Plasminogen Activator Inhibitor 1; D005340:Fibrinogen