Cytokine Activation in Pericardial Fluids in Different Forms of Pericarditis

Abstract

There are many causes of pericardial effusion and it is useful to classify them etiologically, since this disorder is the most common pathologic process involving the pericardium. This report details our experience with pericardioscopy and epicardial biopsy in 101 patients with pericardial effusions in whom pericardioscopy was performed. By means of clinical data and polymerase chain reaction we tried to elucidate the etiology of the pericardial effusion which were classified as follows: we found 41 effusions to be induced by primary malignant tumors or tumors metastatic to the pericardium. Specific diagnosis of viral and bacterial pericarditis was established in 17 patients by examination of the pericardial effusion with PCR, where we found 3 patients positive for adenovirus, 5 patients positive for cytomegalovirus, 2 patients positive for enterovirus-RNA and 5 patients positive for borrelia Burgdorferi-DNA. Additionally, idiopathic effusions (lymphocytic and autoreactive) were seen in 35 patients. In summary immunological and molecular biology investigations seem to provide an additional tool in the diagnostic of pericardial effusion with unknown etiology. If we focus on the ELISA results, there is some evidence, that the demonstration [table: see text] of activation markers and soluble mediators of inflammation such as Il-6, Il-8 and IFN-gamma in pericardial effusion and the simultaneously lack of these mediators in sera of the patients first may be helpful in the discrimination of autoreactive and lymphocytic effusion. Second, this cytokine pattern or distribution indicates a possible local inflammatory process, where these cytokines were all released from activated T lymphocytes present in lymphocytic effusion. In the future, this may have therapeutic implications.

2015 ESC Guidelines for the diagnosis and management of pericardial diseases

“…Badania serologiczne są natomiast całkowicie nieprzydatne w diagnostyce wirusowego zapalenia osierdzia. U chorych na zapalenie osierdzia nie stwierdza się zwiększonych stężeń cytokin prozapalnych w surowicy, natomiast w płynie osierdziowym zwiększone są stężenia TNFa, czynnika wzrostu śródbłonka naczyń, zasadowego czynnika wzrostu fibroblastów, IL-6, IL-8 i interferonu-gamma (IFNg), co jest wykładnikiem toczącego się miejscowo procesu zapalnego [134,135]. Nie stwierdza się też korelacji między mianami przeciwciał przeciwwirusowych w surowicy ani badaniami w kierunku obecności wirusa w wymazach z gardła czy odbytu a wynikami badań metodą łąńcuchowej reakcji polimerazy (PCR)/hybrydyzacji in situ w kierunku obecności wirusów kardiotropowych w prób-kach płynu lub tkanki pobranych z osierdzia [136].…”

“…W krajach uprzemysłowionych większość zachorowań na ostre zapalenie osierdzia jest wywołana zakażeniem wirusowym lub ma charakter autoimmunologiczny [5,6,[133][134][135]. Ostre wirusowe zapalenie osierdzia zwykle ma charakter samoograniczający się, a większość chorych wraca do zdrowia bez powikłań [5,6,9,36].…”

Acute idiopathic pericarditis: current immunological theories

“…Some indirect evidence is the presence of pro-inflammatory cytokines such as interleukin-6 (IL-6), IL-8, and interferon-gamma in the pericardial fluid, but not in plasma, which suggests a local inflammatory reaction. 17 However, the findings of familial forms and of proinflammatory cytokines in the pericardial fluid in IRAP would be in keeping with both O-s AID and AInfD (Table 2). Anti-nuclear antibodies have been detected in 43.3% of IRAP patients, in comparison to 9.8% of healthy controls, and anti-nuclear antibodies might be markers of nonorganspecific autoimmune disease.…”

The Relation of Inflammatory Markers to Idiopathic Pericardial Effusion

“…According to increasing evidences, the usual suspect is the immune mediated pathogenesis. In previous epidemiological studies, the presence of pro-inflammatory cytokines such as interleukin-6, interleukin-8 and interferongamma have been demonstrated in the idiopathic PE (15) . Furthermore, anti-nuclear antibodies, anti-heart and antiintercalated-disk antibodies were detected in the idiopathic PE.…”