Characterization of the immunological features of tuberculous pericardial effusions in HIV positive and HIV negative patients in contrast with non-tuberculous effusions

Objective: To investigate the immunopathogenesis of pericardial tuberculosis (TB) and the influence of human immunodeficiency virus (HIV) on the anti-tuberculous immune response. Design: Consecutive patients presenting with large pericardial effusions were subjected to a full clinical examination and pericardiocentesis. Aspirated fluid was sent for biochemistry, differential leukocyte count, flow cytometric analysis and determination of cytokine levels. Pericardial tissue was sent for TB culture and histopathological evaluation. Diagnoses were made according to pre-determined criteria. Results: Fifty-six patients were included and divided into HIV positive TB (n=22), HIV negative TB (n=21) and non-tuberculous effusions (n=13). Peripheral blood neutrophil, lymphocyte and monocyte counts were significantly lower in HIV positive TB patients. Lymphocytes were the dominant cell type in tuberculous pericardial effusions. CD4+ cells dominated in HIV negative tuberculous effusions, whereas CD8+ cells dominated in HIV positive TB. The difference in the concentration of IFN-γ levels in the tuberculous and non-tuberculous pericardial effusions was statistically significant. Despite significant differences in pericardial CD4+ cell counts, IFN-γ levels were similarly elevated in HIV negative and HIV positive tuberculous effusions. Highest levels of pericardial IL-10 were observed in samples associated with least tissue necrosis, suggesting the possibility of a tissue protective immunoregulatory role for IL-10. Conclusions: Tuberculous pericardial effusions result from a T helper1 (Th1)-dominant immune response. IFN-γ producing CD4+ lymphocytes dominate in HIV negative patients, whereas CD8+ seem to play a more important role in HIV positive patients. Infection with HIV leads to the depletion of immunocompetent cells such as monocytes, NK cells and neutrophils. © 2005 Elsevier Ltd. All rights reserved.