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Original Articles |
Imbalance between intra-alveolar procoagulant activity (PCA) and fibrinolytic activity may lead to fibrin deposition, as described in several pneumopathies, and may eventually contribute to fibrotic changes as observed in Pneumocystis carinii pneumonia (PCP). The aim of our study was to compare these activities in bronchoalveolar lavages of human immunodeficiency virus (HIV)-positive and HIV-negative patients. The material comprised: a) controls (n = 7); b) HIV-positive patients subdivided into PCP (n = 11), bacterial pneumonia (n = 8) and other pneumopathies (n = 22); and c) HIV-negative patients with bacterial pneumonia (n = 8). PCA was significantly increased (p less than 0.05) in all patient groups compared to controls. The urokinase-type plasminogen activator (u-PA) antigen levels were highest during bacterial pneumonia. Regardless of the HIV status, in bacterial pneumonia there was a marked elevation of plasminogen activator inhibitor antigens with little residual fibrinolytic activity. In contrast, the fibrinolytic activity was not decreased in PCP. D-dimer were elevated during PCP compared to controls; the highest levels were found in HIV-negative bacterial pneumonia. These data indicate that transient fibrotic changes seen in PCP may be favoured by increased PCA, but not by a depressed fibrinolytic activity. In bacterial pneumonia PCA is increased and fibrinolysis decreased independently of the HIV status.
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