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Following the unexpected finding of antibodies to GBM in a patient withPneumocystis carinii pneumonia in the absence of kidney abnormalities, the presence of anti-GBM antibodies was analysed in 14 patients with pulmonary P. carinii infection who did not have clinical evidence of autoimmune glomerulonephritis. Patients were divided into three groups: HIV- with P. carinii pneumonia(n = 4), HIV+ with P. carinii pneumonia(n=5) and HIV- carriers of P. carinii without pneumonia (n=5). As control groups, HIV- patients with community-acquired non-P. carinii pneumonia (n=6) and healthy individuals (n=16) were included. Anti-GBM antibodies, studied with a quantitative enzyme immunoassay (EIA) for anti-α3 chain of collagen IV antibodies, were detected in three out of the four HIV- patients with P. carinii pneumonia, but not in any individuals of the other categories. These results suggest that P. carinii alveolar injury or the host response to the organism could affect the basal membrane Goodpasture antigen or a similar antigen, and induces anti-GBM antibody production in HIV- patients, and support the hypothesis that, at least in some cases, Goodpasture's syndrome could be triggered by an alveolar lesion induced by a P. carinii pneumonia.