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There are many causes of pericardial effusion and it is useful to classify them etiologically. In this study 40 patients with pericardial effusion of different etiology were included. By means of clinical data as well as by findings of special techniques such as pericardioscopy, pericardiocentesis and molecular techniques such as PCR and immunological and immunohistochemical analysis of pericardial biopsies the patients were classified retrospectively in the following groups: Group 1 consisted of patients with neoplastic pericardial effusion (n=19 patients), subdivided in a group of patients with cytologically validated malignancy in the pericardial effusion/ pericardial tissue and in a group of patients with malignant metastatic disease but however negative cytology or histology for malignant cells. Group 2 consisted of patients with infectious pericardial effusion (n=5 patients), subdivided in patients with viral or bacterial pericardial effusion. Group 3 consisted of patients with inflammatory and possible autoreactive pericardial effusion (n=13 patients), subdivided in patients with antibody-mediated and in patients with lymphocytic pericardial effusion. Little ist known about the role of cytokines in inflammatory pericardial diseases. The aim of this work was to examine whether a certain cytokine pattern allows to conclude the cause of pericardial effusion and thus possibly offers new therapeutic options. For this purpose the cytokines IL-1alpha, IL-2, IL-6, IL-8, IL-10, TNF-alpha, IFN-gamma and IL-2 sRa in pericardial effusions and sera were determined by means of ELISA and were compared with sera of a control group. For the cytokines IL-6, IL-8 and IL-10 a significantly increased concentration could be demonstrated both in patients with malignant and with autoreactive/inflammatory pericardial effusion compared to the control group, whereas for TNF-alpha this could only be observed in the patients with malignant pericardial effusion. In none of the groups IL-2 and IFN-gamma levels were significantly increased, neither in the pericardial effusion nor in the serum. IL-1alpha was significantly increased both in pericardial effusion and in the serum of all groups in comparison to the control group, except in the serum of the patients with autoreactive pericardial effusion. The concentration of IL-1alpha in the pericardial effusion of neoplastic and inflammatory/autoreactive etiology in median was higher than the autologous serum values. In the group of patients with bacterial pericardial effusion IL-1alpha is increased in the serum in comparison to the control group in particular. IL-8 permits the differentiation of bacterial and viral pericardial effusion and autoreactive antibody-mediated pericardial effusion. Both in sera of patients with viral and in sera of patients with autoreactive antibody-mediated pericardial effusion IL-8 could not be detected, whereas IL-8 levels in the autologous pericardial effusion were increased. IL-2 sRa levels were significantly increased both in patients with neoplastic and in patients with autoreactive pericardial effusiuon in comparison to the control group. A specific cytokine pattern which allows a clear differentiation concerning the etiology of pericardial effusion could not be shown but the results of the analyses of IL-6, IL-8, IL-10 and TNF-alpha show clearly a local inflammatory process, whose better understanding could possibly offer new therapeutic options in the future.