Elevated pleural copeptin levels can distinguish to exudate from transudates

Introduction: Copeptin is released simultaneously along with arginine- vasopressine as a result of different stimuli from the neurohypophysis. Physiological function of copeptin is still unclear. Increased blood copeptin levels is associated with poor prognosis in many diseases. Pleural effusion is a common clinical condition. The most common causes of pleural effusions are heart failure, parapneumonic effusion, pulmonary embolism and malignacy. Tuberculosis is one of the other major causes of pleural effusion in developing countries. In this study, we aimed to assess whether pleural copeptin level may be a new discriminative biomarker for exudates and transudates pleural effusions. Materials and Methods: Research was done at Recep Tayyip Erdogan University School of Medicine in the Department of Chest Diseases. The concentrations of pleural copeptin and typical pleural and serum marker levels were measured in 76 subjects with pleural effusions including 22 transudates caused by congestive heart failure (CHF), and 54 exudates including 18 parapneumonic (PPE), 18 tuberculous pleural effusions (TBPEs), 18 malignant effusions (MPEs). Results: Median pleural fluid copeptin levels were higher in exudates than in transudates (1936 ng/mL and 1313 pg/mL, p value < 0.001). There was no statistical significancy for pleural fluid copeptin levels with in-group exudates (n= 54). Pleural copeptin levels of exudates, with a cut off value of 1469 ng/mL, yielded a 79.6% sensivity, 81.8% specifity, with an are a under the curve of 0.851. Conclusion: Pleural copeptin level is a new biomarker to separate exudates from transudates. Pleural effusion discriminative effect of copeptin is lower than plasma protein level and plasma lactat dehydrogenase (LDH). Pleural copeptin measurement is not recommended for routine clinical use. Pleural copeptin level is not contribute to different iate exudative pleural fluids from each other like PPE, TBPE and