title: [Systemic and lung inflammation in 2 phenotypes of chronic obstructive pulmonary disease].
abstract: OBJECTIVE
  To study whether patients with chronic obstructive pulmonary disease (COPD) at the same level of flow limitation but with different clinical phenotypes present different degrees of systemic and/or pulmonary inflammation.
  
  
  METHODS
  We studied 15 male smokers without COPD (control group) and 39 males with COPD in stable clinical condition. The COPD patients were assigned to 2 groups based on the ratio of carbon monoxide diffusing capacity (DLCO) to alveolar volume (DLCO/VA) expressed as a percentage as follows: a) mainly emphysema (n = 15) and b) mainly chronic bronchitis (n = 24). Classification was determined by comparing both clinical features and diagnostic images.
  
  
  RESULTS
  Mean (SD) concentrations of interleukin 8 (IL-8) and 8-isoprostane in exhaled breath condensate (EBC) were significantly lower in patients with mainly emphysema (IL-8, 0.34 [0.70] pg/mL; 8-isoprostane, 0.07 [0.26] pg/mL) than in patients with chronic bronchitis (IL-8, 2.32 [3.10] pg/mL; 8-isoprostane, 1.77 [2.98] pg/mL) or in the controls (IL-8, 3.14 [4.59] pg/mL; 8-isoprostane, 1.92 [2.84] pg/mL); P < .05 for IL-8 comparisons and P < .01 for 8-isoprostane. IL-8, leukotriene B4, and 8-isoprostano in EBC correlated significantly with DLCO/VA (% of predicted) (r = 0.30, P < .05; r = 0.29, P < or = .05; and r = 0.46, P < .01, respectively) but not with forced expiratory volume in 1 second. There was a negative correlation between EBC and serum levels of both IL-8 (r = -0.31; P < .05) and 8-isoprostane (r = -0.51; P < .001). The correlation between leukotriene B4 concentrations in EBC and serum was not significant, however. No significant differences were found between smokers' and ex-smokers' serum levels of IL-8, leukotriene B4, 8-isoprostane in serum or EBC.
  
  
  CONCLUSIONS
  The results indicate that COPD patients with an emphysematous phenotype have a less intense inflammatory response and less oxidative stress in the lung.
authors.affiliation: Servicio de Neumología. Hospital Universitario. Guadalajara. España. jlizquierdo@sescam.org
authors.forename: José Luis
authors.initials: JL
authors.lastname: Izquierdo
authors.forename: Carlos
authors.initials: C
authors.lastname: Almonacid
authors.forename: Trinidad
authors.initials: T
authors.lastname: Parra
authors.forename: Jaime
authors.initials: J
authors.lastname: Pérez
mesh_terms: D002248:Carbon Monoxide; D004058:Diffusion; D015237:Dinoprost / Q000031:analogs & derivatives / Q000032:analysis; D004646:Emphysema / Q000150:complications* / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D016209:Interleukin-8 / Q000032:analysis; D007975:Leukotriene B4 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D010641:Phenotype; D011014:Pneumonia / Q000378:metabolism / Q000473:pathology*; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D012907:Smoking
chemical_list: D016209:Interleukin-8; D007975:Leukotriene B4; C075750:8-epi-prostaglandin F2alpha; D002248:Carbon Monoxide; D015237:Dinoprost