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In the last 13 years, bronchoalveolar lavage has been widely used to study the mechanisms involved in the defense of the lower respiratory tract and in the pathogenesis of a variety of lung disorders. This technique, which is a relatively safe and simple extension of fiberoptic bronchoscopy, has been proved to be a powerful investigative tool with enormous potential since it has enhanced our knowledge on a variety of disorders, including interstitial lung diseases, lung destruction associated to cigarette smoking and, recently, bronchial asthma. In addition, bronchoalveolar lavage has also been utilized as an interesting test to help in the diagnostic procedures and in the management of patients with a variety of pulmonary diseases. Its actual importance in clinical respiratory medicine, however, is still under debate and the value of some suggested applications remains to be established.

Adriamycin, given to 10 cancer patients at the dosage of 0·4 mg/kg intravenously for three following days (this course of therapy was repeated three times at 10-day intervals), was evaluated in plasma and urine according to a simpler and sensitive fluorimetric procedure. By considering plasma disappearance curves of single patients following the first intravenous injection, quite important differences emerged concerning duration of measurable amounts of the drug. Moreover, adriamycin concentrations in plasma appeared to be progressively more sustained and sometimes more lasting following the subsequent drug injections. Urinary excretion of adriamycin turned out to be of a great variability concerning duration of excretion in different patients, duration of measurable excretion in the same patient relative to the successive therapeutic courses and percentage of the total dose administered. Thin-layer chromatography of plasma and urine extracts did not reveal any fluorescent band other than adriamycin itself.

Alveolar macrophages act as accessory cells in lymphocyte response to mitogens or alloantigens. Because the autologous mixed lymphocyte reaction (MLR), in which HLA-DR-positive non-T cells stimulate the proliferation of autologous T lymphocytes, represents a good model to study macrophage-T cell interaction, we examined and compared the ability of human alveolar macrophages and peripheral blood-derived monocytes to induce T-cell proliferation in autologous MLR. Maximal T lymphocyte proliferation was observed in both alveolar-macrophage- and blood-monocyte-stimulated autologous MLR at a T cell to alveolar macrophage or blood monocyte ratio of 4:1, but the ability to stimulate T-cell proliferation was lower for alveolar macrophages than for blood monocytes (p less than 0.01). Because HLA-DR antigens modulate monocyte-T cell interaction, we quantified the proportions of HLA-DR-positive cells in alveolar macrophage and blood monocyte suspensions and determined the inhibitory effects on T-cell proliferation of masking HLA-DR antigens on stimulator cells with monoclonal antibodies. The proportions of HLA-DR-positive cells were higher in alveolar macrophage than in blood suspensions (p less than 0.01); interestingly, however, the preincubation of the stimulator cells with anti-HLA-DR monoclonal antibodies inhibited to a similar extent both alveolar-macrophage- and blood-monocyte-stimulated autologous MLR (p greater than 0.2). These studies indicate that alveolar macrophages are less effective than blood monocytes are as stimulator cells in autologous MLR and that, although the masking of HLA-DR molecules results in inhibition of autologous MLR, T-cell proliferation is not dependent on the numbers of stimulator cells bearing HLA-DR antigens. The autologous MLR may represent a good model to study the functions of alveolar macrophages during their interaction with autologous T cells in health and disease.

Different lymphocyte subpopulations have been evaluated in bronchoalveolar fluid and blood obtained from six patients with active and six with inactive pulmonary sarcoidosis and from six normal subjects by means of two recently described monoclonal antibodies, 5/9 and MLR4. The percentages of OKT4 positive (helper) and OKT8 positive (suppressor) T cells were also determined. Patients with active sarcoidosis had significantly higher proportions of 5/9 positive T cells in the bronchoalveolar fluid than patients with inactive disease (p less than 0.01) or normal subjects (p less than 0.001). In contrast, the proportions of 5/9 positive blood T cells were similar in the three groups studied. Patients with active sarcoidosis had also a greater proportion proportion of MLR4 positive T lymphocytes in bronchoalveolar fluid than patients with inactive disease or normal subjects (p less than 0.01 for each comparison), but similar proportions of MLR4 positive blood T cells were found in each group. The ratio of 5/9 positive to MLR4 positive T cells was higher in the bronchoalveolar fluid (but not in the blood) in patients with either active or inactive sarcoidosis than in normal subjects. These observations suggest that the MLR4 negative fraction rather than the MLR4 positive fraction of the 5/9 positive T cells is preferentially expanded in the lungs of patients with pulmonary sarcoidosis and may indicate a secondary role for the MLR4 positive T cells in producing lung injury in this disorder. Comparisons of the OKT4 positive and 5/9 positive T cells showed that in patients with active disease most of the lung T lymphocytes expressed both the OKT4 and the 5/9 surface antigens, so the 5/9 monoclonal antibody may be considered a good marker of activity in this disorder. Pulmonary sarcoidosis may be characterised by the preferential expansion of helper T cell subsets at sites of disease activity.

Massive pulmonary infiltration by leukemic cells resulting in respiratory symptoms is a rare complication of acute leukemia. We report the findings in a patient with acute myelomonocytic leukemia presenting with acute onset of fever, dyspnea, and nonproductive cough, in whom the diagnosis of pulmonary invasion by leukemic cells was made by cytochemical analysis of bronchoalveolar cells recovered by lavage.

A pilot study of topical (intrapleural) treatment with Corynebacterium parvum was carried out in 10 patients with malignant pleural effusions complicating primary or secondary neoplasms and necessitating frequent thoracocentesis for symptomatic relief. The method was aspiration of all intrapleural fluid except a small portion left for dilution, and then injection of 7 mg of a preparation of Corynebacterium parvum suspended in 20 ml of normal saline solution. The treatment was repeated in each case as clinical conditions called for further thoracocentesis. In eight of these 10 patients the treatment resulted in prompt reduction of the rate of accumulation of pleural fluid and a striking change of cell sediment composition, with appreciable reduction in or complete disappearance of malignant cells and a rise in lymphocyte and neutrophil polymorph counts. The best responders were patients with primary pleural mesothelioma. Clinical improvement was evident in all responders.