Surgical Strategy and Clinical Outcome in Patients with Bronchial Carcinoids.

Carcinoids are malignant neuroendocrine neoplasms showing good long-term survival after oncologic therapy. The study evaluated the influence of operative strategies and individual decision-making on the outcome and long-term survival in 222 patients with bronchial carcinoids. The patients underwent preoperative pulmonary function tests and bronchoscopy to facilitate surgical decision-making. A hundred and twelve tumors were detected endoscopically, including 32 in the main and lobar bronchi. We performed 5 isolated bronchus resections, 4 segmentectomies, 15 wedge resections, 10 pneumonectomies, 19 sleeve resections, 26 bilobectomies, 138 lobectomies, and 2 chest wall resections. Three patients were technically inoperable. Systematic mediastinal lymphadenectomy was routinely performed although most patients' computer tomography scans showed N0. A hundred and sixty-two patients had typical (155 N0, 7 N+) and 60 patients had atypical carcinoids (39 N0, 21 N+). There was no intraoperative mortality. The hospital mortality was below 2%. Overall, 1-, 5-, and 10-year survival rates were 99%, 94%, and 89%, respectively, in typical carcinoids. Atypical carcinoids show similar 1- and 5-year survival rates, but the 10-year survival rate was below 70%, decreasing in higher N-stages. The N-stage was the most important survival factor. In conclusion, bronchial carcinoids should be surgically treated the way lung cancer is. Anatomic resection and systematic lymphadenectomy are the treatments of choice. The availability of bronchoplastic techniques and preoperative assessment is essential for individual decision-making, focusing predominantly on postoperative quality of life.

Lung fibroblast repair functions in patients with chronic obstructive pulmonary disease are altered by multiple mechanisms.

RATIONALE: Fibroblasts are believed to be the major cells responsible for the production and maintenance of extracellular matrix. Alterations in fibroblast functional capacity, therefore, could play a role in the pathogenesis of pulmonary emphysema, which is characterized by inadequate maintenance of tissue structure. OBJECTIVES: To evaluate the hypothesis that deficient fibroblast repair characterizes cells obtained from individuals with chronic obstructive pulmonary disease (COPD) compared with control subjects. METHODS: Fibroblasts were cultured from lung tissue obtained from individuals undergoing thoracotomy and were characterized in vitro. MEASUREMENTS AND MAIN RESULTS: Fibroblasts from individuals with COPD, defined by reduced FEV(1), manifested reduced chemotaxis toward fibronectin and reduced contraction of three-dimensional collagen gels, two bioassays associated with fibroblast repair function. At least two mechanisms appear to account for these differences. Prostaglandin E (PGE), a known inhibitor of fibroblast repair functions, was produced in increased amount by fibroblasts from subjects with COPD, which also expressed increased amounts of the receptors EP2 and EP4, both of which signal through cyclic AMP. Incubation of fibroblasts with indomethacin or with the PKA inhibitor KT-5720 partially restored COPD subject fibroblast function. In addition, fibroblasts from subjects with COPD produced more transforming growth factor (TGF)-beta1, but manifested reduced response to TGF-beta1. The functional alterations in fibroblasts correlated with both lung function assessed by FEV(1) and, for the data available, with severity of emphysema assessed by Dl(CO). CONCLUSIONS: Fibroblasts from individuals with COPD have reduced capability to sustain tissue repair, which suggests that this may be one mechanism that contributes to the development of emphysema.