2001 Volume 41 Issue 6 Pages 643-648
Objective: This study was designed to understand the pathogenetic mechanism of pleural carcinomatosis.
Patients and Methods: We collected 207 surgical cases of primary lung cancer and identified 43 cases with positiveintraoperative pleural lavage cytology (PLC). We then histologically examined the pulmonary ligament (PL), visceralpleura (VP) and parietal pleura (PP) in these cases and found that 24 cases belonged to either the p0 or p1 categoriesof the Classification of Lung Cancer of the Japan Lung Cancer Society. Unfortunately the surgical cases were unsuitablefor investigation of PL, because of severe operative manipulation involving the ligament. However, 15 autopsy cases of primarylung cancer and 63 of extrapulmonary primary origin were similarly investigated.
Results: Surgical cases: Positive PLC cases showed a statistically significantly higher involvement in lymphatics andblood vessels of the lung parenchyma and hilar lymph nodes, than cases with negative PLC (p<0.001). Autopsy cases: Varying degrees of pleural carcinomatosis were found in 8 cases (53.3%) of primary lung tumors, which were all adenocarcinomain 2 out of the 8 cases, however, tumor cells were found, only in the PL. In addition, varying degrees of pleuralcarcinomatosis were observed in 21 cases (33.3%) of extrapulmonary origin, in which combined PL involvement was onlyobserved in 5 cases. Furthermore, cancer cell clusters were found in the lymphatic cisterns of the PL in 29 autopsy cases (37.2%).
Conclusion: There was also evidence of permeation of tumor cells in the cisterns into the pleural cavity via adjacentstomas in the PL. The PL was found to be a site with numerous lymphatic cisterns with stomas in the thoracic cavity. As aresult, we consider that tumor invasion into the subpleural lymphatics might be a prerequisite for the development ofpleural carcinomatosis.
