Nonresolving pneumonia and rash in an adult: pulmonary involvements in Kawasaki's disease.

, talc not only causes a greater degree of apoptosis of lung cancer cells than bleomycin at equivalent concentrations, but it also demonstrates selectivity of action by sparing the normal mesothelium, which is not observed with bleomycin or doxycyline. Our in vitro observation was further supported by the discovery of a preserved layer of mesothelial cells despite an intense inflammatory pleural reaction in rabbits treated with talc [8]. Interactions between normal PMC and tumour cells are complex. An intact pleural mesothelium appears important for inciting the acute inflammatory response necessary for pleur-odesis by secreting pro-inflammatory interleukin-8 and vascular endothelial growth factor, and for developing pleural fibrosis by the production of transforming growth factor-b and basic fibroblast growth factor [8, 9]. ANTONY et al. [9] demonstrated that patients with extensive pleural carcinomatosis and minimal intervening normal mesothelium had significantly lower quantities of basic fibroblast growth factor in their pleural fluid, compared to those with limited disease who subsequently developed successful pleural symphysis. These findings suggested that a mesothelium free of tumour was necessary for successful pleurodesis [8]. A recent study also showed that an intact pleural mesothelium is critical in modulating the metastatic potential of cancer cells within the pleural space. Malignant cells secrete angiogenic factors that promote tumour growth, proliferation of endothelial cells and invasion of surrounding tissue by neovascularisation. Talc treated pleural mesothelium counteracts these effects by releasing endostatin, an antiangiogenic factor which may be responsible for tumour containment within the pleural space, and account for the improved clinical outcome of patients with malignant pleural effusions successfully pleurodesed with talc [10]. Our preliminary results support the use of talc for malignant effusion as it selectively causes apoptosis of lung cancer cells, and spares normal mesothelium pivotal for inciting inflam-matory processes necessary for pleural fibrosis. Studies are underway to compare the in vitro results with in vivo response, as well as to assess the impact on patient survival.