Spontaneous pneumothorax rates following video-assisted thoracoscopic talc pleurodesis with or without resection of macroscopic bullous disease.

BACKGROUND: Recurrent primary spontaneous pneumothorax (PSP) is routinely treated by video-assisted thoracoscopic (VATS) talc pleurodesis (with or without localized resection of macroscopic bullous disease). There is a paucity of published data regarding durability of the procedure and the rate of recurrent pneumothorax after such surgery, and this has significant implications from a prognostic and employment limitation perspective. METHODS: Patients who underwent a VATS talc pleurodesis (with or without localized resection of macroscopic bullous disease) for the treatment of their second or subsequent PSP or a PSP were followed for recurrent ipsilateral pneumothorax and new contralateral PSP. Follow up was by way of telephone interview and medical record verification out to 48 months. RESULTS: New contralateral pneumothorax occurred in 7 patients (11.1%) in the talc pleurodesis plus wedge resection group and 2 (1.8%) in the talc pleurodesis only group. There was one case of recurrent ipsilateral pneumothorax in a patient who had no inflammatory response to talc insufflation. CONCLUSION: Video-assisted thoracoscopic (VATS) talc pleurodesis (and lung resection for macroscopic bullous disease) is a durable treatment for recurrent PSP. Patients with macroscopic disease have a significant risk of subsequent contralateral PSP.

Successful treatment of pulmonary mucormycosis in a renal transplant recipient with limited pulmonary reserve by combined medical and surgical therapy.

Mucormycosis is a rare opportunistic fungal infection in renal transplant recipients which is associated with exceedingly high mortality when inadequately treated. Risk factors for this infection include diabetes, neutropaenia and immunosuppression. We report a case of pulmonary mucormycosis in a renal allograft recipient with type 2 diabetes and limited pulmonary reserve. The patient was successfully treated with lobectomy and liposomal amphotericin B with preservation of pulmonary and allograft functions. Early recognition of this infection is warranted before dissemination, which carries a poor prognosis.

Defective lung macrophage function in lung cancer ± chronic obstructive pulmonary disease (COPD/emphysema)-mediated by cancer cell production of PGE2?

In chronic obstructive pulmonary disease (COPD/emphysema) we have shown a reduced ability of lung and alveolar (AM) macrophages to phagocytose apoptotic cells (defective 'efferocytosis'), associated with evidence of secondary cellular necrosis and a resultant inflammatory response in the airway. It is unknown whether this defect is present in cancer (no COPD) and if so, whether this results from soluble mediators produced by cancer cells. We investigated efferocytosis in AM (26 controls, 15 healthy smokers, 37 COPD, 20 COPD+ non small cell lung cancer (NSCLC) and 8 patients with NSCLC without COPD) and tumor and tumor-free lung tissue macrophages (21 NSCLC with/13 without COPD). To investigate the effects of soluble mediators produced by lung cancer cells we then treated AM or U937 macrophages with cancer cell line supernatant and assessed their efferocytosis ability. We qualitatively identified Arachidonic Acid (AA) metabolites in cancer cells by LC-ESI-MSMS, and assessed the effects of COX inhibition (using indomethacin) on efferocytosis. Decreased efferocytosis was noted in all cancer/COPD groups in all compartments. Conditioned media from cancer cell cultures decreased the efferocytosis ability of both AM and U937 macrophages with the most pronounced effects occurring with supernatant from SCLC (an aggressive lung cancer type). AA metabolites identified in cancer cells included PGE2. The inhibitory effect of PGE2 on efferocytosis, and the involvement of the COX-2 pathway were shown. Efferocytosis is decreased in COPD/emphysema and lung cancer; the latter at least partially a result of inhibition by soluble mediators produced by cancer cells that include PGE2.

Increased proteinase inhibitor-9 (PI-9) and reduced granzyme B in lung cancer: mechanism for immune evasion?

Cytotoxic CD8(+) T-cells mount immune responses to cancer via cytotoxic pathways including granzyme B. Cancer cells are also known to develop immune evasion mechanisms. We hypothesised that lung cancer cells would over-express the granzyme B-inhibitor, proteinase inhibitor-9 (PI-9) and down-regulate granzyme B expression by neighbouring CD8(+) T-cells. We investigated PI-9 expression in lung cancer cell lines, and primary lung cancer cells obtained at curative lung resection from cancer patients with/without chronic obstructive pulmonary disease (COPD). Granzyme B and PI-9 expression was also determined in CD8(+) T-cells from the cancer and non-cancer areas of resected lung tissue and from bronchoalveolar lavage (BAL). We then evaluated the effects of conditioned media from lung cancer cell lines on granzyme B expression and the cytotoxic activity of CD8(+) T-cells. PI-9 was highly expressed in lung cancer cell lines. Increased PI-9 expression was also observed in primary cancer cells vs. epithelial cells from non-cancer tissue or bronchial brushing-derived normal primary large airway epithelial cells. Expression significantly correlated with cancer stage. Significantly reduced granzyme B was noted in CD8(+) T-cells from cancer vs. non-cancer tissue. Granzyme B production by CD8(+) T-cells was reduced in the presence of conditioned media from lung cancer cell lines. Our data suggest that lung cancer cells utilise their increased PI-9 expression to protect from granzyme B-mediated cytotoxicity as an immune evasion mechanism, a function that increases with lung cancer stage.

Management of a large bronchopleural fistula using a tracheobronchial stent.

Bronchopleural fistula, one of the most serious complications following pneumonectomy, has a complicated treatment protocol and carries a high mortality rate. We present a case report of a 75-year-old female with squamous cell carcinoma of the lower lobe with positive peribronchial hilar nodes who underwent a right pneumonectomy. She represented with a large bronchopleural fistula one month postoperatively, eventually treated by a novel tracheobronchial stenting procedure.