Hemoptysis as the presenting symptom in bronchiolitis obliterans organizing pneumonia.

Bronchiolitis obliterans organizing pneumonia (BOOP) is an uncommon but increasingly recognized pulmonary entity that usually presents with symptoms of dyspnea, cough, and fever. The medical literature describes rare cases of hemoptysis in BOOP, with very small quantities of blood expectorated. We describe two cases of BOOP, one idiopathic and one in association with rheumatoid arthritis, in which large-quantity hemoptysis was the primary presenting symptom.

New treatment modalities for cystic fibrosis.

Refinements in standard therapy for cystic fibrosis have led to dramatic increases in survival and quality of life over the past three decades. Standard therapy has consisted of oral and intravenous antibiotics, chest percussion with postural drainage, and aerosol bronchodilator therapy. The discovery of the cystic fibrosis gene and elucidation of the underlying biochemical defect have broadened our understanding of the pathophysiology of cystic fibrosis and provided a rationale for many new and innovative therapies. Modulation of airway epithelial ion transport may improve mucociliary clearance and delay colonization by infective organisms. Anti-inflammatory therapy may decrease lung injury that results from the host's attempt to limit airway infection. Supplementation of airway antiproteases may limit the destructive effects of unopposed proteases on pulmonary architecture. Genetic biotechnology has already produced agents that preserve pulmonary function and decrease infectious exacerbations by altering the viscoelastic properties of sputum from patients with cystic fibrosis. Both active and passive immunotherapy are currently being investigated as a measure to delay or combat endobronchial infection with Pseudomonas spp. Aerosolized aminoglycoside antibiotics are being increasingly employed to control pulmonary infection while minimizing systemic toxicity. These treatment modalities, combined with the prospects for gene therapy, provide a brighter outlook for the patient with cystic fibrosis than ever before.

The comparative effects of elastase-induced emphysema on costal and crural diaphragm and parasternal intercostal muscle contractility.

Chronically, hyperinflated human subjects with chronic obstructive pulmonary disease and animals with experimentally induced emphysema generate greater than expected levels of transdiaphragmatic pressure at high lung volume because of adaptive changes in the length-tension relationship of the costal diaphragm. The ability to lower intrathoracic pressure during inspiration depends on the mechanical action of all the inspiratory muscles acting in concert. However, the effect of chronic hyperinflation on the mechanical action of inspiratory muscles other than the costal diaphragm remains unknown. This study compares the effect of chronic hyperinflation in the form of elastase-induced emphysema on the contractile properties of the three major inspiratory muscles of the hamster (i.e., the costal and crural diaphragm and parasternal intercostals). Muscles were studied in vitro 6 months after emphysema was induced by intratracheal injection of elastase. Saline-injected animals served as controls. TLC in the elastase-injected hamsters was significantly greater than in controls (12.5 +/- 0.8 ml versus 9.0 +/- 0.3 ml, p < 0.002). Maximal tetanic tension, time to peak tension, maximal velocity of shortening, and the force-velocity relationship differed among the three muscles but for any given muscle were similar in control and emphysematous animals. In contrast, the fiber length optimal for tension generation (Lo) not only differed across muscles but was significantly shorter in the costal diaphragm of emphysematous animals compared with control animals. However, Lo of the parasternal intercostal and crural diaphragm was similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Pleural effusions in right-sided endocarditis: characteristics and pathophysiology.

The incidence, characteristics, and pathogenesis of pleural effusions in patients with right-sided endocarditis (RSE) are poorly defined. We have recently observed four patients with a history of intravenous drug abuse and bacteremia due to Staphylococcus aureus who had pleural effusions during an episode of RSE. We report the pleural fluid characteristics of five effusions in these four patients and attempt to define the pathogenesis of each. We found that (1) an exudative, sterile, serosanguineous, or bloody effusion is common in RSE, (2) empyema occurred in only one patient, and (3) transudative effusions due to CHF were not observed. Possible mechanisms of pleural fluid formation in RSE include parapneumonic effusion, septic pulmonary emboli with or without infarction, and empyema. Congestive heart failure does not appear to be a common cause of pleural effusion in pure right-sided endocarditis.