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The clinical and radiologic presentation as well as the macroscopic and histologic characteristics of lung parenchyma in three HIV-infected patients with Pneumocystis carinii pneumonia (PCP) are detailed. The distinguishing clinical feature in these patients was a prolonged stable clinical course of the disease over at least 4 to approximately 24 months. Serial chest radiographs in two patients demonstrated persistent focal radiographic lesions. In one patient blebs in both upper lobes were not recognized until thoracoscopy/thoracotomy was performed. Biopsy specimens of affected areas revealed extensive interstitial fibrosis, occasional giant cell reactions, and honeycombing. In view of the combined clinical, radiologic, macroscopic, and histologic patterns, it is suggested that these patients had a chronic productive form of PCP rather than the well-known acute presentation of the disease. Data from the literature confirm the impression that atypical histologic lesions of PCP, either of a productive or destructive nature, are frequently related to a prolonged clinical course. It is unlikely that prophylactic pentamidine contributes to this entity. Coinfection with other pathogens may have a role. Given the recent evidence on augmented release of tumor necrosis factor a (TNFα) in HIV-associated pulmonary complications, it is speculated that TNFα may be of importance in producing focal fibrosis in Pneumocystis infection of the lung.

Thirty patients with a history of asthma and ten patients with suspected bronchial hyperreactivity underwent nonspecific provocation testing. The control group consisted of ten normal volunteers without a history of lung disease. The patients' baseline FEV1 (percent predicted) revealed mild obstructive disease (72.9 +/- 8.9 percent and 74.6 +/- 7.7 percent) compared with controls (87.2 +/- 8.5 percent, p less than 0.001). The mean volume of trapped gas (D) (ie, TLCB-TLCHe) was not significantly different between groups (0.11 +/- 0.49 L vs 0.15 +/- 0.4 L vs 0.18 +/- 0.45 L), and no correlation was established with any of the remaining lung function data. Bronchial hyperreactivity in response to inhaling acetylcholine could be observed in the asthma group only. Their mean D increased significantly from 0.11 +/- 0.49 L to 0.62 +/- 0.66 L (p less than 0.001), and returned to baseline (0.26 +/- 0.55, NS) subsequent to inhaling salbutamol. D changes induced by acetylcholine correlated weakly with concurrent changes of FEV1 (r = -0.44, p = 0.01), RV (r = 0.59, p less than 0.001), and Rs (r = 0.59, p less than 0.001). In response to bronchodilating doses of salbutamol, however, D was changed in close correlation with FEV1 (r = -0.82, p less than 0.0001), RV (r = 0.85, p less than 0.0001), and Rs (r = 0.76, p less than 0.0001). Provided that D is a valid parameter of small airways function, these data may give a clue to the site of action of both drugs. Acetylcholine affects small and large airways alike with no clear-cut preference, whereas salbutamol's predominant target appears to be the small airways. These conclusions are only partially supported by the pertinent literature.

The most effective treatment of severe paraquat poisoning in man is uncertain. In order to prevent pulmonary fibrosis, we employed radiotherapy of both lungs in a 23-year-old patient with severe paraquat poisoning; however, it failed to prevent the fatal outcome.