Vascular endothelial cells act as antigen-presenting cells in the lung allograft and stimulate alloreactive host lymphocytes. Activated lymphocytes and cytokines can induce expression of leukocyte-endothelial adhesion molecules that facilitate invasion of the allograft by circulating leukocytes. To define the role of endothelial HLA class II antigen and adhesion molecule expression in lung allograft rejection, we prospectively analyzed endothelial expression of HLA class II, E-selectin, and intercellular adhesion molecule-1 (ICAM-1) antigens in 52 transbronchial biopsy specimens from 24 lung allograft recipients as compared to normal control subjects. Thirty-one of 52 specimens showed histologic rejection and 8 of 24 patients developed histologic obliterative bronchiolitis (OB) by the end of the study period. Increased expression of HLA class II antigen was seen in 32 of 52 (62%) lung allograft specimens, but increased expression did not correlate with acute rejection or OB. In contrast, E-selectin expression was seen in 30 of 52 (58%) biopsy specimens and was associated with acute rejection (p < 0.005) and with the development of OB (p < 0.05). Increased expression of ICAM-1 was seen in only 18 of 52 (35%) biopsy specimens and did not correlate with acute rejection or OB. These data suggest that E-selectin expression may be a tissue marker of acute and chronic lung rejection possibly by promoting leukocyte adhesion to the allograft endothelium. The high levels of endothelial HLA class II expression may reflect long-term antigenic stimulation of the allograft even in the absence of rejection.

Aortic dissection most often is an acute event dominated by excruciating pain and other symptoms which suggest the diagnosis. Our report and a review of the medical literature demonstrate that chronic aortic dissection may, rarely, present as a prolonged febrile illness, with night sweats, weight loss, pleural effusion, and little or no pain. These symptoms may be associated with a markedly elevated erythrocyte sedimentation rate (ESR), anemia of chronic disease, and hyperglobulinemia. Awareness of this unusual presentation, a high index of suspicion, and confirmation by an appropriate imagine technique (CT or MRI of the chest or transesophageal echocardiography have a very high sensitivity) will result in earlier diagnosis and better patient outcome.

To determine the impact of antibiotic treatment of ventilator-associated pneumonia (VAP) on survival.

We investigated the effect of free radical scavengers, micronutrient antioxidants, on antioxidant enzyme activities in cigarette smokers. We measured the intracellular superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities and vitamin E and beta-carotene levels in the bronchoalveolar cells of 14 smokers before and after 6 weeks of supplementation with vitamins E and C and beta-carotene. Eight nonsmokers served as control subjects. CAT and GPx activities were higher in BAL cells from smokers compared with nonsmokers (20.5 +/- 2.3 vs 9.6 +/- 1.3 U/10(6) cells; p = 0.027; 0.90 +/- 0.10 vs 0.46 +/- 0.12 U/10(6) cells; p = 0.049, respectively), while there was no difference in SOD activity between the two groups. Likewise, vitamin E and beta-carotene concentrations were markedly higher in smokers' lung lavage cells (403.3 +/- 81.0 in smokers vs 16.6 +/- 5.3 ng/10(6) cells in nonsmokers, and 1.23 +/- 0.21 in smokers vs 0.15 +/- 0.04 ng/10(6) cells in nonsmokers, respectively). The serum levels of vitamin E and C and beta-carotene increased by 2.0-, 1.6-, and 8.9-fold in smokers after supplementation, which were similar to nonsmokers. Similarly, BAL cell vitamin E increased from 403.3 +/- 81.0 to 477.4 +/- 97.7 ng/10(6) cells and beta-carotene increased from 1.23 +/- 0.21 to 4.32 +/- 0.45 ng/10(6) cells (p < 0.05). Despite increased concentrations of vitamins in serum as well as beta-carotene levels in BAL cells, there was no significant down regulation in SOD, CAT, or GPx activities in the lung lavage cells. These data suggest that augmentation of micronutrient antioxidants in smokers and nonsmokers does not appear to have an effect on antioxidant enzyme activities, suggesting a differential regulation of these defenses.

Fifty-three lung masses were found in 51 (16%) of 325 patients who underwent lung volume reduction surgery. This included 11 non-small cell lung cancers and 42 benign lung masses. Eleven patients (mean age, 69.4 years) underwent a combined lung volume reduction surgery and resection of clinical stage I lung cancers (lymph node dissection with either lobectomy [3] or wedge resection [8]). There were no deaths or major complications. The average length of stay was 8.7 days. The mean FEV1 was 654 mL (21.7% predicted) preoperatively and 1,079 mL (49% predicted) postoperatively. Patients who are screened for lung volume reduction surgery should be carefully evaluated for possible lung masses. Lung volume reduction surgery allows lung cancer surgery in patients who otherwise would be considered to have physiologically inoperable disease.

Torulopsis glabrata is a rare cause of pneumonia in immunocompromised patients. We herein describe the case of an elderly man who presented with fulminant Torulopsis pneumonia and septic shock leading to death. We then review the literature, describe the clinical syndrome, and delineate an approach to diagnosis and treatment of Torulopsis pneumonia.

