Publications

Thirty-two patients with or suspected of having the acquired immunodeficiency syndrome were evaluated for opportunistic lung infection using examination of sputum induced by inhalation of 3% saline. The specimens obtained were stained with Giemsa stain and examined for Pneumocystis carinii. Smears of sputum were also appropriately stained and examined for acid-fast organisms and fungi, as well as cultured for these organisms. Patients whose sputum did not contain P. carinii had bronchoscopy within 24 h of sputum induction. Twenty-five of the 32 patients were ultimately determined to have P. carinii pneumonia. Of these, 14 were detected by examination of sputum (sensitivity, 56%). Of 18 patients whose sputum did not contain P. carinii, 11 had the organism detected in specimens obtained by bronchoscopy (negative predictive value, 39%). There were no clinical features that identified patients more likely to have a positive sputum examination. No additional treatable lung pathogens appeared to be missed by sputum examination. In this select population, examination of induced sputum establishes the diagnosis of P. carinii pneumonia in a significant proportion of patients, thereby decreasing the need for more invasive procedures.

To determine the role of polymorphonuclear leukocytes (PMNs) in the airway edema that accompanies airway inflammation, we studied the effects of a 1-h exposure to 2 ppm toluene diisocyanate (TDI) on tracheal extravasation of Evans blue dye and on the concentration of PMNs in the tracheal wall. Tracheal Evans blue content was significantly increased by TDI exposure (53.6 +/- 8.0 micrograms/g tracheal tissue (mean +/- SE) for animals exposed to TDI and 16.3 +/- 2.0 for animals exposed to air, P less than 0.0025) as were both the intravascular and extravascular concentration of PMNs in tracheal sections (intravascular PMNs were 28.0 +/- 8.4 X 10(3) cells/mm3 for TDI and 1.5 +/- 1.5 X 10(3) for air, P less than 0.025, extravascular PMNs were 10.9 +/- 4.5 X 10(3) for TDI and 0 for air, P less than 0.05). PMN depletion with vinblastine or with hydroxyurea abolished both the increase in tracheal Evans blue extravasation and the increase in the concentration of intravascular and extravascular PMNs in animals exposed to TDI. PMN depletion with hydroxyurea did not significantly inhibit the increase in tracheal Evans blue extravasation caused by intravenous histamine. Administration of donor PMNs to animals depleted of PMNs with hydroxyurea reconstituted the TDI-induced increase in tracheal Evans blue extravasation (80.4 +/- 17.3 micrograms/g tissue (mean +/- SE) in animals exposed to TDI vs. 21.3 +/- 2.9 in animals exposed to air, P less than 0.025) and in the intravascular concentration of PMNs in tracheal sections [18.5 +/- 3.4 X 10(3) cells/mm3 (mean +/- SE) in animals exposed to TDI vs. 1.3 +/- 1.3 X 10(3) in animals exposed to air, P less than 0.0025].(ABSTRACT TRUNCATED AT 250 WORDS)