Recurrent pneumococcal pneumonia in an HIV-positive patient with lymphoid interstitial pneumonitis.

Lymphoid interstitial pneumonitis (LIP) is a rare complication of AIDS in adults. Patients with AIDS and LIP are at high risk for bacterial pneumonia caused by Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus. We have described an HIV-positive patient with LIP complicated by recurrent pneumonia due to Streptococcus pneumoniae; recurrence was apparently prevented by maintenance penicillin therapy.

Evaluation of high-dose tobramycin-carbenicillin therapy in pseudomonal infections in cystic fibrosis.

Fourteen episodes of acute pseudomonal pulmonary exacerbations of cystic fibrosis were treated with high-dose tobramycin (10.1-17.1 mg/kg/d) and carbenicillin (600 mg/kg/d). The Sawchuck-Zaske method of dosing tobramycin was used and resulted in good agreement between the desired and measured peak (8.1 +/- 0.5 vs. 8.2 +/- 1.5 micrograms/ml) and trough (0.5 +/- 0.2 vs. 1.0 +/- 0.4 micrograms/ml) concentrations. Ninety-three percent of cases improved clinically. Forced expiratory volume in one second and forced vital capacity increased significantly (39.3 +/- 24.8, p less than 0.001 and 24.1 +/- 22.8 percent, p less than 0.05, respectively) after treatment. Pseudomonas aeruginosa was eradicated from the sputa of 69 percent of the cases, with recolonization occurring within three months. Significant nephrotoxicity and ototoxicity were not seen. Liver enzymes, however, were elevated in 29 percent of those treated. Combination high-dose carbenicillin and tobramycin satisfies the treatment goals of bacteriological and clinical cure with a minimal degree of toxicity.

A four-year follow-up study of lung mechanics in smokers.

We performed a prospective study of pulmonary function in 21 smokers, 9 ex-smokers, and 12 nonsmokers. The smokers and ex-smokers were preselected, because they were participants in a smoking cessation clinic. An average interval of 4 years separated the first and second (follow-up) studies. The smoking group showed a significant decrease in maximal expiratory flow measured at low lung volume, loss of elastic recoil, increase in lung compliance, increase in total lung capacity; increase in the ratio of residual volume to total lung capacity, and an increase in the ratio of functional residual capacity to total lung capacity. The ex-smokers showed changes similar to those of the smokers, but of lesser magnitude. The nonsmoking group demonstrated few changes in function during the study interval. Commonly measured parameters of function, including the ratio of the forced expiratory volume in 1 sec to the forced vital capacity and the maximal expiratory flow after exhalation of 50 per cent of the vital capacity, did not change significantly in any group. Sensitive tests of lung function were abnormal in a very high percentage of the combined group of smokers and ex-smokers when measured at the time of the second study; only a small number of abnormalities in these parameters were noted in the nonsmoking group. We conclude that there was a deterioration of lung function in smokers far in excess of that predicted by age. These changes suggest the development of emphysema and were predictable for the group as a whole by a high prevalence of abnormality of dynamic compliance, closing volume, maximal mid-expiratory flow, and residual volume at the time of the initial study.

Pulmonary function studies in acute pulmonary histoplasmosis.

We performed follow-up pulmonary function studies on three patients with acute pulmonary histoplasmosis over a period of several months, and found that the disease is benign and usually responds well to treatment or is self-limiting. There are four major changes in lung function, namely a restrictive defect, an impairment of diffusing capacity, stiff lung, and obstruction in small airways. These changes usually lead to disturbance of ventilation-perfusion ratios and impaired gas transport across alveolar capillary membranes, resulting in arterial hypoxemia. There is also hypocapnia from alveolar hyperventilation commonly found in restrictive and stiff lung syndrome.

Effects of intravenous histamine on lung mechanics in man after beta-blockade.

In six nonatopic normal subjects, neither intravenous histamine infusion (0.3 mg.kg-1.min-1) nor intravenous propanolol (10 mg) alone produced significant change in pulmonary mechanics. Histamine infusion after propranolol resulted in an increase in pulmonary resistance (RL) from 2.1 +/- 0.41 (mean +/- 1 SE) to 3.3 +/- 0.76 cmH2O./-1.S-1 (P greater than 0.05); maximal flow at 50% total lung capacity (Vmax 50) decreased from 3.6 +/- 0.35 to 2.7 +/- 0.44 l/s (P greater than 0.01). Similar changes in Vmax 50 were observed during partial forced expiratory maneuvers from end-tidal inspiration (PEFV). On 80:20 helium-oxygen mixture Vmax 50 during maximal expiration (MEFV) decreased from 4.9 +/- 0.61 to 3.4 +/- 0.61 l/s (P greater than 0.005) and during PEFV diminished from 4.6 +/- 0.61 to 2.8 +/- 0.46 l/s (P greater than 0.005). Density dependence (deltaVmax 50) decreased significantly (P greater than 0.05) during PEFV but not during MEFV. There were no significant changes in tidal pulmonary compliance, in closing volume and closing capacity (resident gas technique), and in inflation and deflation pressure-volume curves. We conclude that iv histamine in low doses constricts peripheral conducting airways in man but this effect is masked by histamine-induced release of catecholamines from the adrenal glands.