Self-expanding metallic stents (SEMSs) are used to palliate malignant esophageal strictures. We describe a patient who had an extensive mediastinal tumor for which he was receiving irradiation therapy; chest pain, hemoptysis, and recurrent Gram-negative pneumonia developed in this patient after stent placement. Fiberoptic bronchoscopy revealed protrusion of the SEMS into the tracheobronchial tree, a novel complication for this new type of stent.

A 72-year-old man presented with malaise, weight loss, and cough. Chest radiograph revealed bilateral pleural effusions. On thoracentesis, the left effusion was a clear yellow exudate with more than 90% lymphocytes, and the right effusion was a grossly bloody exudate with more than 90% neutrophils. Cultures of both effusions grew Mycobacterium tuberculosis.

We investigated whether the bronchodilator response to a beta-adrenergic agonist is influenced by the mechanism of induced bronchoconstriction. Normal subjects and asymptomatic asthmatics inhaled a dry aerosol (mass median aerodynamic diameter, 1.5 microns) with increasing concentrations of methacholine or histamine to produce a 35% decrease in specific airway conductance (SGaw), followed by a single inhalation of a metaproterenol aerosol. By studying normal subjects and asthmatics, we were able to compare metaproterenol responsiveness after widely divergent doses of the bronchoprovocative agents but the same degree of bronchoconstriction. Airway deposition of methacholine, histamine, and metaproterenol was measured using a quinine fluorescence technique. Mean baseline SGaw, metaproterenol responsiveness, and metaproterenol mass deposited were similar in normal subjects and asthmatics. Likewise, mean SGaw after completion of methacholine and histamine challenge, and the subsequently deposited metaproterenol mass were similar in the two groups. After methacholine challenge (mean +/- SD provocative drug mass causing a 35% decrease in SGaw, PM35: 8.94 +/- 5.96 mumol in normal subject and 0.30 +/- 0.29 mumol in asthmatics), metaproterenol increased mean SGaw by 89 +/- 33% in normal subjects and by 190 +/- 55% in asthmatics (p < 0.05, two-way analysis of variance). After histamine challenge (PM35, 2.92 +/- 2.49 mumol in normal subjects and 0.17 +/- 0.29 mumol in asthmatics), metaproterenol increased mean SGaw by 111 +/- 38% in normal subjects and 113 +/- 69% in asthmatics (p = not significant). Thus, for the same degree of bronchoconstriction, metaproterenol responsiveness was influenced by the dose of methacholine but not the dose of histamine. The differential metaproterenol response could be related to a functional antagonism between muscarinic and beta-adrenergic agonists.

Although performance of concomitant open heart and pulmonary operations has been described, there is general reluctance to perform pulmonary procedures in patients receiving cardiopulmonary bypass (CPB). Reasons for this include fear of excess bleeding caused by systemic heparinization, limited exposure afforded by median sternolomy, and alterations in the immune system caused by CPB that might lead to dissemination of lung cancer or infection. We have used CPB to facilitate operations on the lung in four patients who did not require concomitant cardiac surgery. In each case, lesions involving central pulmonary vessels precluded safe operation by conventional techniques. There were no complications related to the use of CPB. We believe that CPB can be a valuable adjunct in the surgical treatment of selected tumors and vascular malformations that involve large or central pulmonary vessels.

Congenital bilateral absence of the vas deferens (CBAVD) was once thought to be a distinct clinical entity, but genetic similarities in men with cystic fibrosis (CF) and CBAVD are described increasingly. We evaluated the clinical status, growth and nutritional state, and respiratory function of 18 men with CBAVD to determine whether these men with different CF transmembrane regulator (CFTR) genotypes may have clinical evidence of mild CF. Following a thorough history and examination, pulmonary function tests, sweat test, and renal ultrasound were performed. Genetic evaluation for 50 known CF mutations, screening for private mutations (single-strand conformational polymorphism and direct sequencing), and assay of the length of the polypyrimidine tract in the splice site acceptor of intron 8 was performed. A history of pulmonary disease was present in three, and an additional man had some features suggestive of malabsorption. Results of general physical examination and anthropomorphic measurements were unremarkable in all patients, with a mean (SD) body mass index of 26 (3). Pulmonary function tests of large and small airway function as well as lung volumes were normal in all except one whose results were consistent with moderate asthma. Five men were compound heterozygotes for CFTR mutations, four of whom had positive sweat tests (sweat chloride > 60 mEq/L). Twelve men were heterozygotes for CFTR mutations while no mutations were identified in one man. Although putative etiologic factors may suggest that men with CBAVD and CFTR mutations could be considered within the spectrum of clinical CF, the authors suggest that in men with CBAVD without any other clinical features of CF, the diagnosis of CF may not be made.

To determine whether supraventricular tachydysrhythmias (SVTs) occurring early after thoracic surgery for non-small cell lung cancer (NSCLC) are associated with poor long-term survival.

To determine the outcome of areas of ground-glass attenuation and assess disease progression on serial high-resolution CT (HRCT) scans of patients with biopsy specimen-proved usual interstitial pneumonia (UIP) and desquamative interstitial pneumonia (DIP).