title: Comparative evaluation of serum markers in pulmonary sarcoidosis.
abstract: BACKGROUND
  Although several serum markers have shown their ability to reflect lymphocytic alveolitis and disease progression in pulmonary sarcoidosis, to our knowledge no prior study has made comparative evaluations of these markers.
  
  
  METHODS
  Forty-three patients with pulmonary sarcoidosis were enrolled. BAL fluid (BALF) cells were analyzed, and serum levels of serum amyloid A (SAA), soluble interleukin 2 receptor (sIL-2R), lysozyme, angiotensin-converting enzyme (ACE), and the mucin-like, high-molecular-weight glycoprotein KL-6 were measured at disease presentation. Clinical data, including chest radiographs, were collected at presentation and during follow-ups. Univariate and multivariate analyses were used to identify markers best predictive of increased parenchymal infiltration.
  
  
  RESULTS
  Significantly higher serum levels of sIL-2R, lysozyme, and KL-6 were found in patients with parenchymal infiltration compared with those without parenchymal infiltration. The numbers of total cells and lymphocytes in BALF were significantly higher in patients with parenchymal infiltration. Serum levels of sIL-2R, lysozyme, and KL-6 were significantly correlated with the numbers of total cells, lymphocytes, and CD4(+) T lymphocytes in BALF. At the cutoff levels determined by receiver operating characteristic curves, sIL-2R, lysozyme, KL-6 serum levels, and the number of BAL lymphocytes showed significant correlations with increased parenchymal infiltrations by univariate analysis. However, multivariate analysis revealed that only KL-6 was a predictor of increased parenchymal infiltration.
  
  
  CONCLUSIONS
  Our results suggest that initial serum sIL-2R, lysozyme, and KL-6 levels may reflect lymphocytic alveolitis in pulmonary sarcoidosis. Furthermore, initial serum KL-6 tends to associate with increased parenchymal infiltration in pulmonary sarcoidosis.
authors.affiliation: Department of Integrated Medicine and Informatics, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295, Japan.
authors.forename: Seigo
authors.initials: S
authors.lastname: Miyoshi
authors.forename: Hironobu
authors.initials: H
authors.lastname: Hamada
authors.forename: Toru
authors.initials: T
authors.lastname: Kadowaki
authors.forename: Naohiko
authors.initials: N
authors.lastname: Hamaguchi
authors.forename: Ryoji
authors.initials: R
authors.lastname: Ito
authors.forename: Kazunori
authors.initials: K
authors.lastname: Irifune
authors.forename: Jitsuo
authors.initials: J
authors.lastname: Higaki
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D001999:Bronchoscopy; D003124:Colorimetry; D018450:Disease Progression; D005434:Flow Cytometry; D005500:Follow-Up Studies; D006801:Humans; D007841:Latex Fixation Tests; D016015:Logistic Models; D008163:Luminescent Measurements; D008297:Male; D008875:Middle Aged; D018396:Mucin-1 / Q000097:blood; D009113:Muramidase / Q000097:blood; D009391:Nephelometry and Turbidimetry; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D012372:ROC Curve; D013902:Radiography, Thoracic; D015375:Receptors, Interleukin-2 / Q000097:blood; D012129:Respiratory Function Tests; D012189:Retrospective Studies; D017565:Sarcoidosis, Pulmonary / Q000097:blood* / Q000000981:diagnostic imaging; D000685:Serum Amyloid A Protein / Q000378:metabolism; D018709:Statistics, Nonparametric
chemical_list: D015415:Biomarkers; C060192:MUC1 protein, human; D018396:Mucin-1; D015375:Receptors, Interleukin-2; D000685:Serum Amyloid A Protein; D009113:Muramidase; D007703:Peptidyl-Dipeptidase A