Diagnostic value of broncho-alveolar lavage in certain interstitial and/or immunological pneumonia.
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Biomedical subjects
Publications and source records attributed to C M Mayaud.
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Pulmonary Kaposi's sarcoma may contribute to respiratory dysfunction in patients with acquired immune deficiency syndrome (AIDS) and features of pneumonitis. Opportunistic infections are readily recognised in endoscopic material, but pulmonary Kaposi's sarcoma is easily missed, so that patients are deprived of specific treatment. The clinical and pathological findings from nine cases of pulmonary Kaposi's sarcoma have been reviewed; these were found among 84 patients with AIDS and pneumonitis undergoing fibreoptic bronchoscopy and bronchoalveolar lavage. Diagnosis was established before death in eight patients (in five by bronchial biopsy and in three by open lung biopsy). Examination of lavage fluid showed alveolar haemorrhage in six patients. It is concluded that: (1) fibreoptic bronchoscopy may be useful in the diagnosis of endobronchial lesions of Kaposi's sarcoma; (2) alveolar haemorrhage in patients with AIDS is suggestive of pulmonary Kaposi's sarcoma. Factors that may cause difficulties in diagnosis include the focal nature of some lesions and the pleural or parenchymatous location of others. In addition, in the lung as in the skin, the early stages of Kaposi's sarcoma resemble granulation tissue. Such lesions are far more difficult to recognise than is the late nodular stage.
The results of bronchoalveolar lavage in three patients with a presumptive diagnosis of methotrexate induced lung disease are presented. Lavage fluid was characterised by the presence of large numbers of lymphocytes, which in two patients were predominantly lymphocytes of the T8 phenotype. These findings further support the hypothesis that immune mediated mechanisms may play a part in the pathogenesis of this disorder in some patients, and indicate that bronchoalveolar lavage may be helpful in the evaluation of patients suspected of having methotrexate induced lung disease.
Methotrexate-induced pneumonitis is a well-known clinical entity, but the mechanism for the induction of the pulmonary disease is ill defined. In three patients with this disorder, evidence was obtained for elaboration of a lymphokine, leukocyte inhibitory factor (LIF), by peripheral blood lymphocytes after incubation with methotrexate (MTX) in the direct leukocyte migration inhibition test. Control lymphocytes from normal subjects, as well as from patients receiving methotrexate but without pneumonitis, failed to elaborate LIF in the presence of the drug in this test. Along with these results, we obtained bronchoalveolar lavage (BAL) cell data displaying high grade lymphocyte alveolitis with a lymphocyte subset inverted ratio. This production of LIF suggests that pneumonitis associated with methotrexate therapy is also associated with a specific cellular immune response to the drug.
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Interstitial pneumonitis developed in a patient who had received a cumulative dose of 985 g of amiodarone in nine years. No other cause for pneumonitis was found. The following findings favor an immunologic mechanism of hypersensitivity due to amiodarone: positive skin and basophil degranulation tests with amiodarone; lymphocytosis and inverted ratio of helper/suppressor T lymphocytes in bronchoalveolar lavage fluid; secretion of leukocyte inhibitory factor, as shown by the inhibition of migration of peripheral blood leukocytes; and positive lymphoblastic transformation in the presence of amiodarone.
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We examined by direct immunofluorescence open lung biopsies from seven adult patients with Pneumocystis carinii pneumonia. In all of them, immunoglobulin deposits (especially IgA) were found in alveoli that exhibited by light microscopy the classical foamy exudate infested by Pneumocystis. These immunoglobulins were eluted at an acid pH and were able to fix complement fractions in vitro. Moreover, we could reproduce this fixation by incubating previously eluted tissue sections with concentrated immunoglobulins isolated from a bronchopulmonary lavage performed in another case of pneumocystis. This immunohistological pattern suggests the presence of a humoral response in pulmonary parenchyma of patients infected with Pneumocystis carinii, despite the consistent underlying immunocompromised status. Considering these results, we conclude that humoral immune mechanisms do not constitute the main barrier against the development of Pneumocystis carinii in human lungs.