title: Levels of YKL-40 in pleural effusions and blood from patients with pulmonary or pleural disease.
abstract: BACKGROUND
  YKL-40 (a chitinase-like protein) is an inflammatory biomarker that is associated with lung injury pathogenesis. We aimed to identify the diagnostic values of YKL-40 in pleural effusions and to evaluate circulating YKL-40 levels during multiple etiological pulmonary/pleural diseases and the role of YKL-40 as a monitoring marker of inflammatory pulmonary disease.
  
  
  METHODS
  Pleural YKL-40 (n=197), YKL-39 (the most homologous chitinase-like protein to human YKL-40), and conventional pleural marker levels were measured in patients with pulmonary/pleural disease. Additionally, serum YKL-40 and YKL-39 levels were analyzed in both patients and controls (n=432) and serially monitored in patients with asthma (n=27) or pneumonia (n=22).
  
  
  RESULTS
  Pleural YKL-40 levels were higher than those in the serum and highest in tuberculous pleural effusions (TPEs; 1181 ng/mL), followed by parapneumonic, malignant, and cardiogenic effusions (560 ng/mL). The diagnostic accuracy of pleural YKL-40 (0.78) for discriminating between tuberculous and malignant effusion was comparable to or greater than those of YKL-39, total protein, C-reactive protein and CYFRA 21-1, and lower than those of adenosine deaminase (p<0.05) and carcinoembriogenic antigen (p=0.05). Serum YKL-40 levels were higher in the pneumonia group than in the cancer, asthma, or control groups. Following treatment, serum YKL-40 levels were more greatly reduced in pneumonia patients than in asthma patients. Serum YKL-39 levels did not differ between patients and controls.
  
  
  CONCLUSIONS
  Pleural YKL-40 levels are elevated in TPEs and have fairly good diagnostic efficacy for detecting TPEs. However, adenosine deaminase is more efficient for detecting TPEs than pleural YKL-40. Serum YKL-40 levels are highest during pneumonia compared to common pulmonary/pleural diseases and are more useful for monitoring pneumonia than asthma.
authors.affiliation: Department of Internal Medicine, School of Medicine, Wonkwang University, Iksan, Republic of Korea.
authors.forename: Hak-Ryul
authors.initials: HR
authors.lastname: Kim
authors.forename: Chang-Duk
authors.initials: CD
authors.lastname: Jun
authors.forename: Koung-Sun
authors.initials: KS
authors.lastname: Lee
authors.forename: Ji-Hyun
authors.initials: JH
authors.lastname: Cho
authors.forename: Eun-Taik
authors.initials: ET
authors.lastname: Jeong
authors.forename: Sei-Hoon
authors.initials: SH
authors.lastname: Yang
authors.forename: Young-Jin
authors.initials: YJ
authors.lastname: Lee
authors.forename: Do-Sim
authors.initials: DS
authors.lastname: Park
mesh_terms: D054392:Adipokines / Q000097:blood / Q000378:metabolism*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D000071451:Chitinase-3-Like Protein 1; D005260:Female; D006801:Humans; D037102:Lectins / Q000097:blood / Q000378:metabolism*; D008171:Lung Diseases / Q000097:blood / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010995:Pleural Diseases / Q000097:blood / Q000378:metabolism*; D010996:Pleural Effusion / Q000378:metabolism*; D011446:Prospective Studies
chemical_list: D054392:Adipokines; C084533:CHI3L1 protein, human; D000071451:Chitinase-3-Like Protein 1; D037102:Lectins