BACKGROUND: The intrapleural instillation of a sclerosing agent produces an inflammatory process frequently followed by pain. The treatment can include the use of analgesics or anti-inflammatory drugs. Previously, it was demonstrated (experimental studies) that corticoids and nonsteroidal anti-inflammatory drugs (diclofenac) reduce the inflammation and fibrosis produced by talc but not by transforming growth factor-beta or silver nitrate. The objective of this study was to determine whether parecoxib (COX-2 inhibitor) affects pleurodesis induced by talc or silver nitrate. METHODS: 140 rabbits received intrapleural injection (2mL) of 400mg/kg of talc or 0.5% silver nitrate. A subgroup of 70 animals received additional daily intramuscular parecoxib (1mg/kg). They were sacrificed at 4, 24, 48, 72h or 7, 14, or 28 days after the procedure. The pleural fluid was quantified; biochemical examinations (glucose, lactic dehydrogenase, and proteins) and immunologic dosages (interleukin-8, vascular endothelial growth factor, and transforming growth factor-beta(1)) were analyzed in pleural fluid and blood. Finally, macro- and microscopic pleura and lung studies were performed. RESULTS: Evaluation after 28 days demonstrated that parecoxib reduced pleural and pulmonary inflammation but not pleural adhesions. The changes were observed precociously (congruent with 72h) and were more evident after silver nitrate injection. CONCLUSION: Systemic parecoxib injection does not interfere with talc or silver nitrate pleurodesis. These results suggest that use of COX-2 inhibitors can be considered and depending of the results of other studies, recommended in human pleurodesis.
BACKGROUND: The intrapleural instillation of a sclerosing agent produces an inflammatory process frequently followed by pain. The treatment can include the use of analgesics or anti-inflammatory drugs. Previously, it was demonstrated (experimental studies) that corticoids and nonsteroidal anti-inflammatory drugs (diclofenac) reduce the inflammation and fibrosis produced by talc but not by transforming growth factor-beta or silver nitrate. The objective of this study was to determine whether parecoxib (COX-2 inhibitor) affects pleurodesis induced by talc or silver nitrate. METHODS: 140 rabbits received intrapleural injection (2mL) of 400mg/kg of talc or 0.5% silver nitrate. A subgroup of 70 animals received additional daily intramuscular parecoxib (1mg/kg). They were sacrificed at 4, 24, 48, 72h or 7, 14, or 28 days after the procedure. The pleural fluid was quantified; biochemical examinations (glucose, lactic dehydrogenase, and proteins) and immunologic dosages (interleukin-8, vascular endothelial growth factor, and transforming growth factor-beta(1)) were analyzed in pleural fluid and blood. Finally, macro- and microscopic pleura and lung studies were performed. RESULTS: Evaluation after 28 days demonstrated that parecoxib reduced pleural and pulmonary inflammation but not pleural adhesions. The changes were observed precociously (congruent with 72h) and were more evident after silver nitrate injection. CONCLUSION: Systemic parecoxib injection does not interfere with talc or silver nitrate pleurodesis. These results suggest that use of COX-2 inhibitors can be considered and depending of the results of other studies, recommended in human pleurodesis.