Comparative evaluation of serum markers in pulmonary sarcoidosis.
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.
Miyoshi
Seigo
S
Department of Integrated Medicine and Informatics, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295, Japan.
Hamada
Hironobu
H
Kadowaki
Toru
T
Hamaguchi
Naohiko
N
Ito
Ryoji
R
Irifune
Kazunori
K
Higaki
Jitsuo
J
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
D015415:Biomarkers; C060192:MUC1 protein, human; D018396:Mucin-1; D015375:Receptors, Interleukin-2; D000685:Serum Amyloid A Protein; D009113:Muramidase; D007703:Peptidyl-Dipeptidase A