title: Systemic levels of cotinine and elastase, but not pulmonary function, are associated with the progression of small abdominal aortic aneurysms.
abstract: OBJECTIVE
  to study whether smoking and impaired pulmonary function are associated with the expansion of abdominal aortic aneurysms (AAA).
  
  
  METHODS
  seventy-nine men with small (3-5 cm), screen-detected AAA underwent a simple 5-step smoking history, measurement of the forced first second expiratory volume (FEV1), venepuncture and annual ultrasound scan for mean follow-up period of 3.5 years.
  
  
  RESULTS
  all but one patient had a significantly reduced FEV1 (p<0.05, Mann-Whitney). The FEV1/expected FEV1 ratio (rFEV1) was not related to AAA expansion but was negatively correlated with P-elastase-alpha1-antitrypsin-complexes (P-Elastase). P-Elastase was positively correlated with smoking and S-cotinine. Smoking, S-cotinine, and P-elastase were positively correlated with the mean annual AAA expansion rate but not rFEV1.
  
  
  CONCLUSIONS
  in general, patients with AAA have impaired pulmonary function. A simple five step smoking classification is as predictive of AAA-expansion as S-cotinine. Smoking may cause elastase secretion leading to pulmonary and aortic elastin degradation but the lack of association between AAA-expansion and rFEV1 suggest that other mechanisms are important.
mesh_terms: D000368:Aged; D017544:Aortic Aneurysm, Abdominal / Q000097:blood / Q000503:physiopathology*; D003367:Cotinine / Q000097:blood*; D018450:Disease Progression; D005541:Forced Expiratory Volume; D006801:Humans; D008297:Male; D010196:Pancreatic Elastase / Q000097:blood*; D015656:Respiratory Mechanics; D012907:Smoking / Q000097:blood*
chemical_list: D010196:Pancreatic Elastase; D003367:Cotinine