Ischemia modified albumin in the differential diagnosis of pleural effusions

The differential diagnosis of pleural effusion often requires invasive procedures. Up to 25 percent of pleural effusions can remain undiagnosed with an unclear pathogenesis. Therefore new biological markers may increase diagnostic yield and provide better understanding of pathogenesis of pleural effusion. We hypothesized that new ischemia biomarker, “ischemia modified albumin (IMA)” would help in both the differentiation of the underlying etiologies and provide a better understanding of pathogenesis of pleural effusions. This study was done between December 2009 and September 2010 in the Department of Pulmonary Diseases of Gaziantep University Hospital. One hundred and sixteen subjects with pleural effusion were included. Pleural and blood IMA levels were measured by ELISA. The underlying etiologies of pleural effusions were as follows: transudates (n = 50), malignancy (n = 32), tuberculosis (n = 12), pulmonary thromboembolism (n = 6), pneumonia (n = 16). The median pleural IMA levels were significantly different between the groups (p < 0.000). There were no such differences in the blood levels of IMA. The most striking difference in the median pleural IMA levels was between transudates and exudates (7986 (25-75%, 5145-56.505) ng/mL; 3376 (25-75%, 1935-4660) ng/mL; respectively, p = 0.000). The area under the ROC curve was 0.837 ± 0.038 for the cut-off level higher than 4711 ng l/mL for the differentiation of transudates from exudates (sensitivity, 82%; specificity, 78%; 95% CI, 0.76 to 0.91; p = 0.0000). In conclusion, the pleural IMA levels are higher in transudates compared to exudates. No such differences were observed in blood levels of IMA suggesting that there are reasons other than ischemia that cause an increase in pleural fluid IMA levels.