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(Chest. 1998;114:1542-1545.)
© 1998 American College of Chest Physicians

Sialyl Stage-Specific Embryonic Antigen-1

A Useful Marker for Differentiating the Etiology of Pleural Effusion

Yu-Chin Lee MD, FCCP1; Jia-Haur Chern MD2; Shinn-Liang Lai MD, PhD, FCCP1; and Reury-Perng Perng MD, PhD, FCCP1

1 From the Chest Department, Veterans General Hospital-Taipei; and the Department of Internal Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan
2 From the Department of Internal Medicine, Taipei Municipal Chung Hsiao Hospital; and Department of Internal Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan

Objectives: To assess the usefulness of sialyl stage-specific embryonic antigen-1 (SSEA-1) levels in differentiating the etiology of pleural effusion (PE).

Design: A solid-phase immunoradiometric sandwich assay with an FH6 monoclonal antibody was used to measure sialyl SSEA-1 levels in PEs of 132 patients with various diseases. Paired serum sialyl SSEA-1 levels were measured simultaneously in 47 patients with various subtypes of lung cancer

Results: The pleural sialyl SSEA-1 levels were significantly higher in patients who had adenocarcinoma of the lung with positive cytology than in all the other patients, including those having malignancies other than adenocarcinoma of the lung, adenocarcinoma of the lung with cytology-negative PE, and benign diseases. There were no significant differences among sialyl SSEA-1 levels in the pleural fluid containing no adenocarcinoma cells. Using the cutoff value of 265 U/mL, the sensitivity was 64% (25/39) and the specificity was 95% (88/93) for the pleural sialyl SSEA-1 level to differentiate adenocarcinoma from other effusions.

Conclusions: With high specificity and modest sensitivity, the pleural sialyl SSEA-1 level is a useful biochemical marker for differentiating the etiology of PEs caused by adenocarcinoma from other diseases.

Key Words: adenocarcinoma • lung neoplasms • pleural effusion • sialyl SSEA-1 • tumor markers

Submitted on March 31, 1997
Accepted on October 17, 1997




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